Note: This post follows Extraordinary claims require extraordinary evidence about Don Huber’s alleged letter to the USDA that claims a never before seen “micro fungus” is endangering all of agriculture.
While claims about “micro-fungi” are too extraordinary to even consider until extraordinary proof is provided (and preferably replicated by another lab and peer reviewed), Don Huber’s claims that Roundup (specifically the active ingredient glyphosate) weakens crops by binding minerals in the soil seems to have at least some merit, at least enough to be taken seriously and examined further.
Over the years since Roundup Ready (RR) crops have been released, independent researchers have conducted many studies to determine whether there is a specific problem with some crop varieties with the RR gene, with all crops with the RR gene, or with glyphosate itself. Overall, the research shows that there may be some concern about glyphosate reducing availability of some minerals when the soil is deficient in those minerals. The research hasn’t found a problem with the RR gene itself.
It is important to note that the stack of peer reviewed papers indicating glyphosate to be a problem with disease or yield is much smaller than the stack indicating there is no problem. We must look at the entire body of evidence, not just cherry pick one or a few papers, in order to get a clear understanding of what’s really happening. Happily, extension experts from multiple universities have summarized the research for us, but if you want to look for yourself, PubMed is a great place to start.
Claims of interactions between glyphosate and minerals
In February of 2010, Dr. Huber appeared in an article by Martha Ostendorf titled Are We Shooting Ourselves In The Foot With A Silver Bullet? in No-Till Magazine along with Bob Streit, an agronomy consultant in Iowa. That article is no longer available from the No-Till Farmer website, but thankfully a Biofortified reader found another source (linked from the article title). Another article written by Huber at about the same time is Ag chemical and crop nutrient interactions. In these document, a lot of claims are made that aren’t consistent with the majority of peer reviewed research on the subject.
Since 2010, Dr. Huber has continued publicly claiming that glyphosate binds up minerals in the soil, making the minerals unavailable to crops and increasing susceptibility to disease (specifically fungal disease), thus decreasing yields. He spoke to the Innovative Farmers Association of Ontario in March 2010, one of many talks he’s given on this topic. In February 2011, he gave a talk in Des Moines at a seminar organized by the same Bob Streit and Amie Brandy. Dr. Huber has published some peer reviewed studies to back up his claims as well.
Dr. Huber is not the only scientist that has found interactions between glyphosate and minerals. Back in 2007, Barney Gordon published some research in an industry newsletter indicating that glyphosate treated soybeans may require manganese fertilizer for optimal yields: Manganese Nutrition of Glyphosate-Resistant and Conventional Soybeans. Of course, this research was used inappropriately as “evidence” that genetic engineering reduces yields, but that’s another story.
Dr. Gordon and Dr. Huber’s work has been used eagerly by fertilizer companies and organizations that promote fertilizers to encourage farmers to apply minerals to their crops. For example, see Glyphosate and Micronutrients by Jim Halbeisen of Growers Mineral Solutions and Missing Micro Nutrients by Larry Reichenberger of ProfitPro (who sells liquid fertilizer).
Dr. Huber has published directly in fertilizer promotion materials, such as the Fluid Journal (sponsored by the Fluid Fertilizer Foundation): What About Glyphosate-Induced Manganese Deficiency? Dr. Gordon’s Manganese Nutrition of Glyphosate-Resistant and Conventional Soybeans was published in Better Crops which is run by the International Plant Nutrition Institute which encourages use of a variety of fertilizers.
Response from extension
Understandably, farmers have been actively pursuing more information from extension agents as soon as they hear about a possible decrease in yields with glyphosate use. University extension has responded with multiple documents and presentations to help guide farmers using known research and by conducting additional research. Extension agents have a unique ability to bring research directly to farmers and other people near the university and can quickly conduct field tests to help farmers make science-based decisions.
In February of 2010, Iowa State University Extension produced a great overview of the research that includes analysis of some papers of which Dr. Huber was a co-author: Glyphosate-Manganese Interactions in Roundup Ready Soybean by Bob Hartzler, Extension Weed Specialist and Professor of Agronomy. He concludes that manganese uptake varies depending on which soybean variety is being used, not on whether or not the RR gene is present. He also concludes that while it is known that glyphosate will bind to soluble manganese, this is only a problem in manganese deficient soils.
In November of 2010, Bob Hartzler released Glyphosate Interactions with Micronutrients and Plant Disease, with the conclusion:
Due to the complexity of the processes that occur within the root zone, it is impossible to completely rule out negative effects of glyphosate on mineral nutrition or disease development in GR crops. However, results from field research and our widespread experience with glyphosate on GR crops for over a decade do not indicate widespread negative impacts of glyphosate on these factors.
In April of 2010, University of Minnesota Extension put out a short commentary that also discussed Dr. Huber’s claims: Roundup and Manganese for Minnesota Soybeans. Extension agent George Rehm conducted experiments in Minnesota and found that additional manganese was not needed due to adequate manganese in Minnesota soils. The April commentary was actually a followup to a post about manganese from January of 2010, Magnesium In Minnesota, that attracted some critical commentary from none other than Bob Streit.
In January of 2011, Ohio State University Extension released a presentation (Flash needed) by Robert Mullen, extension specialist and associate professor, summarizing their work on this subject: Manganese / Glyphosate antagonism? Their research shows that applying manganese to soy does increase the concentration of manganese in plant tissues, but did not find that glyphosate caused decreases in yield or manganese. Adding manganese can cause yield increase or yield decrease depending on environment, specially soil type. They did find that soil type and pH causes significant differences in manganese uptake.
In February of 2011, Dr. Huber’s colleagues at Purdue University Extension put out a paper titled Glyphosate’s Impact on Field Crop Production and Disease Development that seems to be in direct response to the flurry of blog posts and “news” articles about Roundup that were spurred by Dr. Huber’s recent letter. While they don’t mention Dr. Huber directly, they do cite and express concern about articles that are credulous about Dr. Huber’s claims regarding glyphosate and plant and animal disease. They conclude:
Overall, the claims that glyphosate is having a widespread effect on plant health are largely unsubstantiated. To date, there is limited scientific research data that suggest that plant diseases have increased in GM crops due to the use of glyphosate. Most importantly, the impact of these interactions on yield has not been demonstrated. Therefore, we maintain our recommendations of judicious glyphosate use for weed control. We encourage crop producers, agribusiness personnel, and the general public to speak with University Extension personnel before making changes in crop production practices that are based on sensationalist claims instead of facts.
This isn’t the first time that Dr. Huber’s colleages have attempted to do damage control in response to “greatly exaggerated” reports by Dr. Huber about minerals and glyphosate. In April of 2010 Dr. Huber’s colleagues at Purdue University Extension released Glyphosate – Manganese Interactions and Impacts on Crop Production: The Controversy, referring interested persons to Iowa State University Extension. They state that high pH, high organic matter soils cause manganese to be less available to the crop whether or not glyphosate is present.
Update: Extension agents are still working to correct what they see as misinformation spread by Dr. Huber. Anne Dorrance, expert in soybean pathology and extension agent at Ohio State has a 14 March 2011 article in Ag Professional: Glyphosate Effects on Soybean Diseases. She directly assesses the claims that glyphosate use has increased incidence of disease, backed up with literature and her personal experience.
Have you seen any other extension or other articles by professional agronomists on this topic? Let us know and I’ll include them here.
Consider the data, not the source
I have read some claims that university researchers can not be trusted because many universities accept some grants from agricultural companies. Specifically, some bloggers have claimed that the Purdue extension agents’ scientific integrity is compromised, which is something that I think needs to be addressed, especially when it is clear that fertilizer companies and foundations are so eager to use Dr. Huber’s research. Potential conflicts of interest go every which way.
Purdue, like Iowa State and every other university, has strict standards of scientific and professional ethics. In addition, the amount of research funding granted by companies is small compared to funding from other sources. For example, at Iowa State, publicly available detailed reports of funding show that the research being conducted with corporate funding are far from the majority of funding and that most grants are extremely specific in scope. While there are isolated examples of inappropriate conduct of public universities regarding private companies or company interests, that is no reason to denounce every employee at every public university.
Instead of smearing the names of extension employees and researchers, we should examine the veracity of their work. We need to consider the data available. The identity of the source needs to be known in order to determine if a person has relevant expertise. We can look at the source to get a feeling for how much skepticism we need to apply. Go too far beyond that, and we get dangerously close to ad homs.
“He has published some peer reviewed studies to back up his claims as well.”
It is worthwhile to check this claim — go to Google Scholar and search with this string: “Don Huber” glyphosate
It looks like he has peer-reviewed work on this topic, but the papers are found on websites for lawn & garden stores, etc.
Anastasia wrote:
« Over the years since Roundup Ready (RR) crops have been released, independent researchers have conducted many studies to determine whether there is a specific problem with some crop varieties with the RR gene, with all crops with the RR gene, or with glyphosate itself. »
I take (some) exception at the word « independent ». We have to face an attack on science and regulation based upon the allegation that the scientists and regulators are not « independent ». Seralini and CRIIGEN, for instance, are fans of this kind of tactics. We do not need to play into their hands.
This is somewhat cured in the conclusion – which I fully endorse, and which can be adapted to skepticism applied to peer review – of a great piece.
I should probably have been more clear. There has been both independent research at universities (which is the sort of research I personally prefer to refer to) as well as corporate research (which isn’t necessarily less valid, but perhaps something to be a bit more careful about).
PS: Can you tell I am an extension fan girl? 😉
André,
I, too, have long been concerned by the use/misuse of the term, ‘independent’. I have noticed that the use of the term by the anti-people is fairly consistent, and generally indicates that the person to whom it is applied knows nothing about the field. That is, for them, the ultimate independence.
Consider: Mae-Wan Ho is a cosmologist. Vandana Shiva is a physicist. Erwina Ermakova is a neurobiologist. Francisco Chapela is a mycologist. Jeffrey Smith is a dance-hall instructor.
Without training in the field of agricultural biotechnology, they are almost completely innocent of anything which might subject them to the ultimate accusation: being ‘linked with’.
Monsanto might provide grants to agricultural colleges and universities, and sponsor research — but to my knowledge, Monsanto is not involved in cosmology, physics, neurobiology, mycology, or dancing.
And, since the anti-people focus on Kapitalism, AmeriKKKa, Korporations, globalization, natural harmony, feminist deconstruction of reductionary science, etc., they actually don’t need to know a durned thing about agriculture or biotechnology, anyhow.
If glyphosate does restrict Mn uptake by plants (while at the same time having no impact on yield apparently, at least in Mn sufficient condtions) then shurely this is a great victory for healthy soil everywhere as the mean ole plants can’t suck all the nutrients out of the soil and leave it dead – bacteria can chew on the glyphosate (yummy carbon, nitrogen and phosphorous) and get a nice batch of Mn as an added bonus.
I mean, isn’t the fact that plants suck the nutrients out of the soil the big issue with conventional Ag and “soil health” – we should be working on stopping ’em doing so, not making sure they can suck up more than they need. That way madness lies.
There seems to be some confusion as to how the review of a new chemical takes place. What often happens (in simplified, hopefully, layman terms) is that a limited amount of research is presented that indicates that something is OK. The product is approved, introduced, and the “beta testers” ie, the public, then put the product through normal use (ie “real world” testing). If problems are observed, then scientists go back to their research “drawing boards” and attempt to duplicate the observed problems under controlled conditions and explain what is causing the unexpected “real world” behavior.
If you read the enclosed paper, I feel that you will see an example of what I have outlined. The following 2010 publication that appeared in a respectable ( Published on behalf of the Society for Applied Microbiology) reviewed scientific journal and has a UDSA scientist as the second author (United States Department of Agriculture, Agricultural Research Service, Cropping Systems & Water Quality Research Unit, University of Missouri, Columbia, MO, USA).
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2672.2010.04864.x/pdf
In the introduction you find the reason(s) for doing the follow up research (what “real world” experience has indicated that a closer look is merited).
The reviewers (who are considered the “scientific peers” of the authors) may point out to the editor additional papers that should be included in this section.
Then the experimental details are give. The reviewers may suggest additions/modifications which result in further (normally minor) experiments or rejection of the paper.
The conclusion section wording is closely examined by the reviewers to ensure that the authors conclusions are consistent with the experimental findings.
Concerning manganese Fig 3, page 123 shows what the quantative effect of glyphosate application is.
Regarding affects of glyphosate on the plants themselves. Fig 6, page 125 shows the decrease in shoot weight as a function of applied glyphosate. Fig 5, page 124 shows the root weight for the same conditions.
If you are interested in what happens to the soy seeds, you may find this 2010 American Chemical Society reviewed scientific article abstract of interest (I have the full paper, but the ACS only makes the abstract available to the general public. I am allowed to e-mail a limited number of copies for educational purposes so if you have the background and interest please e-mail me a request for a copy with a short explanation corncerning your background and reason for the request. (Remember I will only be able to send a few copies.) kuska@neo.rr.com
Since this is in an ACS journal, your local university will probably have the journal.
http://pubs.acs.org/doi/abs/10.1021/jf904342t
Please note that this paper has authors affiliated with 2 USDA laboratories.
Agricultural Research Service, Cropping Systems and Water Quality Research Unit, United States
Department of Agriculture, Columbia, Missouri 65211,
)
Agricultural Research Service, Crop Genetics and
Production Research Unit, United States Department of Agriculture, Stoneville, Mississippi 38776
Henry – first glaring thing with both papers is that they’re conducted in the greenhouse in pots, making assumptions about performance in the field from performance in the greenhouse (where amongst other things bacterial recolonization is next to impossible) unreliable at best (if greenhouse was a good predictor of field performance then there would be no arguements about whether or not GMOs could drastically increase yield for instance)
It is also surprising to see that root biomass, shoot biomass etc are significantly reduced in both experiments – along with SPAD readings as one would expect this to cause drastic reductions in yield (less photosynthesis, less dry matter accumulation, less end season yield) – something not reflected in the yield data for soy despite the near ubiquity of the RR system in soy production in the US – if you look at yield data for the US and for Iowa at this link for instance and plot the data (hurrah for excels ability to separate data by space deliniation, and boo to tables that don’t copy correctly into excel in the first place) you’ll see that in soy there is a consistent increase in yield from 1960 through 2009 which rather casts doubt on the expectation that soy yields should drop considerably due to the use of glyphosate (unless you propose the rather bizarre notion that soy bean yields jumped spectacularly coincidentally with the introduction of RR but that there was a cancelling effect) – R squared values for the trends are .85 for the US trend and .71 for the Iowa trend (Iowa appears to have had 4 particularly bad years (each coincidental with bad US years but generally of higher magnitude in terms of displacement from the trend – damned weather) which reduce the R squared there.
