Evolving Pesticide Resistance

Written by Matt DiLeo

It’s been estimated that genetic resistance to every pesticide that will ever be invented already exists in some microbe in some field, somewhere in the world (simply because there are so many individuals of each species). If you invent an incredible new spray that kills, say, Phytophthora infestans, you’d know that somewhere in the world there is a little P. infestans mycelium or spore that is already resistant. If you start spraying thousands and thousands of acres with your new pesticide, you may have a season or a few without late blight, but it’s only a matter of time before this little guy gets into your field and finds a smorgasbord all for himself (to a lesser extent, this probably also applies to multicellular weed and insect pests).This is one of the primary critiques of modern ag monocultures. The 1970 Southern corn leaf blight epidemic is a great example of what happens when a lucky germ stumbles onto a crop that can no longer defend itself. Luckily for us, this is pretty rare. Simple mutations that provide microbes instantaneous resistance to a pesticide (or to a plant’s genetic disease resistance) tend to have pretty nasty side effects (think human resistance to malaria via sickle cell anemia). This means that stacking up multiple disease resistance genes (natural or transgenic) in a single plant increases the chance not only that no local microbes will be resistant, but also that any microbe that has multiple resistance mutations will be so crippled that it won’t be a very effective pathogen anymore. Stacking up multiple resistance genes in one plant variety is called “pyramiding.” Another strategy, “multilines,” places different resistance genes in different individuals of the same variety, creating a field-scale mosaic that should mimic the genetic variation of natural plant populations. This second strategy always appealed to me aesthetically, but it hasn’t been used successfully much in modern ag.
A stunning exception is described in the linked Nature article.* Magnaporthe grisea causes one of the most devastating diseases of rice – rice blast. This fungus chews necrotic spots in rice leaves and panicles, hurting yield and spreading spores. Like many pathogens, M. grisea is a diverse species, containing many separate “races” that are optimized to attack different varieties of rice. New races of M. grisea are constantly evolving. If you develop a new variety of rice that’s resistant to all known races of rice blast, it’s only a matter of time before a new race appears to attack it. Even with the use of fungicides to slow the fungus down, new resistance genes begin to “break down” after just a few years as new races of M. grisea continually appear and proliferate.
Rice varieties, like those of any crop, differ in many respects. As described in the article, farmers in this region grew some combination of hybrid rice (great yields, tastes terrible) with glutinous “sticky” rice (poor yields and extra-susceptible to rice blast, but very valuable). Most farmers grew big plots of reliable hybrid rice with small plots of sticky rice on the side – but some planted occasional rows of sticky rice within hybrid rice fields. It occurred to the researchers that this trick may allow farmers to produce more rice (especially more valuable sticky rice) on the same amount of land than traditional methods allowed.
Over a few years, the scientists worked with farmers to plant various monocultures and mixes of the two rice varieties (e.g. 1 row of sticky rice for every 4 or 6 rows of hybrid rice). In the end they found that the severity of rice blast on hybrid rice was slightly lower in mixed plots than monocultures, but the severity on sticky rice fell from about 20% in monoculture plots to 1% in mixed plots!
So why did this happen?
The authors suggest a range of possible explanations. Since different races of M. grisea attack sticky and hybrid rice varieties, spreading out the sticky rice plants in a big field of hybrid rice (instead of concentrating them in a small plot) makes it harder for the fungus to spread from plant to plant. Also, the mixed canopy of short (hybrid) and tall (sticky) rice plants alters the microclimate around the rice leaves, perhaps producing an environment less conducive to disease. They also studied the genetic structure of the pathogen population in monoculture versus mixed fields – while M. grisea populations from monoculture fields were dominated by the few races that were best adapted to the planted variety, M. grisea populations from mixed fields were more diverse, not dominated by any one race. It’s possible, they suggest, that the constant (failed) attempts of the M. grisea individuals in the mixed field to attack the wrong variety increased induced immunity of the rice plants – in a way, “vaccinating” them against the few races that could really hurt them.
This experiment was so successful, that fungicide sprays were discontinued by the end of the two year project!
Humans have been in an arms race with crop pests for thousands of years – we keep trying to develop new varieties and sprays that keep the pests away, and the pests keep finding new ways to get back in. While scientists are getting a lot better at designing resistant crop varieties and pesticide sprays that the pests have a very hard time adapting to, we still need new (and old) cultural techniques to load the dice in our favor.
This requires an understanding of the evolutionary pressures that drive pests to adapt. Slowing down the evolution of pesticide resistance is a key aspect of integrated pest management (IPM). For example, the transgenic gene in corn that produces Bt toxin (which specifically kills certain inspect species), is a great trait for limiting pest damage – but planting thousands and thousands of acres of it presents an extremely strong selective advantage on the lucky individual insect that happens to be resistant. This monoculture doesn’t increase the chance that an insect will develop resistance, but it does increase the ease with which it can reproduce and pass on the resistant mutation (in the absence of competition). We can defuse this selective advantage by intentionally supporting a thriving population of the original, susceptible insect – e.g. by planting rows of old, susceptible varieties of corn among the new, resistant corn. Some yield is lost to the planting of these sacrificial “refuge” plants, but in the long run, it helps the protect the integrity of the plant’s pest resistance for as long as possible.
At their blog, Martin Family Farms demonstrates how they include such refuges on their commercial farm – as required by EPA regulations and Monsanto contract.**
*Zhu, Y., Chen, H., Fan, J., Wang, Y., Li, Y., Chen, J., Fan, J., Yang, S., Hu, L., Leung, H., Mew, T., Teng, P., Wang, Z., & Mundt, C. (2000). Genetic diversity and disease control in rice Nature, 406 (6797), 718-722 DOI: 10.1038/35021046
**I’ve heard buzzing that some think this practice in this specific case isn’t useful enough to justify having the EPA require farmers to do it, but I haven’t seen strong empirical evidence in either direction. It may be one of those cases that evokes different opinions from people based on their faith in our ability to keep inventing new and better mousetraps vs. taking extra measures to protect the ones we already have…

