Much of this work has been done on the hardy arabidopsis – the “laboratory rat of plants”, as he puts it. There are a few things that make it the perfect test subject. One is that the genome of the humble weed is quite short, part of the reason why it was the first plant to be fully sequenced. Another is the unique way its code can be changed. For most plants, the process is careful. New genetic material is introduced into a petri dish, carried by bacteria that slip into the plant’s cells. When this happens, the modified cells must be grown and lured to new roots and stems. But arabidopsis offers a shortcut. Biologists only need to dip the plant’s flowers in a solution filled with gene-bearing bacteria, and the messages will be carried directly to the seeds, which can simply be planted. In the painstakingly slow field of botany, it takes place at chain speed.
Still, it took years to figure out what all these SA-producing genes were doing under perfect greenhouse conditions. Only then could He’s team start tinkering with the environment to test what’s going wrong. Their mission: to find a gene (or genes) that controls the step that stopped SA production when it got hot. It took 10 years to find the answer. They modified gene after gene, infected the plants and looked at the effects. But no matter what they did, the plants still withered from disease. “You wouldn’t believe how many failed experiments we had,” he says. Larger leads, such as someone else’s laboratory identification of heat-sensitive genes affecting flowering and growth ended in crushing disappointment. Generations of graduate students kept the project going. “My job is primarily to be their cheerleader,” he says.
Eventually, the lab found a winner. The gene was called CBP 60g, and it appeared to act as a “master switch” for a number of the steps involved in making SA. The process of taking these genetic instructions and producing a protein was suffocated by an intermediate molecular step. The key was to get around it. The researchers were able to do this, they found out, by introducing a new line of code – a “promoter” taken from a virus – that would force the plant to transcribe CBP 60g and restore the SA assembly line. There was another apparent benefit: The change also seemed to help restore less-understood disease-resistance genes that were suppressed by heat.
His team has since begun testing the genetic modifications on food crops such as rapeseed, a close cousin of arabidopsis. In addition to the genetic similarities, it is a good plant to work with, he says, because it grows in cool climates where the plant is more likely to be affected by rising temperatures. So far, the team has been successful in re-activating the immune response in the laboratory, but they need to do field tests. Other potential candidates include wheat, soybeans and potatoes.
Given the ubiquitous SA pathway, it is not surprising that Hes genetic fix would work broadly across many plants, says Marc Nishimura, an expert in plant immunity at Colorado State University who was not involved in the research. But it is only one of many climate-sensitive immune pathways that biologists must explore. And there are variables other than heat waves that will affect the immunity of plants, he points out, such as rising humidity or a persistent heat that lasts throughout the growing season. “It may not be the perfect solution for every plant, but it does give you a general idea of what is going wrong and how you can fix it,” he says. He considers it a gain to use basic science to decipher plant genes.
But for any of this to work, consumers will have to accept more genetic manipulation with their food. The alternative, Nishimura says, is more crop loss and more pesticides to prevent it. “As climate change accelerates, we will be under pressure to learn things in the laboratory and move them faster out into the field,” he says. “I do not see how we can do this without more acceptance of genetically modified plants.”