Edit: Hopefully this works.
To insert images in the future, use this code (except with < instead of ( and > instead of ) and with the full image url including http where it says image url):
(img src=”image url” alt=”” /)
-Anastasia
Thanks Anastasia… I had thought that was what I had done… apparently though, not so much!
Other… unrelated question – how would one have no pic as avatar while having pics in the gallery – it is rather bloody bizarre of me to be a pumpkin all this time, particularly a pumpkin that I didn’t have anything to do with!
(and that is how to derail a topic completely!)
🙂 All you need to do is click on your name to link to your Community Page on Biofortified. Then click “More user pictures” and on that page you’ll find “Manage your photo gallery” where you can choose a main picture and an avatar. Of course all this only works if you are logged in.
Well yes but that rather presupposes I didn’t like the weird little dooberry that I had previously – it seems (unless I’m doing it wrong, and I often am) that I have to pick a pic, and as I don’t have any pics that I’d want to pick I’m forced to pick a pic I wouldn’t pick.
Perhaps I should get a pic of a pickled pepper, just to make things interesting.
“Text to Columns” is your friend, friend 🙂
Interesting tends, BTW.
As for avatars, they’ve gone to the dogs…
I guess I was too cryptic – although admittedly I learned to use text to columns specifically because of this… don’t tell anyone though…
That’s one reason why I think extension is so great. They typically do field studies that are obviously better than greenhouse studies in many cases. Soil type and composition has a HUGE effect on mineral availability to plants, absorption/binding of different fertilizer and pesticide treatments to the soil, and so on. We can still make general conclusions about some types of field research but when soil is involved, it’s best to get information from studies that were conducted near where you want to be farming – which is what extension does.
I do not want to “hijack” this thread. But since comments were addressed to me, I will give a short response to Ewan R.’s last post to me.
The first point of greenhouse studies being “unreliable at best” did not include any reviewed literature references. If you are correct, I wonder why the editors of 2 different journals and 2 sets of peer reviewers allowed the papers to be published in their present form.
Your utilization of that graph is interesting. The graph presents data from 1960 to 2010 that has a (crude) fit to a straight line. GMsoy was introduced in 1996 and the second “improved yield” form in 2008. What has happened to the yields between these two dates? When you look at the graph for this time period keep in mind that the adoption of GMsoy did not jump from zero to 100% in one year.
I looked for “yield” papers that examined GMsoy “field experiments” AND involved Extension university research that would allow viewing the entire manuscript, here is one:
http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1028&context=agronomyfacpub
I cite personal experience and experience of others – note that I didn’t say they were unreliable at best in general, just at predicting field performance. I don’t think you’d find anyone who does both greenhouse and field studies of plant performance who’d disagree particularly for traits as complex as yield (there’s at least one wheat paper which shows this spectacularly – I’ll dig it up tomorrow) – the data aren’t unpublishable, just not necessarily applicable to the real world.
Sorry but an R2 value of .8 is hardly a crude fit by any standards when looking at multi year field data.
Soy has increased gradually in that period. (blue dots are more telling than red, as they represent US yield – Iowa appears to have had a bad time at that particular juncture) RR2Y soy was only, afaik, broadly released last year and the acreage onto which it went wasn’t enormous so one wouldn’t expect to see a huge leap – my point is that you don’t see a yield effect which one would expect if all of a sudden plants were incapable of getting enough nutrition, or were photosynthetically impacted as those in your linked paper were – it may well be that glyphosate can kill off beneficials and whatnot in a closed pot environment – I would however suggest that jumping to conclusions about activity in the field is unwarranted – it does however provide the evidence that should lead to a grant to actually do the field study.
I’ll take a look at the paper tomorrow.
Henry Kuska:
This is often a function of the field of study. Agronomy, weed science and agronomic entomology, for example, typically require experiments be repeated in both space and time, and in the case of greenhouse work, a comparable field study be done. Looking at the first paper, I am not familiar with journal, but it would not be unexpected that microbiology, typically studied in the lab, would find greenhouse experimentation to be sufficient. I suspect that the topic had come up, however, as the authors make a point to mention a field survey paper citing apparent Fusarium increases in glyphosate treated soy. Someone, somewhere along the way thought it necessary to imply a broader perspective.
The study itself seems reasonably executed. While I would quibble with the dose response analyses themselves, it seems that they did induce a microflora response. That said, Ewan has a point regarding extrapolation of this to a wider setting. The environment, for example, was ideally set with water held to 80% field capacity, no intra or interspecific competition between plants, temperatures kept in a constant range with 12 hr light/dark cycles. Conditions that might well favor something like Fusarium, but not likely in the real world.
Overall, the results are intriguing and warrant further study, but I think the authors over reach in the title, abstract and conclusions; More appropriate would be “Glyphosate affects micro-organisms in rhizospheres of glyphosate-resistant soybeans under controlled conditions“
So I’m coming back at this with a little peer review on the effects of GR soybeans in agronomic use in (sort of…) the areas discussed in Henry’s first paper (Still haven’t read the second paper – I’m a bad bad person I guess – I’ll get to it!)
this paper Gives a brief overview of the use of transgenic corn and soy – there are conflicting studies cited on the yield effect of the transgene (note – not the herbicide itself) but I do think there is a general acceptance that the initial offerings in soy had a 0-4% yield drag (which if glyphosate impacted photosynthesis as negatively as the GH study suggests should be amplified to closer to 10% one would think) which explains the allure of RR2Y if nothing else
This paper in done in the field in Brazil suggests that using glyphosate increases the N uptake from soil – in the conclusion it suggests that this is because glyphosate inhibits bacterial N fixation although from the tables I would have to disagree with this assessment – the amount of N fixed per m^2 is similar between regimes but there is a large difference in the size of the plants which to me suggests that weed competition results in reduced quantities of available soil N which in turn means that a higher proportion of plant N will come from fixation – I also note that grain yield in the RR varieties sprayed with roundup are either significantly higher than hand weeded varieites/imazethapyr treated or are trending that way (for the double shot of roundup treatment (late roundup treatments can impact yield – I wonder if this treatment was on the late side?)
Certainly suggests that at least in the case of macronutrients the plants aren’t inhibited, and given the significantly higher dry matter accumulation one assumes that micronutrients aren’t limiting either (micronutrient limitation leads to sickly plants that can’t put on dry matter (or don’t because they sense low nutrients and realize that getting bigger means getting deader (to anthropomorphize horribly!))
Which rather begs the question – is reduced nutrient uptake a good or bad thing if yields don’t actually change? I’d posit it’s a good thing (I believe the authors of the 2nd paper would agree) as you leave more in the ground (whether or not more is left in the ground in their method isn’t clear – I personally think the weeds were sucking up that difference, but that’s not founded on anything other than armchair science) and would happily predict that if you can find a gene (or combination thereof) that’d have a corn plant take up 30% less N and yield the same as its isogenic control you’d have a $500M+ product on your hand (at the very least you could retire on the licensing fee you could charge Monsanto, Pioneer or Syngenta to test it fully after you run some proof of concept experiments)
Back to the U.S. yearly Yield data. For the years that GM soy was available (1996-2009) the best fit linear equation is Y=0.2949(X) – 551.76. The R(squared) is 0.2575.
What does this mean? The slope (yield improvement per year)is much lower than the slope for the total yield data presented earlier in this thread (0.3761). This suggests that the annual yield improvement has dropped since the introduction of GMsoy. I say “suggests” because with an R(squared) of 0.25, I feel that this data is not worth discussing in a quantative way.
Back to a discussion of the topic of this thread: “Does glyphosate restrict crop mineral uptake?” see: the following USDA scientist’s 2009 reviewed scientific paper, “Glyphosate and glyphosate-resistant crop interactions with rhizosphere microorganisms”
http://etmd.nal.usda.gov/bitstream/10113/35795/1/IND44260932.pdf
To add a little more to the discussion – I encountered a technical paper by Benbrook (hardly a non-partisan source, but given that he’s the enemy or whatever I think I can cite him without being accused of whatever it is I might be…)
Evidence of the magnitude and consequences of the Roundup Ready soybean yield drag from university-based varietal trials in 1998
Which details yield drag in RR soybeans across a ton of university trials – what strikes me however is that across the board the numbers are significanly whooping the ass of the national average, which in the late 90’s was sitting around 38-42 Bu/Ac – nothing in his paper is even close to this value which to me suggests that the insertional effect impacts the intrinsic yield of the bean, but this difference may not be seen if the bean isn’t grown in conditions which allow it to reach the intrinsic value (which was a distinction made by another dear friend of the GMO lover – DGS (laziness forbids more than a shortening as I can never remember the guys full double barreled name)) – which would, I feel, explain why you don’t see a change in the yield graph above despite the yield drag of RR1 being a very real thing in near – perfect agronomic conditions. (you’ll note the values for most trials in Benbrook’s paper exceed the national average in 2010 also, which is testimony to the awesome job done by university farms at keeping their fields in tip-top shape, but also illustrates that farmers operate outside this perfect world as it costs too bloody much to do)
I need to interject here. What you guys are doing is not really appropriate. The variability in this data relative to the short time spans you are extracting from the larger set is too large to say anything definitive. I suspect that the slopes you are reporting are not even significant (compared to zero) and, hence, interpreting there sign and magnitude is pointless. Given the full data set, things are fine, but trying to extract slopes or correlations for these short time spans is not possible to do accurately without further information (such as the variability associated with individual data points). Essentially, this data tells us little to nothing about changes between 1996 and 2009 without interpreting those years in the context of the full time line.
I would also concur, and add that
a) He started it (wah!)
b) This is exactly what climate change denialists do, so I deserve a smack on the wrist
c) Toldja I needed you to keep my statsy math stuff in check.
Or something!
Henry – I’d have to concur with your Huber comments on Google Scholar – I tried the search myself and didn’t come to the conclusions stated above about the articles appearing in lawn and garden stores etc anyway.
Henry – Taking it decade by decade, rather than 38 years vs 11 (which is going to alter R^2 quite significantly) you get
60’s .32x-600 R^2 0.55
70’s .28x-534 R^2 0.13
80’s .37-713 R^2 0.14
90’s .32-616 R^2 0.14
00’s .64-1257 R^2 0.37
or
00’s with ’03 removed as it looks like a huge outlier – bad year environmentally for soy?
00’s2 .46-878.53 R^2 .42
while there are some slight differences in slopes the decades with the biggest slope is the 00s regardless of whether or not the ’03 data is included (inclusion increases the slope enormously) So no, your assumption that the slope is lower doesn’t hold when the comparison is fair (equal size of grouping) (excluding 03 for your analysis changes the slope to .3083, which while still lower than the average isn’t that far removed from most decades performances other than the 80’s or the 00’s (so one decade either side of adoption did significantly better)
The linked paper there makes a much stronger case on changes in the bacterial ecology due to use of glyphosate – the question still remains however – if it doesn’t effect plant productivity (and I see no evidence that it does) does it matter enormously? If the plants are as productive but take up less nutrients (therefore leaving more in the soil, and I don’t believe that the paper shows differential nutrient uptake, just altered soil ecology – if enough Mn remains that the plants are healthy then does it matter whether it is available or not?)
To tackle your paper on soy cultivars and reduced yield – couple of points – first, nutrient availability isn’t established here, and the suggestion is that it is the modification itself that is causing yield differences (yield drag due to transgenic insertion isn’t anything to do with glyphosates capacity to alter nutrient uptake), second it is interesting that the within group comparisons only show 2 cases where there is a significant yield difference between the control and the transgenic and one of these cases is only a single year entity – so out of 5 direct comparisons only 2 were sig different and one of these was only in a single year – you’ll also note that transgenic comparisons (non-sister lines) can perform just as well as the high yielding checks.
Also, for clarity – the paper says nothing about the effects of glyphosate on nutrient availability as the test was fair in that all cultivars were treated the same (ie no glyphosate use on the plants as that’d skew the yield results pretty badly)- so any yield differences here don’t actually support the notion that glyphosate does anything at all, merely that yield drag is potentially an issue (but not in all lines all the time)
Because I’m an enormous dork…
Yeah, an enormous dork who can’t make img tags work even when explicity shown how!
pdiff, thank you for your comments regarding the yearly U.S. yield data. But, I do not understand why you said “you guys” as I thought I was saying the same thing.
“This suggests that the annual yield improvement has dropped since the introduction of GMsoy. I say “suggests” because with an R(squared) of 0.25, I feel that this data is not worth discussing in a quantative way.”
I am sorry if my statement was misunderstood. For the record I completely agree with your conclusion.
Agreed. I said you guys because both gave examples extracting smaller data sets from the larger. Your conclusion was correct, however 😉
The following was stated earlier in this thread:
““He has published some peer reviewed studies to back up his claims as well.”
It is worthwhile to check this claim — go to Google Scholar and search with this string: “Don Huber” glyphosate
It looks like he has peer-reviewed work on this topic, but the papers are found on websites for lawn & garden stores, etc.”
H. Kuska comment. Anything put in quotes has to be found exactly to be reported. Scientists normally do not publish under their full first name. Also, they would normally use their middle initial (unless their name is so unusual that the middle initial is not needed). Further problems arise in using the quotes “D. M. Huber”, “D.M. Huber”, and “DM Huber”, “D M Huber” plus probably other variations (I have problems when my Russian work is translated) will miss hits found by the other combinations.