Written by Guest Expert

Matt DiLeo has a PhD in Plant Pathology from UC, Davis. During his postdoctoral research at Boyce Thompson Institute, he researched unintentional effects of genetic engineering. Matt builds R&D teams and biotech platforms: genome editing, gene discovery, microbials, and controlled environment agriculture.


  1. Matt,
    A couple points. I enjoyed your perspective on how there will always be a representative of a microbial pest species somewhere out there with pre-existing resistance to a pesticide.
    A recent discovery would seem to demand a broadening of that perspective. That is, the pest species need not have a representative with pre-existing resistance to become resistant, when that resistance can be ‘borrowed’ from a different species, via horizontal gene transfer.
    “Reporting in the journal PLos Pathogens, the AGH team documents for the first time that bacteria engage in a process called horizontal gene transfer to evolve rapidly during the course of a single infection. *** And they are doing so through a dynamic, real-time process of altering their genetic code that until now has not been understood and which is counter to conventional wisdom about the typical pace of species evolution,” Dr. Ehrlich said.” [1]
    I don’t know if this could be generalized to fungi, though. If so, it would greatly magnify the challenge of managing resistance.
    Second point, regarding the utility of requiring a refuge for Bt maize. It is thought be some that the mode of action of the Bt protein is such that resistance would likely never develop. According to that theory, the Bt protein opens pores in the insect’s gut–but does not kill the insect. Rather, beneficial bacteria in the gut move through the pores created by the Bt, and they kill the insect. To gain resistance to Bt on this mechanism, the insect would need to become resistant to its beneficial gut flora — which is said to be highly unlikely.
    The theory seems to have been confirmed by an experiment where corn borers were given antibiotics to wipe out the native gut flora. When fed Bt, the critters survived. Those not first receiving antibiotics were wiped out when fed Bt. The ‘buzz’ I get about this, though is that the jury is still out.
    Great post!
    1. http://www.medicalnewstoday.com/articles/201652.php

  2. Eric,
    Wow! That’s pretty fascinating about Bt toxin.
    Fungi do participate in horizontal gene transfer – though I don’t know if anyone’s looked for it occurring in the same way as you cite with bacteria. I’ll check out that paper, thanks!

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