In the mid 1990s a team of computer engineers came up with a new way to plug devices into computers and called it a USB port. It was different from the old ports so it wasn’t compatible with older peripherals and they became useless. Computer companies called this progress but many users called it a big pain in the neck.
Plants sometimes do this with crucial enzymes. An odd gene mutation may change them slightly, so older herbicides can’t bind to the active sites and older formulations become useless. Biochemists call this target-site mutation, but farmers call it an even bigger pain in the neck. Everyone calls it herbicide resistance.
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“Plants are very, very, clever and they’ve evolved all sorts of mechanisms to overcome herbicides,” says Stephen Lindell of Bayer CropScience in Frankfurt, Germany. “There was a guy called Charles Darwin who predicted what we should have predicted. If you have a big selection pressure, plants will evolve to live and cope with it.”
And so it goes. Before there were herbicides we controlled weeds through tillage and rotation. This certainly kept weeds at bay for 10,000 years but we suffered the occasional civilization crash as the relentless cultivation degraded the fertile soil. Herbicides appeared after the Second World War and seemed like a miracle. Now we could put land into continuous production without breaks for summer fallow. Later, even zero till became possible with the development of glyphosate.
Then 50 years later, a nasty little problem arose in the fields where herbicide treatments left increasing numbers of resistant weeds behind. When we started using farm chemistry, the weeds responded by calling on 70 million years of experience shuffling genes. They showed their cards and we started losing. This shouldn’t surprise anyone with a passing understanding of how plants behave genetically.
Every biology student gets an elementary grounding in genetics that, for the sake of simplicity, deals with diploid species. Diploid means there are two sets of chromosomes in total with one set coming from each parent. Dominant and/or recessive genes line up on the chromosomes and then wrestle for control of protein production within the cell.
While diploid animals, such as ourselves, are relatively simple beasts, angiosperm plants, the most evolved so far, are a three-ring genetic circus. Some are diploid with two sets from each parent, but many are tetraploid (like canola) with four or even hexaploid with six (like bread wheat) or beyond (like triticale). They’re referred to as polyploid, and considering that plants exchange gammetes (pollen) via the wind or carried by insects such as bees, it’s not surprising that there would be some strange crossing going on out in those fields.
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Many such crosses don’t live, but some do survive and thrive in spite of polyploidy’s big disadvantage. With that much genetic information in the nucleus, dividing it perfectly several billion times confers a greater chance that something will go wrong. It’s a cumbersome and risky process, so mutations will happen and this is why we animals don’t like to do things this way.
On the other hand, if the local surroundings are not to our liking, we animals can get up and move somewhere else. Plants have no such luxury so they must endure what’s thrown at them. In that scenario, the more genetic resources you have, the more likely you’ll have some trick up your sleeve that will get you through a crisis. If those extra chromosomes give you a slightly different active site that keeps a marauding herbicide from jamming your crucial enzymes, you survive. You pass on that gene and your offspring are immune.
That’s why we’re losing the game right now. We’re playing poker with an octopus and we can’t bluff. It’s a big numbers game and if we want to win we have to see how he plays it, what cards he has and what’s up all those eight sleeves, because he has no reservations about cheating.
“At the end of the day it’s all down to genetics, isn’t it?” Lindell says. “If you have a selection pressure on plants you’ll always see resistance, the plants will always find a way. We will come up with new technologies but if we continue as we have done in the past, resistance will develop.”
One of the tricks that our card shark octopus plays when we’re not looking is called target-site mutation. If you could actually look into a DNA strand you would see what looks like rungs in a ladder. These would be the base pairs and, to put things simply, 1,000 to 1,500 of them line up in combination to create a gene. If one of those base pairs changes, this can bring about subtle changes to the structure of the gene, so the coding changes.
“One base pair can change, and this results in the target enzyme of one amino acid changing too,” Lindell explains. “That’s typically in the active site, and what that means is that this new amino acid sticks out a bit more, so that the herbicide no longer binds. Since the herbicide is no longer binding to the enzyme, it can no longer exert its herbicidal activity.”
It’s not restricted to one base pair either. It might involve more than one base pair or even more then one gene. When combinations of things within sets of billions start shuffling, it becomes very difficult to find. Not only that, it seems our octopus has friends to help him cheat.
Target-site mutation is probably the most common way a plant population develops herbicide resistance. Some populations of plants can develop what’s called enhanced metabolism. Some weeds survive spraying because they can ramp up their ability to metabolize the herbicide and detoxify it. For example, Palmer amaranth in the southern U.S. cotton belt overproduces the ESPS synthase enzyme, so when glyphosate gums it up, there’s still enough to continue running the shikimate pathway. The plant continues to live, and its offspring continue to survive the annual glyphosate dousing.
“Some plants delay germination so that they lie in the soil longer and wait for the herbicide effects to be gone before they germinate,” Lindell says. “Or when resistant giant ragweed sees glyphosate all of the leaves drop off so it stops the herbicide from getting down to the roots to kill the plant. Then it just grows new leaves, and away it goes again.”
Genetics is still a relatively new science and agriculture has been one of our grander experiments in genetic selection. From our deliberate attempts to husband super organisms as crops and livestock to our accidental successes with super organisms as pests, we’ve seen many of these processes first-hand. As we learn more about the rules, we’ll have to use our chemistry in conjunction with biology and play a much more complex and subtle game. Otherwise some very valuable herbicides will become impotent.
“It’s a fascinating science and it’s a science which I think has a very important application in society and in agriculture. But the results from this science need to be preserved, taken care of and fostered a little bit,” Lindell says. “I really feel that we need to introduce more diversity into agriculture. We can’t be just using up herbicide modes of action and going on to the next one, because we’re starting to run out of next ones.”