To be safe I suggest using Huber and glyphosate as the key words. Then, look at information in the abstract such as the author’s affiliation to see if the hit can be rejected.
http://scholar.google.com/scholar?q=huber+glyphosate&hl=en&btnG=Search&as_sdt=1%2C36&as_sdtp=on
If the abstract is too vague, you often can find the actual journal at:
http://www.e-journals.org/botany/
Another question for Ewan or others: In the plot above, why does the variability of the US trend suddenly increase post ’73? Was there a change in how these yields were measured (collated from larger sets I’m guessing). Maybe a change in how things were reported?
I was wondering that myself, I’ll ask a few folk who know Ag backwards and forwards and see if I can get good details.
Could be what you’re saying, 70’s could be the oil crisis making inputs mad expensive? Seems to really be the 70’s and early 80’s which are wildly fluctuating and then things calm down somewhat into the 90’s and 00’s (although not as steady as the 60’s) – there was a massive uptick in acreage in the 70’s and early 80’s – perhaps new adopters got spotty performance? (baseline for the US is 22M acres in 60, 40M by 70 up to 70M in the mid 80’s followed by a slump then a recovery in the late 90’s.
All the above is highly nonsensical speculation though and should be taken with a pinch of salt.
I feel it is very confusing (even sometimes misleading) not to have the posts appear in chronological order.
True. Chronological ordering can be effective in a flat thread, but in a multiple-thread section like this, it seems to work well where subtopics are kept together. The problem I have with that is finding new comments that are buried somewhere in the middle. Perhaps a flag indicating newness could be indicated.
I can see if there is a plugin for wordpress that can flag new comments – it might be rather useful!
I feel that this article should be brought to the groups attention.
http://www.animalwelfareapproved.org/2011/03/04/gm-crops-further-cause-for-concern/
A bit of misdirection in this article. First we get the author correctly stating:
Then we get the conclusion:
Reminds me of “fair and balanced” from elsewhere. The reality is this is really not a GM issue. Roundup tolerant crops were around and used before GM versions and would, therefore, have the same issues. GM crops could all disappear tomorrow, and the seed companies would still be pushing RR varieties developed through other techniques. This should be about the effects of glyphosate, not GM. But the author here isn’t interested in that.
Uhhhhh …, so what’s the problem here? What “data”? He claims there is a new pathogen. So, go find it. The burden of proof is on him, not anyone else. And since this is a glyphosate issue, not proprietary GM technology, he should have no trouble collecting data or carrying out research, as implied by this author:
Science is rewarded by acclaim from discovery. If Dr. Huber is this sure he is correct, he (and every other pathologist worth the title) should, could, will be out there chasing the evidence. Until then, it’s just his opinion. Without evidence, the USDA did what they should, rely on the available science.
“After all, he’s just doing his job”
Someone needs to look up the meaning of the word ‘Emeritus’!
Must admit I’m eagerly awaiting Huber’s publication on this new-to-science organism. Maybe it will be in the same edition of Nature as the now long-overdue paper from Alexey Surov and co-workers 😉
Jonathan
What I find astounding in this mess is the claim that nearly half of a herd of 1,000 cows aborted.
A result like that would be impossible to cover up. It would make its way into the news regardless of any precautions relevant to publication prior to peer review.
I’m sticking with the theory that this whole thing is a grand hoax until I hear otherwise.
I suggest the following recent articles if one is interested in where the published science is now concerning gm crops:
Inventory of observed unexpected environmental effects of genetically modified crops, a non peer reviewed report that was commissioned by a group that advises the Netherlands government about the environmental concerns of genetic engineering (PDF).
The second paper is still “in press” but the abstract is available. J.L. Domingo, J. Giné Bordonaba. A literature review on the safety assessment of genetically modified plants. Environment International xxx (2011) xxx–xxx. I have a pre publication copy. It is my understanding that I do not have the right to distribute it.
Editor’s note: hyperlinks and clarification of what the links are was added.
I’ve just read the summary of the Netherlands report for now. They essentially say that while there have been some environmental effects, most have been anticipated or just make sense based on what we know about each transgene. Overall, glyphosate resistant and Bt crops have had a positive effect on the environment through reduction of more harmful herbicides and reduction of insecticides respectively. I do take issue with their conclusions that glyphosate tolerant crops are less disease tolerant – as the studies I’ve looked at show any such effect to be caused by glyphosate and not by genetic engineering. Perhaps they explain further in the report.
Edit: yep, they do!
More data is always better than less so when the authors of the Env Int article call for more studies I won’t say nay. However, they say “Published literature on GM plants over the past 4 years concerns only 3 products.” which indicates to me they haven’t got good coverage of the literature. We shall see when it comes out.
Another new paper coming out:
http://www.enveurope.com/content/23/1/10/abstract
Seralini’s “creative” use of statistics and known biases have been discussed elsewhere on Biofortified, I won’t go into them here. I hope Mary or another commenter with more experience with feeding studies than I will discuss the article (perhaps in a guest post?).
Really, Seralini again? Lets guess, he’s expounding the differences he saw in his previous 2 papers again and adding a couple more papers which didn’t actually find any real differences, jsut the normal couple of statistically significant oddballs you’d expect to see, and shouting booga booga about it.
One hopes this is his swansong considering his recent anti-science education statement.
For background information, Huber’s 2010 report.
http://u-trough.com/docs/Articles/Fluid%20Fert%20%202-10.pdf
That report was already linked to in my post, in the first paragraph under “Claims..”.
Perhaps someone has some comments on the following:
http://www.aaemonline.org/gmopost.html
The only citation to this paper found by Google Scholar is in Chinese. The automatic translation did not yield anything that I could see as relavent.
Seralini has recent comments please see the following 2010 communication.
http://home.biolsci.org/v06p0590.htm
It’d be especially helpful to the conversation if you’d post a few thoughts about or a summary for a source rather than just posting a naked link.
The AAEM is using the same old debunked studies to support their claims, and as such isn’t worth anyone’s time. They cite Jeffery Smith for goodness sake.
I’m fine with Seralini’s proposal for better designed tests. There are plenty of experts in toxicology out there who can analyze current animal testing methods and recommend better ones, and we should get them to do that ASAP. But he’s basically saying “the tests might have false negative results so it’s ok for me to focus on what may be false positives and crow about them from the rooftops”. It’s not ok.
The following was stated concerning the March 1, 2011 review paper by Seralini et.al. that I linked to on March 5, 12:53 pm. “But he’s basically saying “the tests might have false negative results so it’s ok for me to focus on what may be false positives and crow about them from the rooftops”. It’s not ok.”
H.Kuska comment. Please look at the link provided as to what the abstract approved by the the editor after reviewer input states that the review is saying.
If you are concerned about where this was published please see:
http://www.enveurope.com/about
Please remember/consider the Precautionary Principe.
I don’t see any editorial comments from the journal anywhere, so I don’t know what you mean.
An abstract is just a summary, I like to read the paper whenever possible. In the section “Debate on statistical tests” of this paper:
And then they go on to say why they think their stats are better and why they think their interpretation of the data is correct. I am not alone in disagreeing that these are superior methods, and if the methods are indeed problematic then the conclusions are as well.
As for the precautionary principle, I think we must be cautious about any ideology that does not consider the impact of both acting and not acting. For some discussion that is far more eloquent than I could ever provide, see bioethicist Clark Wolf’s Cost of Caution.
In the case of RR crops we have to consider the overall negative impact and the overall positive impact. The document “Inventory of observed unexpected environmental effects of genetically modified crops” that you posted seems to do a good job of doing this. Do the negatives outweigh the positives? I do not think so, but I’m always ready to accept solid data that I can use to reevaluate my conclusions. A hotly debated statistical twisting does not seem like solid data to me.
I also am interested in documented cases of positives. The so called “yield advantage” in the “real World” has been brought up in this thread. I feel that I was successful in showing that the data presented did not support a yield advantage. I then presented University of Nebraska data to support a real world example where there was a reduction. I hope it is clear to the readers that all that has been established is that under some conditions there has been reported a “yield advantage” under other conditions there was either no advantage or a disadvantage. This is important because in order to feed an expanding population addition land (normally/often? poorer will have to be utilized.) We now have have a choice of varities to select from that nature has conditioned over centuries to exist in various condition such as low mineral content, drowth, temperature, sunlight, etc.
Please see the following recent reviewed scientific paper titled: Plant immune system incompatibility and the distribution of enemies in natural hybrid zones which I intended to show what (sometimes/often?) happens when new hybrids are formed. In nature, natural selection eliminates these “unsuitable hybrids”. If they are gmos that do not have the ability to prosper in the variability of a given local environment, people may starve (crope failure).
The concern is that the spread of the non “nature developed” GMO genes through pollen release(which “poisons” the gene pool) will leave us without the ability to adjust quickly to nature’s “challenges”.
“One of the points that there is probably no question about is that GMO farming is “easier” (requires less manpower). Unfortunately, manpower is not the limiting factor in much of the world where hunger is a major problem.
Please see the following reviewed 2011 paper by two US scientists from two US universities, Department of Environmental Studies University of California, Santa Cruz, USA and Community, Agriculture, Recreation and Resource Studies Michigan State University, USA.
http://www.eee.hku.hk/~ccst9004/Notes/CaseStudy-GMCrops-DowdUribe2011.pdf
I assume that water can be considered as a “mineral” for purposes of being included in his thread. (Of course it is not a mineral in the geology sense.)
The following quote is referenced below. “at later stages the stems were dryer after Roundup application”
http://tools.laba.lt/marc/getobj.php?obj=LT-eLABa-0001:J.04~2006~ISSN_1392-3196.V_93.N_1.PG_22-32
Concerning the comments about the wording in the abstract: “I don’t see any editorial comments from the journal anywhere, so I don’t know what you mean.”
In a reviewed accepted scientific paper everything written in the paper (particularly the abstract) was subject to scrutiny by the reviewers who send their comments to the editor. The editor then decides reject, send the manuscript back for revision, or accept the paper as submitted.
Thus, any statement that you chose to challenge has been through the review process. You can of course prepare your own manuscript and submit it as a communication or letter to the editor as no review process is perfect. Your manuscript will also be subject to the review process.
To create a link, select the text that you want to have the link attached to, then click on the blue “link” button above the comment box. Paste in the link, click ok. This should work regardless of link length. You can also enter the HTML tags yourself, but be careful to close all tags or strange formatting can happen including disappearing text.
On yield:
There are 2 parts to yield. The first part is the ability of a plant to produce more of what you want, and the second part is the plant’s (or the farmer’s) ability to protect the yield. Yield itself as in producing more is a complex multigenic trait that is best improved with breeding (there may be exceptions where a single gene can be overexpressed with genetic engineering to increase yield). Yield protection includes things like disease resistance and insect resistance as well as ability to withstand stress. Yield protection can include both bred and genetically engineered traits. From the farmer’s side, yield protection can include removal of pressure from weeds and insects (and addition of fertilizer to increase yield but response to fertilizer is a result of breeding). So, the yield gains we see come from both breeding for increased yield and the biotech and bred traits that help protect that yield (and methods used by farmers).
If unrelated pollen “poisons” then gene pool then we’re poisoning things just fine without genetic engineering. However, we know that introducing unrelated germplasm is actually often beneficial, something that breeders can use to improve traits from yield to disease resistance and beyond.
Gene flow and hybridization can be good for plant populations, it can be bad, and it can be neutral – whether or not genetic engineering is involved. The paper you cite has nothing to do with genetic engineering but shows that hybrid plants in their specific test situation fare worse than the parents. Should we erect barriers to keep these plants from intermating? Should we prevent movement of germplasm from one place to another? No. Of course that would be silly. The offspring that are well suited for that environment will survive and the ones that aren’t won’t, whether in natural populations or due to human induced conditions.
As for “gmos that do not have the ability to prosper in the variability of a given local environment” – do you think it would make any sense to take a plant variety that does well in Florida and try to grow it in Montana? Can we take a variety that grows well in Iowa and expect it to grow well in Nigeria? Whether nor not genetic engineering is involved we can expect that varieties that aren’t adapted for the local environment will not do well. That’s why seed companies don’t just sell one variety. Even if one managed to get germplasm unsuited for a local environment into an area, those genes wouldn’t last long. For a fairly simplified discussion of gene flow and its consequences, see my post Those naughty plants!
Genetic engineering is a process that can be used to develop different traits. Any conclusions we come to about herbicide resistance, for example, may not apply to other traits. Resistance to herbicides is obviously not a trait that would be useful for low-income farmers who can’t afford herbicides in the first place. Bt on the other hand, does not require additional inputs so would be useful to a low income farmer – if the crop was under pressure from the insects that are affected by the Bt protein.
In the case of Bt cotton in Burkina Faso (again, if you would provide at least a title instead of a naked link that would be really really nice, pasting the author names really isn’t useful) the wide climatic variability means that a single variety introduced (genetically engineered or not) into the area most likely would not do well in all micro climates. What they should have done is backcrossed the Bt gene into the locally adapted varieties and then they’d have both Bt and the benefits of being adapted for each microclimate.
Has nothing to do with genetic engineering. As I described in this post, there may be effects of glyphosate with mineral uptake (yeah, I’m not comfortable with your water=mineral thing here) but that is due to the herbicide not to the resistance gene or the genetic engineering process.
I understand how the review and editorial process works. It doesn’t mean that the reviewers or editors accept every statement in a paper that is accepted, which is what you seem to be implying. There isn’t any ownership of ideas or approval of ideas implied in the process at all. In addition, many papers get through the process with mistakes, which is why in many ways it is futile to pick apart a single paper rather than looking at the full body of literature on a subject. Disagreeing with a statement of a paper or the entirety of the paper isn’t a disagreement with the reviewer or editor, though we may argue whether the review process for a given paper was stringent enough.
The following was stated: “It doesn’t mean that the reviewers or editors accept every statement in a paper that is accepted, which is what you seem to be implying. There isn’t any ownership of ideas or approval of ideas implied in the process at all.”
H.Kuska reply. Regarding editing, here is one set of instructions that in my experience as both a reviewer for a number of different journals and an editor, (board of editors Mag. Res. Rev. no longer published) are pretty typical.
If you see words such as “may” or “suggests” in a conclusion section or an abstract, there is a possibility that the editor required a softhening of a too strong statement/conclusion that was not merited by the data (according to the opinions of one or more of the reviewers).
The following was stated: “Should we erect barriers to keep these plants from intermating? Should we prevent movement of germplasm from one place to another? No. Of course that would be silly. The offspring that are well suited for that environment will survive and the ones that aren’t won’t, whether in natural populations or due to human induced conditions.”
H. Kuska reply. Setting up a “straw man”?????
Perhaps I did not make it clear that the difference is that in the natural formation of hybrids, every hybrid is genetically different (every hybrid has a unique set of genes). Some /many/most? may not survive or they will be “weak plants” as the 2 immune systems not only are normally not additive but actually fight against each other. (In addition to my cited literature I base that statement on my experience hybidizing roses.)
When a farmer plants his/her field with a gmo product, he/she may be planting a variety that does not have a well “tuned” immune system for his/her long term conditions. He/she is risking the crop (as indicated in the literature, the crop failure may not occur in the first year but may be in a later year when a required mineral is depleted or there is less rainfall (this is where the water article fits in. Why use a gmo glyphosate resistant product if you are not going to use glyphosate?), etc. I gave a literature reference that scientists from 2 respected universities voiced a similar concern in a reviewed scientific journal. Unfortunately, the suggestion that was given for their concerns: “What they should have done is back crossed the Bt gene into the locally adapted varieties and then they’d have both Bt and the benefits of being adapted for each micro climate.” simply does not normally work in several generations of crosses (this can be understood by reading the paper that I cited that “(shows that hybrid plants in their specific test situation fare worse than the parents.” It would normally take a very large number of generations of crosses and even then there would be no guarantee of success.
Henry:
Why would this be unique to GMO? Any bred crop (or animal) would be susceptible to these types of problems. GMO, in fact, promises the ability to quickly breed around such difficulties.
This wasn’t a straw man at all. You are implying that allowing plants to cross introduces too many unknowns. I took that to the logical conclusion, that’s all.
The following was stated: “in fact, promises the ability to quickly breed around such difficulties.”
H.Kuska comment. Please cite references. I thought that I was presenting points that it is/will be very difficult “to quickly breed around such difficulties”.
Some background reading:
“Conclusions and future prospects
Although many exciting insights have emerged from
recent research on plant defense signaling, our overall
understanding of the process is still fragmentary. For
example, we still know very little about the structural
basis of pathogen recognition. In fact, we are less sure than
before about what R proteins actually recognize (Avr
proteins, modified guardees, or complexes that include
both?). Furthermore, many gaps remain in our models of
the defense signal transduction network and these must be
bridged before we can design truly rational strategies to
activate the network. Nevertheless, useful applications
are already being developed from our relatively limited
knowledge base and others will undoubtedly follow as our
level of basic understanding grows. In the short term, we
expect that additional useful R genes will be cloned and
that models of resistance signaling developed in Arabidopsis
will continue to be evaluated for applicability in crops [49]. We also anticipate the application of functional
genomic tools to disease resistance [50], which will greatly
accelerate the pace of discovery and provide new insights into interactions between defense signaling and other plant
processes [51]. In the longer term, a detailed understanding
of the structural basis of recognition will enable us to approach the holy grail of designing R proteins that recognize essential virulence factors (or important guardees).”We emphasize that the problem of disease resistance is being addressed on many fronts – this review covers only a
subset of the exciting approaches being explored [2]. Given
the diversity of strategies that pathogens use and their
ability to rapidly adapt, it would be rash to predict the
development of a magic bullet for durable, broad-spectrum
resistance. However, it is reasonable to expect a forthcoming
array of sophisticated weapons that will provide
effective protection in certain contexts, when judiciously
integrated with other control measures.”
“How many maize/corn genes have actually been studied? (Not a lot)”
http://www.jamesandthegiantcorn.com/2010/02/22/how-many-maizecorn-genes-have-actually-been-studied-not-a-lot/
“New plant species arise from conflicts between immune system genes”
http://blogs.discovermagazine.com/notrocketscience/2009/08/02/new-plant-species-arise-from-conflicts-between-immune-system-genes/
It’s true, there is a lot we don’t know. The thing is, not knowing everything really isn’t a good example for not doing something.
Regarding complex in-plant gene interaction, we would do well to consider David’s recent Biofortified post about omics in genetically engineered vs non genetically engineered plants. While the omics approach is likely not yet developed enough for use as a regulatory tool, the 44 studies reviewed showed greater changes in RNA, protein, and/or metabolites between conventionally bred varieties and between genetically identical plants grown in different environments than between genetically engineered plants and their isolines. How’s that for unintended effects, now?
You are neglecting genetically engineered traits that bypass all the complex pathogen response mechanisms such as RNAi. It is entirely possible to quickly develop a genetically engineered disease resistance trait for a disease it might take a decade to breed for. It’s also possible that some crop diseases it would be easier to breed for. Again, genetic engineering is a tool, and like any other tool it isn’t always the best for a job while for other jobs it is the best.
Thank you for the lead to the “omocs” Plant Physiology very recent actual full paper link.
I could go into a discussion of the various “possibilities” available for wide crosses in hybridizing, as I have found this area a very interesting read. My own experience is with the gamma cell that I had in my laboratory. I produced “monsters” (if the roses lived). Of the few “monsters” that lived none survived the first winter. By monsters I do not mean large plants, I mean twisted, almost not recognizable lifeforms similar to what was observed around atomic bomb explosion test sites. Another interesting (to me) example in the rose literature is the succesful crossing of a rose with an apple. This is from memory so I cannot give the number of hybrids that survived but at least one did. It/they? was/were? completely sterile and apparently had no traits of interest. It was done early (in the 1960s ?) by a commercial rose company.
The final statement in the abstract of the recent “omocs” Plant Physiology paper is consistent with the Precautionary Principle:
“Mandatory use of “omics” techniques in reglementary GE food safety assessment cannot be recommended. More basic research is required before non-targeted large-scale methodologies can be internationally certified and accepted.”
No, that is not PP. They’re just saying the technology/methodology of the various omics is not ready for prime time yet.
Henry,
You have mentioned the precautionary principle here twice now. There are many definitions and interpretations of the PP. Can you provide a statement of how you see this applied in regards to GE?
As a side note, how would you view your own research via Gamma Cell (assuming you mean radiation treatment here) in light of the PP? How did you know it was safe?
I have not neglected RNA interference (RNAi) in my reading and in discussions. For example:
“Posted by henry_kuska z5 OH (kuska@neo.rr.com) on Sun, Nov 15, 09 at 15:21
One of the easiest ways to catch up in a new (to the reader) field is to read recent Ph.D. Theses in the field. Each thesis normally has an historical section at the beginning which covers the pertinent literature with much more detail than is allowed in a published, reviewed paper. The link below will download a 2005 thesis titled:
“Antiviral RNA silencing and viral counter defense in plants”
I should warn you that it is a long download and took me 4 or 5 tries as my server kept timing out.
In Chapter 4 there is an interesting tie between human flu virus and plant viruses:
“RNA silencing comprises a set of sequence specific RNA degradation pathways that occur in a wide range of eukaryotes, including animals, fungi and plants. A hallmark of RNA silencing is the presence of small interfering RNA molecules (siRNAs). The siRNAs are generated by cleavage of
larger double stranded RNAs (dsRNAs) and provide the sequence specificity to degradation of cognate RNA molecules. In plants, RNA silencing plays a key role in developmental processes and in control of virus replication. It has been shown that many plant viruses encode proteins, denoted RNA silencing suppressors, that interfere with this antiviral response. Although RNA silencing has been shown to occur in vertebrates, no relation to inhibition of virus replication has been demonstrated to date. Here we show that the NS1 protein of human influenza A virus has an RNA
silencing suppression activity in plants, similar to established RNA silencing suppressor proteins of plant viruses. In addition, NS1 is shown to be capable of binding siRNAs. The data presented here fit with a potential role for NS1 in counter-acting innate antiviral responses in vertebrates by sequestering siRNAs.”
“(Posted by Henry Kuska [email] on Sat, Jun 4, 2005)” I posted the following:
“The following 2 very recent papers describe where the field is and where it expects to go in the near future. The first is the paper most applicable to explaining why all roses do not get infected (” This mechanism is conceived as a natural antiviral defense system in plants that is activated as a response to double-stranded RNA (dsRNA) formed during virus replication. “).
Title: RNA interference as a new biotechnological tool for the control of virus diseases in plants
Authors: Tenllado, Francisco; Llave, Cesar; Diaz-Ruiz, Jose Rarnn
Authors affiliation: Ctr Invest BiolDept Biol Plantas, CSIC, Ramiro Maeztu 9, Madrid, 28040, Spain.
Published in: Virus Research, volumn 102, pages 85-96, (June 2004).
Abstract: “RNA silencing occurs in a wide variety of organisms, including protozoa, fungi, plants and animals and involves recognition of a target RNA and initiation of a sequence-specific RNA degradation pathway in the cytoplasm. In the last few years, there have been considerable advances in our understanding of post-transcriptional gene silencing (PTGS). This mechanism is conceived as a natural antiviral defense system in plants that is activated as a response to double-stranded RNA (dsRNA) formed during virus replication. To develop new approaches for plant protection against virus diseases based on PTGS we have expanded previous findings on RNA interference (RNAi) in animals by Using dsRNA to specifically interfere with virus infection in plants. This approach differs from strategies based on transgenic expression of RNAs but still relies on PTGS as a means to achieve pathogen-derived resistance (PDR). Our findings suggest that exogenously supplied dsRNA could form the basis for the development of an environmentally safe. new biotechnological tool aimed at protecting crops against virus diseases. provided that some limitations of the current status of the approach Could be overcome.”
Title: RNA interference and mRNA silencing, 2004: How far will they reach?
Author: Pederson, Thoru
Author affiliation: Department of Biochemistry and Molecular Pharmacology and Program in Cell Dynamics, Medical School, University of Massachusetts, Worcester, MA, 01605, USA.
Published in: Molecular Biology of the Cell, volumn 15, pages 407-410, (2004).
Abstract: “The discoveries of RNA interference and RNA-mediated posttranscriptional gene silencing have opened an unanticipated new window on the regulation of gene expression as well as a facile and highly effective tool for knocking down gene expression in many organisms and cells. In addition, RNA interference and RNA silencing may conceivably be exploited for human therapeutics sometime in the future, possibly bringing greater clinical impact than have the so far disappointing antisense endeavors. This essay summarizes recent developments and offers some personalized perspectives, with emphasis on what we do not yet know.””
Posted by henry_kuska z5 OH (kuska@neo.rr.com) on Thu, Dec 17, 09 at 10:09
A 2010 book titled “RNA Interference and Viruses: Current Innovations and Future Trends” with a chapter on “RNA Silencing in Plants and the Role of Viral Suppressors” is now available:
http://www.horizonpress.com/rnai
Posted by henry_kuska z5 OH (kuska@neo.rr.com) on Sat, Dec 19, 09 at 16:01
The field of “RNA interference” appears to be advancing almost daily. This article (which utilized siRNAs) just appeared and is being touted as a possible breakthrough in the knowledge needed to fight flu viruses.
http://www.hhmi.org/news/elledge20091217.html
It is interesting how research in one field can create a breakthrough in what first seems to be an unrelated field. I once attended a scientific award ceremony in which the recepient in his acceptance speech stated that he never had an original idea in his head, but he had developed the ability to read the scientific literature of other fields and see the possible utilization of their discoveries to his field.
Posted by henry_kuska z5 OH (kuska@neo.rr.com) on Tue, Dec 22, 09 at 11:51
Another “RNA interference” very recent (still in proof) research paper:
http://www.nature.com/nature/journal/vnfv/ncurrent/pdf/nature08699.pdf
“Using these methods, we were able to confirm 295 cellular genes for which at least two siRNAs reduced viral infection by 35% or more….”
You may not have neglected RNAi in other conversations but here in this conversation your argument seems to be that pathogen response systems are too complex to ever engineer a pathogen resistance trait when RNAi clearly invalidates that idea.
Going to just slap a response at the end of the thread here as there is apparently a lot to cover and Henry seems to prefer a non-threaded discussion (so at least we can agree on some things!)
On the dutch paper – I’m not 100% sure this paints the picture you think it does, or perhaps you’re not quite as partisan as it first appears – all the negative effects in the paper, are, as Anastasia has already covered, relatively minimal and don’t particularly outwiegh the positive aspects (this is actually, I think, the first time I’ve seen anything mention that HT fields sprayed with glyphosate have increased biodiversity) – I think the pertinent bit about nutrient uptake effects are that they don’t have an economic impact, so again I’d pose the question (and it isn’t rhetorical! Feel free to chime in) as to why a reduction in the removal of minerals from the soil, with no effect on plant growth, would be a bad thing?
Hm, I may have brought this up – my point was that the university studies don’t really represent the real world – which may explain why the yield drag of RR1 (which is real under great conditions) doesn’t show in a plot of actual on farm soy yields (I don’t think anyone can look at the graph above and say that average soy yields havent increased year on year – if there was a consistent 7-10% yield drag (which apparently there is with RR1 in near perfect agronomic conditions) it should be obviously visible – it ain’t though – unless you assume that for some reason the linear increase in soy yield became more than linear at exactly the time GM crops were introduced.
So your point is that you don’t understand modern agriculture? Noted.
GMOs have been shown to dramatically increase yields in these non-ideal agronomic conditions Like in India The manpower issue is really a non-issue here (given that subsistence farmers use either themselves or their kids to do the labor rather than hiring folk an arguement against reducing labor is an arguement for backbreaking labor rather than schooling, so I’m not sure I’d necessarily persue that line of thought too far)
I assume here you’re simply trying to baffle us with an article which isn’t readily available in translated form? The article apparently has nothing to do with water use efficiency in roundup treated crops but with the moisture retention of flax which is being retted (which, as far as I can tell, is the process of allowing flax to partially rot in the field to facilitate fiber removal) given that this document appears to suggest that faster dry down is a good thing I’m not at all sure what point you’re trying to make with the paper as regards water use?
While the review process is the best thing we currently have for assessing science it is far from flawless, as you really should know as a reviewer/editor (Wakefield…?)
Anastasia on Burkino Faso –
Actually if you read the paper this is precisely what they did. (The whole article seems a tad doom and gloomy to me particularly given that This paper on burkino faso adoption of GM cotton estimates an approximate 18% increase in yield and no significant change in production costs (average across 3 zones and 3 different production styles – large farm, small farm, manual farm (farm size dictated by number of animals used for assistance, to give an indicator of farming conditions in general)
So you’re arguing against agriculture in general? (Those mean old hybrids put out in the field might hybridize badly with erm, I dunno, volunteers from last year? Themselves?)
What exactly are you getting at? You’re aware that for the most part farmers purchase new seed every year right? Farmers don’t save hybrid seed and re-utilize.
Ah the old “farmers are idiots” ploy – well played sir. You are, of course, aware that GM traits can be introgressed into lines which are “tuned” to the local environment (to suggest anything is tuned to long term conditions, ie predictive of the future, rather than simply guessing at the past, is somewhat silly, although this is tangential) If you’d actually read the Burkino Faso article you’d linked you may have got a hint of this, and if you had an understanding of how agriculture works, rather than simply making it up as you go along, then you’d probably get this also.
A good question for a certain P.Schmeisser, I guess, but meaningless here – nobody is suggesting that any farmer who isn’t going to use glyphosate would utilize a glyphosate resistant line, this again rather plays on the “farmers are stupid” trope. They aint.
You clearly have little to no understanding of how modern breeding works. It is the work of but a few years to introgress a trait into a different line with pretty much no genetic carryover from the parent other than the little slice of awesome that you wanted to carry over. Who’d have thunk that marker assisted breeding would have been of use to anyone huh? You also illustrate your incomplete reading of the article (Anastasia I feel can be forgiven as it wasn’t her link) by blindly assuming that the backcrossing hadn’t occured (and from the literature appears to have worked admirably) when even the article you links clearly states that it has.
It is almost as if you’ve come to your conclusions already and are only picking information which matches your preconceived ideas, and are then trying to Gish gallop (with a multi-lingual twist, which is at least novel) the topic – which alas, in a written format with no word count or time constraints is a tactic doomed to failure.
How one can yammer on about the precautionary principle while apparently trying to create monsters in your garage is beyond me – the precautionary principle would suggest that as you do not know the outcome at all you should probably only do this experiment in a bunker half a mile underground (halving the chromosome number surely has far greater effects on plant physiology than inserting a single gene)
I have to admit I am a little confused about the Burkina Faso paper.
I now see the note on the last page “The particular variety adopted in Burkina Faso, Bollgard II, a Monsanto technology, contains two proteins, Cry1Ac and Cry2Ab, and has been backcrossed onto local cotton varieties to improve viability.”
I didn’t see the note the first skim through, sorry. In the text I think they are saying that the Bt variety are less able to survive in the climactically variable environments than the locally adapted varieties were. “Given the high climatic variability of the cotton-growing zone, all Bt cotton adopters will bear the brunt of increased risk associated with climatic variability.”
My first question is – how many generations? I’m thinking they need 5. And second question – was it backcrossing with selection for similarity to the local variety? Because that would produce a variety more similar to the intended variety. If they don’t have 5 backcross generations with selection then yeah, the Bt variety won’t be as locally adapted as the local variety, and wouldn’t have the ability to respond to that high climactic variability (assuming that the local variety does, which I didn’t see in the paper, I guess it just doesn’t matter if the saved seeds fail because those seeds were free).
There are other confusing things about the paper, though.
On the left side of page 65 the authors say that differences in farm management practices among small holder farmers means some will profit and some will loose money with Bt seed (and presumably with non-Bt seed as well). They then use this as a reason to reconsider use of Bt cotton – but to me it’s a reason to get some extension agents down there to talk to the farmers whose practices cause them to loose money when their neighbors are doing fine. Or maybe those failing farmers need to just talk to their successful neighbors.
Then they say “since Bt seeds are only sold
in 10-kilogram sacks this could potentially exclude producers with plots smaller than one
hectare.” Call me crazy but couldn’t multiple farmers go in on a sack? Or one farmer buy a sack and parcel it out to his neighbors maybe with a small fee for his trouble?
I get that the goal of this paper is to explore the problems not propose solutions but when the solutions are so obvious you’d think they’d at least mention them.
Also, it seems to me that the low input system is the problem, not the Bt seeds. If rainfall isn’t dependable at all then duh the crop is going to fail in those years when there isn’t enough rain. That’s not an argument against Bt (which at least solves one of the problems while not solving all of them) – it’s an argument for irrigation or at least crop insurance, and maybe some fertilizer to boot. Yeah, Bt seed is a false hope if you are expecting it to solve every problem. It only solves one very specific problem. They sort of say this in the last paragraph but they only say it in addition to saying Bt isn’t going to help. People need to realize that a specific trait, whether genetically engineered or not, isn’t expected to fix everything like magic. It needs to be a part of a multi pronged intervention strategy.
Oh yeah, and obviously a specific Bt toxin isn’t going to control all insect pests. So if field testing shows that the local pests aren’t deterred by these two specific Bt toxins then that’s obviously not worth it for farmers to use. Either don’t bother with Bt, do a cost benefit analysis to see if Bt really does help reduce number of pesticide sprays needed, or develop Bt toxins that do kill other pests like the cotton leafworm.
It just seems like such a weird paper. I guess if someone is pushing Bt cotton as the be all end all for Burkino Faso then one might have to respond with such a paper but honestly it all seems pretty obvious. Confused.
Anastasia – a little digging turns up
This french document about Bt cotton in Burkina faso (Dunno where I got Burkino from… I think championship manager… or just a bad bad memory) contains the following snippet about how the crosses are to be done (I assume they were done this way, I may or may not try and find out for sure dependant on how bothered I can be!)
(Thanks to microsoft translator for that, my French is a little too basic to make any sense of the linked document)
So to me it appears that multiple varieties will have the (or have had the) transgene introgressed and backcrossing is to be (or was) done for 6 to 7 generations. Looking at the literature while it is clear that low inputs are a big issue it does appear that the introduction of Bt can cause significant improvements in yield (I’ve lost the paper now, may try and find it again, but one study showed that compared to conventional varieties Bt cotton yielded almost the same (slightly lower) than conventional when the conventional was sprayed 7 times and the Bt zero – increasing the Bt sprays to 2 increased yield to more than 25% higher than covnentional with 7 sprays)
The following was asked: “As a side note, how would you view your own research via Gamma Cell (assuming you mean radiation treatment here) in light of the PP? How did you know it was safe?”
My main field was electron magnetic resonance. This is abbreviated ESR. This means I studied free radical formation. Gamma irradiation was being considered as an alternate for sulfur vulcanization of rubber. I also had support from the US Army and the Atomic Energy Commission. As I already mentioned the plants around the atomic bomb blasts were mutated. I studied those types of mutations in a controlled laboratory environment. My Army findings are classified. I got a “good feeling” when years later I received a phone call from a major contract laboratory that they had some questions about my report as they had a contract for further investigation. Within the last 3 months I saw a news report that I interpreted as indicating that my report was the basis for something practical (at last).” A summary of my non classified studies can be gleamed from the following:
H.A. Kuska and M.T. Rogers, Electron Spin Resonance of Transition Metal Ions, in Radical Ions, E.T. Kaiser and L. Kevan, Eds., WileyInterscience, New York, 1968, pp. 579-745.
H. Kuska and M. Rogers, EPR Transition Metal Complexes, MIR, Moscow, USSR, 1970. (Book in Russian).
H.A. Kuska and M.T. Rogers, “Electron Spin Resonance of Transition Metal Complex Ions”, in Coordination Chemistry, Vol. 1, ACS Monograph 168, A.E. Martell, Ed., Van Nostrand Reinhold, New York, 1971, pp. 186-263.
H.A. Kuska and M.T. Rogers, “Electron Spin Resonance of Coordination Compounds”, in Spectroscopy in Inorganic Chemistry, Vol. 2, C.N.R. Rao and J.R. Ferraro, Eds., Academic Press, New York, 1971, pp. 175-196.
Regarding “safe”. I attempted to learn from the literature what the safeguards were and apply them. For example as far as I know I was the first to apply a “Faraday Cage” around the instrumentation. If you had a medical magnetic resonance imaging scan, you may not have noticed the Faraday Cage; but every MRI that I have seen in commercial use has one. I got the idea from the Ham Radio Handbook of that time.
Regarding the Precautionary Principle as scientists (and specifically me) interpret it. Also see the petition linked to here. I feel that in most cases the research should be done, but the application in cases like a major food crop should wait until independent research satisfies all major reasonable concerns about negative effects.
I say “that the basic research should be done in MOST cases” because it appears that we have the ability to take a cell of a human and the cell of “say for example” a frog. We can then utilize digestive enzymes to dissolve the cell walls, force the two cells together into one, and try to regenerate a human frog hybrid.
Henry,
Thanks for getting back on my question(s). I asked the safety question because you mentioned you had created the “mutant” roses and that “they did not survive the winter”. This implies that they were, in fact, somewhere in the environment. I find this no different than researchers testing GE plants. What if they had escaped and created “super roses”? Their pollen could have traveled to wild species and caused unforeseen problems. Many weeds are related to roses you know. These may sound silly, but they are exactly the same types of arguments used against GE. GE is looked down upon, while mutigenesis (mainly chemical) is used commonly in “traditional” breeding. This in spite of the fact that mutated plants would likely have far more genetic alteration than a selective GE insertion. In my mind, they would pose more of an unknown “risk” than GE, if we can even consider it a risk (I don’t).
Consider further that, if you had been working in contemporary Europe, you would be subjected to self proclaimed vigilantes that actively strive to prevent researchers from doing this type of research by destroying, burning and digging out research plots. They do this, by the way, in the name of the precautionary principle, which is why I asked about that. Researchers are caught in a catch 22 situation where they need to demonstrate safety because of the PP, yet can’t do the research because of … the PP.
My Opinion: The PP is pie in the sky idealism. It is one of those things that looks good on paper, but has zero value in the real world. It is the antithesis of the scientific method. The later is centered around the concept of hypothesis testing. To do a test, one must objectively assume a neutral position, aka the null hypothesis, a hypothesis of no effect. The experimentation phase is then carried out to disprove this position, i.e. reject the null hypothesis. If the experimentation does not show this, we say we fail to reject the null hypothesis.
In it’s various forms (see Wikipedia), the PP boils down to one concept. We must prove the entity in question is safe. That is, we must prove the null hypothesis. This is never done in science. One never proves “no effect” because it simply is not possible. The PP can never be practically applied. How safe is safe? How many negative tests do you require before calling it good? The only way we can logically proceed in such matters is to assume a specified level of risk and call anything below that safe. This is similar to the approach taken in the report you link to. I would argue, however, that this is not the PP. Note that by assuming a level of risk, you are actively admitting that some level of harm could arise, but is either worth it or negligible. That is, it is not “safe” at some level.
One must also consider the risk of not adopting the entity in question. This is a point Karl has brought up many times, but has been often overlooked. What are the risks if we play ignorant, turn our heads from this technology, and walk away. The petition you link to does exactly this. They set the bar to zero. No research should be done, no applications should be made, no knowledge gained. As a scientist, I find this appalling and unacceptable. Tell me Henry, how do you feel about those out there who feel exactly the same way about nuclear research? Those out there who have been scared into believing anything to do with radiation is bad?
By the looks of it, you are an accomplished chemist and scientist. I’m curious on your opinions here. I am, by the way, quite familiar with classified work. My father spent 30 years in the national labs doing nuclear research. I never really knew what he did until a few years before he passed. That makes for some awkward answers in 3rd grade when the teacher asks “What do your fathers do?” (no worries, my mother set her straight 🙂 )
Pdiff
This is an excellent description of PP. If you’re ever interested in polishing it up a little to make it a blog post please let me know.
From Henry’s petition, apparently signed by 800+ scientists.
“GM crops offer no benefits to farmers or consumers. Instead, many problems have been identified, including yield drag, increased herbicide use, erratic performance, and poor economic returns to farmers.”
So all the undersigned are either utter liars, or are cherry picking the bad data out of a mountain of good.
“These include the spread of antibiotic resistance marker genes that would render infectious diseases untreatable, the generation of new viruses and bacteria that cause diseases, and harmful mutations which may lead to cancer.”
(the risks of GM crops..)
Weapons.
Grade.
Crazy.
800+ Scientists are apparently crazier than a sack full of monkeys on LSD. Good to know.
I’d like to redact my 800+ scientists comments.
I don’t consider a NAMBLA pediatritian to be viable signatory, so that reduces our number by one. The 20 duplicate signings can be pared down to 10, so we’re down 11.
I’m going to assume anyone who works for an organization with poopy in the title probably isn’t a serious signatory, so we’re at 13. Chiropractors are out, so that’s another 2 gone (15 out), I don’t think that journalists can be considered scientists, so another 2 bite the dust, lawyers aren’t scientists, so another 3 out (20), acupuncturists aren’t scientists… so 21, herbalists… (23), anyone associated with vedic doodadery shouldn’t count (28), or maharishi u (31)
So – somewhat less that 800 scientists are crazier than the aforementioned sack of monkeys. (That’s all the analysis I had time for, I’m sure there are a lot more non-scientists in the list, which makes it a rather dishonest letter as it claims to be from scientists – one wonders, given the online form for signing the letter, how many of the signatories are actually for real)
Ewan R, wow! What a group of comments in your last 2 posts.
I will let the readers of this thread judge their validity.
I am disappointed that you are including what I consider personal attacks myself and other scientists among your “points”. I would have been delighted to address your scientific based topics (some of which I feel are worthy of further discussion) as I did when you presented the 1960 to 2009 yield graph. However, I refuse to further participate in a thread that allows this type of non scientific based discussion.
I expected this thread to be at a level reflecting the statement: “Biofortified’s volunteer authors are devoted to providing factual information and fostering discussion about agriculture, especially plant genetics and genetic engineering. The site is written by grad students, professors, and guest experts.”
Sadly, Goodby.
Perhaps instead of judging tone you could simply ignore the perceived slights and continue with the discussion.
I’m afraid that I am a great believer that the best way to respond to the ridiculous is with ridicule – if you don’t feel that your points are ridiculous then perhaps you should explain why not, rather than flouncing off.
I would expect a similar level of ridicule if I started pontificating on electron spin resonance from an ideological footing rather than actually grasping what I was talking about. Perhaps not, which would be a shame I feel.
The editors of this site (myself and Karl) don’t police comments. If there is one that makes personal attacks then we might edit it, and as you’ve seen we occasionally edit for clarity. So if you see a comment you do not like, unless it is from myself or Karl personally, you should credit that comment to the author themselves and not to the site at large.
That said, while I don’t personally use the conversational style of Ewan I think it is important to note that there are no personal attacks there. Frankly, I agree that the grand majority of all text on the ISIS site is made up of nonsense claims that don’t hold any scientific value, including most of the text of that petition. I’m all for seeking knowledge and free exchange of information, but when things like ISIS are put forth, really there’s nothing else to do but state how useless it is in a science based conversation.
Please see https://biofortified.org/about/
Comment Policy
We encourage discussion in the comments section below each post. Comments that are civil are most likely to foster meaningful discussion, so we ask you to refrain from being rude when commenting, no matter whether you agree or disagree with the authors. The only comments that will be moderated are those that include profanities, threaten others, are illegal, or engage in trolling (deliberate antagonization of authors or other commenters).
Yep. To restate – while we prefer that commenters aren’t rude, if they are rude we will not remove the comments unless they are threatening, profane, illegal, or include deliberate bating of others.
So I’m partially guilty of not complying 100% with a request. (I don’t think that anything I’ve said here falls into the “will be moderated” section) Although personally I don’t think I’ve been all that rude, perhaps I have become cynical and hard skinned from a decade long exposure to the internet – when you’ve been called scum, worthless, told you should die and have heard stories that people “on your side” have been threatened with rape (if I misremember Anastasia’s shocking story here I apologize – it was something repugnant like that) simply for participating in the debate then it’s rather hard to see what all the fuss is about when you point out where people are either lacking in understanding, cherry picking the data, or flat out making stuff up (which I’m sorry, but the undersigned to the isis letter have to be based on the claims they’re undersigning)
I’d again, therefore, ask that you see past the tone and address the issues.
The statement was made: ” I asked the safety question because you mentioned you had created the “mutant” roses and that “they did not survive the winter”. This implies that they were, in fact, somewhere in the environment. I find this no different than researchers testing GE plants. What if they had escaped and created “super roses”? Their pollen could have traveled to wild species and caused unforeseen problems.”
H. Kuska reply. At the time that I did the research (in the 60s, 70s), I was probably (memory question – I am an old man) not aware of the concerns stated above. I even consulted with the local Monsanto research laboratory on ESR matters. But, they did not discuss (and possibly did not even know) the big picture. My consulting was free as it was a local company and did not involve major costs such as overnight lodging and airplane travel. As a state university scientist I feel that I was expected to do “public service” for local Ohio companies. This turned out to be not exactly free as afterwards Monsanto kindly donated a routine ESR spectrometer. At that time I only had a complex research ESR. The 2 complemented each other nicely. In fact it would probably be pretty accurate to say, that after that, 70% of my ESR research was on the “Monsanto” instrument.
If I was doing the experiment now I probably would have protected the plants with individual screening “nets”. (“would have”, “should have”, etc. are great words.) I would like to point out that I was the Chemistry Department Safety Officer and at one time was asked to be the University Safety Officer (I declined).
On March 6, 2011 at 11:33 pm · I replied to a earlier statement.
“Reply
The following was stated: “in fact, promises the ability to quickly breed around such difficulties.”
H.Kuska comment. Please cite references. I thought that I was presenting points that it is/will be very difficult “to quickly breed around such difficulties”.”
As of today no one has cited any references.
A reply was received on March 7, 2011 at 1:21 am: that maybe was intended to be a response: “Reply
You are neglecting genetically engineered traits that bypass all the complex pathogen response mechanisms such as RNAi. It is entirely possible to quickly develop a genetically engineered disease resistance trait for a disease it might take a decade to breed for.”
H. Kuska comment. The (March 7, 2001, 1:21 am) post did not include any references where RNAi has been successfully applied to gmo crops. The statement “entirely possible” is not sufficient (to me) in a scientific discussion as I have seen many promising techniques not succeed due to unforeseen “roadblocks”
This 2011 book “Banana Breeding and Production” summarizes where the field of molecular breeding is now (as I understand it). The link covers a chapter on potato, cassava, and sugarcane. I could not cut and paste the paragraph of interest. It is on the bottom of page 322 and a small amount on the top of 323.
I interpret it (and the other references that I have read) to indicate that RNAi methods require a lot of knowledge about the complex biology of the species.
Also, please read the information given about conventional breeding also on page 322. I interpret it to be very similar to what I said about the difficulty of cross breeding a gene inserted variety GMO with a local “naturalized” variety. It is my understanding that you have to keep the Gene from the GMO and breed OUT all of the genes that are not optimized for the intended location. Not only the genes but the location and order of groups of genes as properties are often determined by groups of complex relationships.
Well yes, but that’s a lot of knowledge that is pretty readily accessible on any plant that has been the focus of a lot of research – banana’s aren’t, as far as I am aware, as hot a topic as corn, soy etc – so even if the requisite knowledge doesn’t exist for bananas (and I am sure it could in a handful of years should this be a viable prospect)
You’re interpreting it wrong. Conventional breeding for new varieties is tough as you don’t know, from the outset, what the offspring of various parent crosses will do – so you take your best effort and do massive factorial experiments from which you can select the best offspring (sorry breeders if I’ve massively oversimplified here) – this isn’t what you do when crossing a gene into a variety of interest – you have an established variety of interest, so you know precisely how you want your end product to look – you know precisely how to make it, you know precisely what it is you are putting in – assuming you are introgressing into an inbred plant your first cross will give you offspring that are 50% where you want them to be, the next cross (target variety x offspring of cross 1) will be 75%(target variety x cross 2) of the way there, then ~87.5(target variety x cross 3), then ~93.75% (target variety x cross 4) then ~97% (target variety x cross 5) – by the time you hit these last crosses, given a large enough population, you’ll have some that contain only your insert of interest (plus a little bit of genomic DNA either side from the transformation line) – I’m sure breeders have better tricks to improve the process (I’d imagine for instance that finding crossovers in early generations which isolate the sequence of interest would be a good thing(tm)) – this is entirely the logic (watered down somewhat no doubt) behind Anastasia’s early comments that you’d need 5 generations of backcrossing to make a decent local variety with an introgressed transgene – which it appears the Burkina Faso cotton project planned to exceed by 2 generations (which adds an extra layer to my calculations above leaving you at ~98% which’d no doubt statistically leave you with a spectrum between 99.9% and probably 96% of the original – so long as you weed out the offspring from each generation that don’t have the gene, and that have the most carryover from the transformation line you’re golden – and molecular breeding techniques offer precisely this (third gen sequencing will make molecular breeding of this nature even less hit and miss, as you won’t rely on markers to assess % genome, you’ll be able to do it base by base)
Henry,
The comment you mention is mine, and was made to the best of my understanding. I freely admit here that, while I have a fair amount of knowledge on these matters, I am a statistician, not a geneticist or plant breeder. As much as I would like to directly respond to you, I must defer to others here on this topic. I still believe it is true, but will wait for others more qualified in this specific area to respond.
I also note that my original comment from March 6 was in response to your stating that a farmer’s GMO crop would possibly be “not tuned” to their particular environment which could result in crop failure down the road (my paraphrasing). While I concur, I, in return, asked you why this would be unique to GMO, as it is obvious to me that any variety/hybrid/crop marketed to a wide array of environmental conditions could exhibit such shortcomings. As with the potential glyphosate environment interaction that started all this discussion, I contend this is not a GMO issue, but rather an agronomic one.
Regarding the difficulties involved in RNAi utilization.
I think that it will be useful to look at a 2007 USDA in progress research report:
http://www.reeis.usda.gov/web/crisprojectpages/201045.html
Please compare the above to the link below that gives their 2011 published paper:
http://onlinelibrary.wiley.com/doi/10.1111/j.1467-7652.2011.00601.x/full
(The conclusion section gives a “quick read”.)
I see nothing here to support your position Henry. In the progress report they suggest that this might be a quick method for solving certain problems. In the paper they indicate their first shot at it was fruitful, but not complete (hardly surprising for a novel approach to something). I used the word promised (as did they) and meant it in terms of “has the potential for”. I did not say “in actuality” for a very good reason. You might find the work of Philip Tetlok on expert opinions interesting in this regard. Consider me a fox, Henry, not a hedgehog 🙂 .
The following was stated by (Ewan R March 9, 2011 at 8:49 am): “assuming you are introgressing into an inbred plant your first cross will give you offspring that are 50% where you want them to be, the next cross (target variety x offspring of cross 1) will be 75%(target variety x cross 2) of the way there, then ~87.5(target variety x cross 3), then ~93.75% (target variety x cross 4) then ~97% (target variety x cross 5) – by the time you hit these last crosses, given a large enough population, you’ll have some that contain only your insert of interest (plus a little bit of genomic DNA either side from the transformation line)”
H.Kuska reply. No reference given. I assume that this is based on a Mendel approach for a diploid. Is this what is taught in advanced graduate plant genetics courses as applicable to real world plants?
I looked at what Purdue’s Department of Agronomy has stated: “Harnessing Plant Breeding and Genetics to Identify and Develop Economically Important Crop Traits” (No date given, 2007?)
I feel that the description adequately describes the complexity of real world research.
(Please note that the following is is a response to the sub topic of this thread started by the statement: “March 6, 2011 at 10:07 pm · Reply
“Henry: ………. GMO, in fact, promises the ability to quickly breed around such difficulties.”
I(H.Kuska) am focusing on the word “quickly”
I will pick out one example that I feel is stated clearly:
“Repeated failures in demonstrating greater NUE in the field has prompted recent conversations with faculty working in plant nutrition, soil fertility, and physiology aimed at understanding the intricacies of N cycling in the soil-plant-atmosphere continuum.”
NUE is an abbreviation for “N use efficiency (NUE)”.
To repeat.
My responses are an attempt to show that “quickly” is not an accurate statement based on real world experience. The comments about banada that were made in the (Ewan R March 9, 2011 at 8:49 am ·) reply appear to be relevent:
“Well yes, but that’s a lot of knowledge that is pretty readily accessible on any plant that has been the focus of a lot of research – banana’s aren’t, as far as I am aware, as hot a topic as corn, soy etc – so even if the requisite knowledge doesn’t exist for bananas (and I am sure it could in a handful of years should this be a viable prospect).
Please note “focus of a lot of research” and “could in a handful of years”. Are these consistent with “easily”?
Concerning the (pdiff March 9, 2011 at 10:01 am) reply
“I see nothing here to support your position Henry. In the progress report they suggest that this might be a quick method for solving certain problems. In the paper they indicate their first shot at it was fruitful, but not complete (hardly surprising for a novel approach to something).”
H. Kuska comment. The second paper is a REVIEW paper that was subjected to the review process “Received 19 November 2010; revised 27 January 2011; accepted 30 January 2011”.
In the reviewed published REVIEW CONCLUSION SECTION the following appears: “Results from RNAi experiments have been very encouraging in regard to sedentary plant-parasitic nematode controls, although additional research is needed.”
This conclusion statement indicates (to me) that the topic area (“Biotechnological application of functional genomics towards plant-parasitic nematode control”) is still in development and was viewed that way either by the research group themselves or by the editor after receiving comments from the peer reviewers.
This is standard trait introgression into an inbred line that Ewan is talking about. Each time you make a cross, only half of the DNA from the parent is inherited in each generation. If you had a corn plant, let’s call it genotype A, and you were crossing it with a plant of genotype B, and you are trying to eventually get a plant of genotype B with one snippet of DNA from genotype A. (A transgene, or allele of interest) Since you lose 50% of the DNA of the parent each generation, on average you will lose half of the remaining genotype A DNA each time you cross it to a plant of genotype B. Crossing repeatedly to the same genotype is called backcrossing. Now this is the average likelihood, so you could get 90% or 85% genotype B at the third generation instead of 87.5%, for example. Ewan is exactly right that as you get to almost none of the original parent DNA (genotype A), you will have some plants that pretty much only inherited just that one snippet of DNA you are interested in. The crossover boundary can be within hundreds of base pairs of your gene, even.
I’ve been doing this sort of back-crossing in maize, and before that, mice – the principle works the same. Tetraploids (and higher ploidy levels) can be a little more difficult to eliminate heterozygosity (Aa Bb), but still each time you make a cross you will lose 50% of the genotype you are trying to breed out.
While Karl’s description of backcrossing is excellent it may be worth noting here that what is simple to describe in a few sentences is not always as simple to accomplish.
In order to arrive at a final plant with >95% genotype of parent B AND still have the “snippet” of DNA from the donor parent (A) one needs to select for offspring that have in fact inherited the snippet. Selecting for the desired phenotype may be quite obvious, and it may not. Herbicide resistance is an example of the obvious phenotype – spray a collection of progeny from the A X B cross and those with resistance will live (F2 progeny can be sprayed when the trait is dominant… F3 progeny can be sprayed if the trait is recesive.)
Karl also points out the complicating effect ploidy level can have on the process. Wheat can be more difficult to work with than corn because of ploidy issues. Strawberries must be a nightmare. One piece of the puzzle that Karl left out is that with marker assisted selection (MAS) one can actually speed the process along in terms of the number of backcross generations needed. If sufficiently large populations are grown at each stage of the process one can select markers that are unique to parent B and recover more of B (or eliminate more of A) than 50% in a given generation.
When selection for the desired phenotype is not so simple (lets use Henry’s example of nitrogen use efficiency (NUE) here – should get Ewan’s attention)… you don’t have such a simple scenario to work with. To use backcrossing effectively for quantitative traits (traits controlled by many genes) is hardly a walk in the park. Even when a transgene lead is available (as I suspect Monsanto uses for their NUE project) one is constantly dealing with genetic background affects. So, Henry’s comments above needn’t be dismissed out of hand.
No reference is given because it is a conversational discussion of how things operate based on my experience talking to actual corn breeders who actually do these crosses. I haven’t taken a single advanced graduate plant genetics course so couldn’t comment, although given Karl’s response it would appear that I’m really not that far off the mark (mathematically and logically I don’t see how breeding could operate enormously different other than the obvious bit of variation one way or the other in terms of percentages from original parent as discussed by Clem) – generally I’d assume references are only required when non-trivial information is brought to light – basic breeding approaches really don’t, in my mind, require referencing.
Papaya viral resistance and rice flooding tolerance says otherwise – things will vary from trait to trait – some traits will be easier than breeding, others harder, some will be worthwhile developing in parallel, others not so much.
Yes, depending on how you define easily. Could you do it in your garage without any training? Probably not, but then you couldn't do plant breeding that way either (not for succesful commercial lines). You can't really go ahead and say something isn't easy because to make it easy requires a vast amount of pre-knowledge, it's amazingly easy for me to respond to your post, but doing so requires a vast amount of technology all of which is the result of years and years of research and development. It's amazingly easy for a surgeon to remove an appendix – I wouldn't however try it myself – therefore just because it is easy (and I guess the statement should be relatively easy, and also be qualified that it will only be so in some cases) to GM around something that would be difficult to breed in (ask Pam Ronald about flood tolerant rice – if they hadn't found the gene in a wild relative an amazing agricultural advance would have been only achievable through GM, or through an amazingly torturous breeding process – as far as I recall breeding in the wild gene was still a lot harder than doing the GM work) for people who know what they;'re doing doesn't mean they'll be doing it in French high school classes any time soon (they'll have to find something else to take the place of E.coli transformation sadly)
Things like NUE, and intrinsic yield, are enormously difficult things to bugger about with – and yet we do actually see success – Monsanto advanced an NUE gene to phase 2 testing this year, Pioneer are in phase 1 with similar but have taken the rather grandiose step of already donating it to a WEMA like project – as far as I am aware Monsanto and Pioneer are the only major biotech companies trying this, because it is such a difficult area to impact – we test hundreds of gene candidates every year for their potential to positively impact NUE – Clem is also right however – genetic background effects could pose a major roadblock for wide releases (one then has to consider the commercial viability of releases in a sub-set of germplasms in which the gene does what it is supposed to) and licensing.
Henry re: my statement above on gmo promising to be quicker:
Ha, Ha! Ok. You want to play the semantics game. I know this music. How about we change the tempo? 🙂
I’m sorry you mis-interpreted my use of the word, but I thought, since we were discussing the development of plant varieties, that it would be read as “quickly relative to classical breeding approaches, aka selective breeding”. I was not implying immediate, over night changes. Under this clarification, I stand by my statement. I believe this to be true for technical reasons. As Clem has pointed out below, genetic innovations such as Marker Assisted Selection (MAS) help speed the traditional selection process by identifying phenotypically positive individuals earlier in the development process. Then there are the more advanced techniques of directly inserting desired traits, thereby avoiding the carryover of unwanted traits inherent in the sexual breeding process, which are time consuming to remove afterward. As noted earlier, this is not my forte, so I await correction on this, if I have things wrong.
It is important to note that these methods rely on the ability to read and identify genetic material. In the last 15 years, the techniques and computing power to do these tasks has advanced so markedly as to be virtually unrecognizable from their former iterations. Keep this in mind with the two examples I demonstrate below, as they are from the former era, using older technology, and yet, even under this constraint, they still soundly verify my initial premise. Please also note that current technology has only refined these abilities.
Example 1: Rice Resistant to Destructive Blight. A research effort led by Dr. Pamala Ronald (coincidentally an editor on this site). This is a general news article on the effort, but the published results are available elsewhere. From the article, quoting Gary Toenniessen, deputy director of agricultural sciences at the Rockefeller Institute in New York: “What would normally take several years or decades to do through classical breeding techniques can now be done in a year or less“.
This meets my definition and intent of “quicker” above. I’m sure Dr. Ronald could provide more contemporary examples in her rice research (for example water tolerant rice). Her book, Tomorrow’s Table is also an excellent resource.
Example 2: Transgenic Papaya in Hawaii A well known and documented case of GMO use. From the abstract: “Coincidentally, a field trial to test a PRSV-resistant transgenic papaya had started in 1992, and by 1995 the ‘Rainbow’ and ‘SunUp’ transgenic cultivars had been developed. These cultivars were commercialized in 1998. ‘Rainbow’ is now widely planted and has helped to save the papaya industry from devastation by PRSV. “ This was an effort that took a bit longer, however, the crop in question was a perennial tree fruit, not an annual, requiring 5-6 months to bloom.
Again, I believe this meets my intended use of “quicker”.
I also note that both these examples illustrate GMO use to circumvent a disease, and were not directed at enhancing or changing yield characteristics.
As to your NUE example, yes they made advances, and yes the hit some roadblocks. As an accomplished scientist, I know that you are fully aware that many, if not most, research efforts do not lead to their intended goals. Such is the nature of science. This is why I explained the use and definition of “promised”, i.e. “has potential for”, in my previous post.
I have given you two documented examples of “GMO quicker than traditional”. This validates my position :GMO, in fact, promises the ability to quickly breed around such difficulties.
Foxes:1 ; Hedgehogs: 0
I am sorry that I have been unable to give responses in a timely manner since yesterday. My cable service is having problems. I have started to write a number of respones only to loose them.
Here I will comment about the use of the word “quickly”.
The statement was made on
March 7, 2011 at 1:21 am ·
H.Kuska comment. Thus, we are comparing to a time period of 10 years. What is “quickly” compared to that? I would suggest 5-6 years or less would fit. 7 or 8 would be boarderline.
The following “Please cite references” was stated by me:
Henry Kuska
March 6, 2011 at 11:33 pm ·
H.Kuska comment. Please note that I use the word “please” and “I thought” in my request. I am here to learn, but as a scientist, I expect to see scientific evidence if something is stated that is not consistent with what I have read.
I do not want to risk loosing this (again) so I will not cover additional topics in detail here.
But I will give some things to consider (please feel free to discuss any of these topics before I get back to them ).
Is using a Mendel diploid inheritance pattern in a discussion of whether 5 or 6 backcrosses a suitable model for tetraploid cotton Bollgard II that has 2 inserted independent pieces of foreign DNA and a number of traits from the local variety that are desired to be preserved?
Does a tetraploid Mendel inhertitance pattern give any information about the number of backcrossing steps required to place the local genes in the correct order (with a high probability)? (Properties often depend on both a number of genes and having the correct spacial arrangement of the genes.) If not, is it not underestimating the number of backcrosses if you only have a finite number of crosses at each backcross?
Is the Mendel model ignoring important “real world” behavior such as “preferential pairing” and other observed failures of normal meiosis.
This patent describes backcrossing in cotton to introgress – I may try and find more pertinent peer reviewed literature tomorrow if time allows – patent suggests 7th or 8th generation is enough here, so 5 or 6 should work.
I’m not sure precisely what you’re getting at about placing genes in the correct order, genes don’t jsut randomly jump about during breeding – if you cross a single donor onto an elite inbred and then breed subsequent generations with the inbred then the genes will be in the right position (I’m actually baffled by the concept that within a species genes would be in completely different places in the genome – this may just be my ignorance at play however – does this happen?) even if there are totally different positions in different varieties. (the bollgard II question is an interesting one, and I’ll have to find someone at work who knows cotton to get an answer I think)
Uhg! I hate that! But, it happens to me as well. I’ve taken to typing into notepad or word first, and then copying to the browser when I’m ready. The 21st century is great, but not always reliable! 😉
I hope we’re all here to learn, and thank you for your discussions. I look forward to your posts. Keeps us on our toes, Henry 🙂
Pdiff
Anastasia,
Once again, thanks for the sober, well thought out commentary on the glyphosate/nutrient uptake issue. You can bet agchem fertilizer companies are doing their own small plot field testing as we speak. They certainly have an interest in selling more micronutrient blends to remedy the situation real or perceived. Guess it makes that eternal dance between dealers and growers a little more interesting. Have done some small plot testing myself with Mn, Mg, and Zn supplemented as a foliar spray on RR corn after glyphosate application and haven’t seen any significant differences in yields or disease pressure. Turns the corn nice and green though.
I did not get a copy of this program “A Software Tool for Teaching Backcross Breeding Simulation”. Has anyone used it?
Purdue is in the news today. “Hybrid plants with multiple genome copies show evidence of preferential treatment of the genes from one ancient parent over the genes of the other parent, even to the point where some of the unfavored genes eventually are deleted.”
http://www.purdue.edu/newsroom/research/2011/110309DilkesScience.html
Interesting but dunno whether it is pertinent to the current discussion or not – parental genes which are overexpressed and end up doing all the work would be subject to natural selection whereas the parental genes which are practically silenced would wander on their own evolutionary track unperturbed by the forces of natural selection (free to be deleted or mutated beyond recognition) – however we’re not talking about natural selection here, we’re talking about human selection of plants which display a phenotype of interest (or a genotype of interest if you get into MAS) – doing so removes the importance of one parental set of genes overexpressing when introgressing a trait (given that you swamp out the genes of one parent with successive introductions of a full set of genes from the parent you’re introgressing into (as illustrated in the paper accompanying the backcross breeding simulation – it is rather nice that the simulation generation time to get almost complete recovery of one parents phenotype is ~5-6 generations)
Henry:
Thanks for the link – pretty interesting. And I don’t care whether Ewan appreciates its value or not.
I’ve been breeding soybean for over 30 years now and for most of this time have been of the impression that the more one has a feel for how genes behave in nature the better prepared one is to be an effective breeder.
Further, I like to think of myself and many of my fellow Homo sapiens as natural members of this world. So from that perspective I imagine that even deliberate plant breeding is in effect a special subset of “Natural Selection”. And of course it should be obvious to any of us paying the slightest attention to the natural world that there are quite a few instances where a given species is practicing selection on another species… effectively “breeding” the other.
So if Ewan delights in being offensive, just give him his space. Like an undesirable gene in a population, selection will eventually push it aside.
I didn’t think the previous post was particularly offensive – I acknowledged the coolness aspect of the paper (spectacularly so), just questioned whether it was pertinent or not to discussions on trait introgression.
The (admittedly forced) distinction between natural and human selection was just to indicate that with a conscious guiding force such things aren’t going to, in my opinion, have a drastic effect on trait integration.
Regarding where the the Purdue paper that I cited on March 11, 2011 at 10:49 am fits into a subthread.
On March 10, 2011 at 8:09 pm I (H.Kuska asked): “Is the Mendel model ignoring important “real world” behavior such as preferential pairing and other observed failures of normal meiosis?”
H.Kuska comment: I feel that the paper is a very recent reviewed, published real world example of Mendel genetics breakdown.
“Our findings suggest an additional network dependence, where genes fine-tuned to work together within either parental species prior to hybridization are more likely to be expressed together in the hybrid.”
ie. Where in Mendel genetics is “preferential expression” allowed for?
Would mendelian genetics prevent preferential expression? Mendelian inheritance is about inheritance, not gene expression – if I remember correctly (and it’s quite possible I don’t!) we’re talking about a hybrid species brought together from two distinct although closely related species some 12 – 130 thousand years ago – what this supports is the darwinian idea (I believe Dawkins made a lot about highly tuned metabolic pathways and their resistance to changes or introduction of non-fine tuned variants of proteins in one of his early books (I want to say extended phenotype)) on fine tuning of metabolic pathways potentially locking a given organism into a particular mode of working which cannot switch to another, more efficient, system because any individual change towards the better system would reduce fitness despite the final result, a complete switch, being fitness increasing.
To illustrate how I think this system would come to be, without even remotely violating mendelian inheretance (and again, apologies to folk who do genetics on polyploids day in day out, for the injustice I’m about to do the discipline) assume that a given gene A, has 2 forms A (Species 1), and A(species 2) – the hybrid would therefore be A A A A* – if the pathway in which A sits is superior, in terms of fitness, to the pathway in which A* sits, then selection will work to maintain A, whereas selection will either ignore A*, or potentially even work to silence it so that pathway A can operate by itself – so even with perfect mendelian inheritance of traits natural selection would maintain one set of genes (A and its compatriots in whatever pathway we’re discussing) while getting rid of, or ignoring (which to all intents and purposes is the same thing – as in the case of cave dwellers that lose pigmentation and eyes etc because there’s no reason to have them anymore) the other set of genes (A* and its compatriots)
And to be somewhat less dickish than normal – I’d like to thank Henry for transforming a discussion on the nutrient uptake capacity (or lack thereof) in plants sprayed with glyphosate into a discussion on a rather cool illustration on evolution in plants (I’d almost suggest, so this isn’t lost, that Henry may like to post on the forums discussing papers like this – as my initial response, while dismissive in terms of the current discussion, didn’t do any justice to the fascinating nature of the paper.)
Ewan:
This I like:
And I like it so much I would like to retract some of what I suggested earlier. You can be a prince when you try.
The piece I’m less excited about is how you jumped from Mendel to Darwin/Dawkins and evolution in one fell swoop. Mendel was about explaining the mechanism of traits passing from parents to offspring. And as such Henry’s question is fair… but I still think preferential expression can coexist with simple genetics in a Mendelian world.
I rather doubt Gregor was wise to polyploidy. But I’m not sure he needed to be. Preferential expression, imprinting, parent-of-origin effects, epigenetics, are often described as non-Mendelian. And for epigenetic phenomena (where a DNA sequence is methylated and passed to offspring such that the offspring inherits a new sequence not found in the original sequence of either parent) I suppose a case could be made to frown on Mendel’s results. A mutation too is a “new” event in a DNA sequence, and in the case where a viable offspring inherits a mutated sequence it has accomplished a somewhat similar result – it now possesses a sequence that neither parent possessed at their respective conceptions. So another non-Mendelian example.
But once these “creative events” occur, the resulting genotype may go on to reproduce according to Mendel’s model.
Preferential expression is different from epigenetics and mutation in that the effect is caused by the interactions between genes. Epistasis occurs in simple diploid organisms where two different genes interact with each other in creating a phenotype. Epistasis doesn’t violate Mendelian principles; it just adds a layer of difficulty in discovering how the phenotype is derived. Likewise I’d like to suggest that preferential expression is a gene interaction (here between homologous sequences rather than two different sequences).
Holy cow… is all of that merely making a distinction without a difference? Won’t argue that. In the end, if you are trying to breed your roses and preferential expression is active you might be inclined to cuss Mendel. But don’t get too hard on the guy. He did an awesome job with what he had at hand.
Not sure why you don’t like the jump to evolutionary theory as that’s what explains the differences seen in the hybrid species – keep in mind the paper isn’t discussing traits, or genes passed from parent to child, but retention of genes and expression patterns passed from parent species anywhere between 12 and 130 thousand year ago (is that perhaps a typo for 120-130 or 12-13 – seems an awfully large margin of error) – the differential expression is caused (again if I’m remembering the paper correctly) by loss of genes and a return to a more diploid genomic environment – and this, is fully explained by evolutionary forces (and I’m sorry but I have an intellectual love of Dawkins, so if I can paraphrase the guy badly I will! Plus despite Mendel and Darwin never achieving a synthesis within their own lifetimes the modern Darwinian synthesis would be a sad state of affairs if Mendel’s work hadn’t come to the fore – so I always tend to see the two as intimately linked regardless that this linkage post-dates both of the theory namesakes) and has little to do with Mendelian inheritance of traits as far as I see it.
I guess, and this is speculation which hopefully an actual breeder or grad level geneticist can correct as they see fit, that exact mendelian inheritance of traits won’t work quite the same way for a tetraploid genome as rather than each allele segregating off by itself it will be paired with at least one other copy of itself (working or not in the case of transitional Arabidopsis hybrids) but will be mathematically modelable (and therefore maybe mendelianesque rather than hardcore classic mendelian) and will still be fully particulate in nature (which in my mind is the most awesome aspect of Mendel’s work)
I hope that you find this article of interest concerning producing plants from a callus of a single plant. “Since all cells of an organism are derived from a single cell, researchers assumed that plants derived from cells of a mother plant would yield plants identical to the mother plant. However, according to Scowcroft (1985), who has researched somaclonal variation since it was formally acknowledged, “clonal uniformity is now recognized as the exception rather than the rule.”
I would also like to direct your attention to another aspect of genetics in the real world – inbreeding depression.
Quote from page 1236 of the first link (callus research). “…..involving backcrossing can also yield improved forms of a clone, but the process can be …….. unsuccessful, and only work for plants that are self-compatible. Many important food crops, such as apple and pear (Pyrus spp. L.), are either self-incompatible or exhibit severe inbreeding depression.”
Page 1077 of second paper. “The genetic basis of inbreeding depression in rice (Oryza sativa), a highly self-pollinating species, potentially offers an interesting contrast to the more outcrossing maize. Despite a highly selfing mating system, F1 hybrids between two inbred lines showed strong heterosis for biomass (as much as a 101% increase over the midparent
expectation) and grain yield (a 120% increase; Li et al.
2001). RILs descended from these F1 plants after 10 generations of selfing showed strong inbreeding depression
(ranging from 40 to 47% for the grain yield), and
backcrosses and testcrosses using the RIL showed significant
heterosis.”
I (H.Kuska) interpret inbreed depression to indicate that Mendel genetics is having trouble again.”
It is well known that tissue culture, a technique used not only in genetic engineering but in other breeding techniques as well, can introduce some epigenetic changes. That is why backcrossing or at least selection post-tissue culture is so important.
Mendelian genetics explains inbreeding depression just fine. We know that a lot of detrimental traits are recessive. An inbred (selfed) individual is more likely (due to Mendelian rules) to have two copies of a detrimental recessive allele that thus expresses that detrimental recessive trait.
H.Kuska reply. The link I gave summarizes the thinking as of 2003. Lets look at the masking of the phenotypic effect of alleles at one gene by alleles of another gene (epistasis – “A gene is said to be epistatic when its presence suppresses the effect of a gene at another locus. Epistatic genes are sometimes called inhibiting genes because of their effect on other genes which are described as hypostatic” – from dictionary).
It is my understanding that Mendelian rules only consider the stastical appearance of the possible combinations of genes. The rules are of course an important contribution to the explanation of Nature, but Nature is complex and there are other influences.
An expression in math language is that a rule that coverns the general behavior is a “first order” rule. One then adds terms for smaller effects (ie. exceptions). These are called “second order” terms.
Perhaps this is where some of the confusion comes from – I have a feeling that molecular geneticists (my own area of training) tend (probably wrongly…) to view mendelian inheritance at the level of the gene, rather than getting worked up about phenotypic effect – as such epistasis and gene silencing won’t be seen, under this view, as interfering with Mendelian inheritance (the silenced gene will still segregate and pass from generation to generation in a mendelian fashion) whereas if you’re looking at the trait the gene normally causes then I can see that it would look, from this level, like Mendelian inheritance breaks down.
At least I think that explains the confusion. Maybe not. I’ll at least try a little harder to differentiate between “trait” and “gene” in the discussion – by default I go straight to thinking in terms of DNA, and it generally takes a bit of effort to even bump up to the cellular level, nevermind organismal.
In general, the capitalization of “Nature” makes me want to ignore you.
Concerning Nature or nature,
“often capital, esp when personified ) the whole system of the existence, arrangement, forces, and events of all physical life that are not controlled by man.”
What is the problem?
http://dictionary.reference.com/browse/nature
There still seems to be a feeling that the failure of Mendel genetics is a one time rare occurrence and that after that, the following generations will return to Mendel genetics.
It may be useful to start at a more basic level. Molecular processes are governed by 2 terms, one an energy term and the second a randomness term. One can say the 2 terms fight each other. Mendel’s model is based on randomness (statistical probability).
It is my impression that some/many? so called failures are actually cases when energy considerations become important. The following Rose Hybridizing thread illustrates a case in rose where every generation of meiosis does not follow basic Mendel genetics.
This type of behavior falls under the general concept of asymmetric division.
Henry – I think taking it to an energy/randomness term would be somewhat akin to discussing how the motor car operates in terms of quantum mechanics (the only reason energy is discussed in either paper is to identify pseudogenes which may have been making evolutionary trees look funny)- dog roses still follow mendelian type inheritance, one simply has to take into account there is an 80/20 split rather than a 50/50 split in terms of genes allocated from maternal/paternal – so I wouldn’t call this a failure of mendelian genetics, it’s just a far more complicated system (mendelian genetics, like darwinian evolution, has grown up considerably since its inception – to account for weirdnesses like this – you would still be able to back cross a trait into roses, but rather than having to deal with only 50% of your genes coming in each generation you’d have a more optimal system whereby you could ensure 80% of the genome was back to wildtype within a single generation (I think))
The plant cell paper isn’t particularly on topic here – it seems to be far more about cellular differentiation within a single plant rather than dealing with any sort of inheritance of genes or traits generation to generation.
The following was stated: “Henry – I think taking it to an energy/randomness term would be somewhat akin to discussing how the motor car operates in terms of quantum mechanics (the only reason energy is discussed in either paper is to identify pseudogenes which may have been making evolutionary trees look funny”
H.Kuska. Please think about why these things happen. When an author says something like selective pairing”, what do you think causes the “selective”?
H.Kuska comment. It is not as simple as just passing 20% random each backcross. The 20% just passes the same 20% each generation.
Quote from link below: “Moreover, alleles that were shared between the species in each cross combination comparatively often appear to reside on the bivalent-forming chromosomes, whereas species-specific alleles instead occur comparatively often on the univalent-forming chromosomes and are therefore inherited through the maternal parent only. Recombination then takes place between very similar genomes also in interspecific crosses, resulting in a reproduction system that is essentially a mixture between apomixis and selfing.”
The following is the link 2009 article concerning this meiosis.
The following was stated: “(mendelian genetics, like darwinian evolution, has grown up considerably since its inception – to account for weirdnesses like this”
H.Kuska comment. Please note that I have brought up the concept of “first order” mendelian genetics and also my use of “basic Mendel genetics” in the last post.
The following was asked:
H.Kuska reply: Does the following answer your question?
“A translocation is a form of structural alteration that occurs between non-homologous chromosomes. It often occurs during meiosis when the chromosomes are close together. During a translocation, portions of non-homologous chromosomes break off from the original and are then interchanged. The result of a translocation is that the structure of the two chromosomes has now been changed.
Different chromosomes do not carry the same genes in the same location, so different genes are interchanged during a translocation. Translocations do not affect the number of genes in the cell as no parts of the chromosome are lost. They can affect how the genes are expressed by the cell because the sequence of the genes is changed. Since a translocation does not cause a loss of genes in a cell, it rarely affects a somatic cell, a non-reproductive cell.”
http://www.wisegeek.com/what-is-a-translocation.htm
Well yes Henry, but translocations (which I’m aware of)aren’t enormously common in the grand scheme of things – certainly not common enough that breeders would have to be overly concerned about them – there is a certain fluidity to genomes that isn’t captured by simple models, but given that this fluidity is only apparent over relatively long timescales (or in large populations where the effects are often deleterious)
On the dogroses and the 20% passing each generation – it isn’t necessarily the same 20% – during meiosis 7 bivalent chromosomes will pair together and go their merry way – pollen contributes 7 bivalents, and ovum contributes 7 bivalents to the progeny – therefore you have swapping here – what is interesting is the univalents in the mix which are matrilinear also and can therefore be considered asexual – it seems that the interest in dogroses is that they must be evolutionarily recent as the univalent chromosomes haven’t degenerated significantly this paper goes into some of the gory details
So admittedly here, for a brief blink of the evolutionary eye, one might expect mendelian looking inheritance (at least in a pure sense, one assumes you can still do the math when you exclude the asexual chromosoes) to be semi broken down here – but it appears that the view in the literature is that such systems won’t last very long (hence the dating of pentaploid dogroses as relatively recent) – although to vaguely get back to the topic that spawned this – I’m not sure this is pertinent to the discussion of cotton, which doesn’t have a similar system, and which demonstrably has traits integrated into inbred lines on a commercial scale.
This all of course makes my prior post nonsensical – which a bit of further reading often does.
I’m not sure what you’re referring to here – which paper specifically, or what sort of selective pairing (obviously things like selective DNA pairing have energy terms and whatnot at their root, but that really doesn’t matter when discussing higher level interactions as we’re doing – and afaik chromosome pairing is a pretty complex regulated process which doesn’t rely (other than in the way everything relies on lower level interactions – cars and quantum mechanics) on such things – perhaps however you can illustrate precisely what you mean and I’ll stop rambling tangentially.
The following was stated by me: “H.Kuska comment. It is not as simple as just passing 20% random each backcross. The 20% just passes the same 20% each generation.
H.Kuska comment: Sorry I misinterpreted “maternal” as the father (my wife caught this). It is the 80% that keeps coming back. Please see the following RHA discussion:
“There are probably only 14 chromosomes (2 sets) of R. canina chromosomes that can/will pair up. Because the remaining 21 chromosomes don’t pair up, the exact same group of chromosomes are passed unchanged from generation to generation (in the maternal line only).”
The following was stated: “Well yes Henry, but translocations (which I’m aware of)aren’t enormously common in the grand scheme of things – certainly not common enough that breeders would have to be overly concerned about them.”
H.Kuska comment: Comments like “enormously common” “not common enough”, and “overly concerned ” are difficult to “pin down”.
As stated “A translocation is a form of structural alteration that occurs between non-homologous chromosomes. It often occurs during meiosis ……”. Please see the following 2010 paper as an example”
“Development of a wheat genotype combining the recessive crossability alleles kr1kr1kr2kr2 and the 1BL.1RS translocation, for the rapid enrichment of 1RS with new allelic variation.”
The following is a search with the keywords “plant translocations meiosis breeding”.
Ok lets pin it down – under mutagenisis translocations occur at the following frequency in Vicia faba
~7-8% of the time in lines mutated by xrays and neutron bombardment (~160 times out of 2400 lines mutated)
0-3% of the time under chemical mutagenisis (one of the chemical treatments resulted in zero translocations in 614 treated lines)
Therefore to lock down what I mean by enormously common I mean rarely happen at all (0 out of 614 times under mutagenic pressure high enough to cause 7.8% partially sterile lines, and 1.5% chlorophyll mutations) and not being overly concerned by would equate to not worrying about in any way shape or form as the breeder could rely on likely hundreds of instances of their desired cross occuring for every instance where a translocation occured.
Now if we can pin down what is meant by “it often occurs during meiosis” we’ll be golden – I read it as of all instances where it occurs (regardless of how common – indeed this is what I vaguely remember being taught in second year biology – long enough ago now that I don’t remember the course name) it often occurs during meiosis (so while it may only occur in one in a million meiosesese 75% of the time it does happen it is during this rare meiosis) – rather than the alternative read which would be that it often occurs in meiosis (as in commonly as compared to number of meiosese (or whatever the plural is!)
Looking at translocation frequency in lines which have been selected to have high translocation frequency is a bit of a non starter – I assume (and perhaps Clem or someone who actually does breeding professionally could chime in on our utterly non-expert discussion to tell us how things are) such lines are really useful for getting the right bits of chromosome set up for sticking into lines which subsequently have low translocation frequency)