Much of this work was done on hardy Arabidopsis—the “lab rat of plants,” as He puts it. There are several things that make him the perfect interviewee. One is that the genome of the humble weed is quite short, which is one of the reasons why it was the first plant to be fully sequenced. The second is the unique way in which its code can be modified. For most plants, the process is painstaking. The new genetic material is introduced into the petri dish, and it is carried by bacteria that invade the plant cells. Once that happens, those modified cells must be grown and coaxed into new roots and stems. But arabidopsis offers a shortcut. Biologists need only dip the plant’s flowers into a solution filled with gene-carrying bacteria and the messages will be transmitted straight to the seeds, which can simply be planted. In the painstakingly slow field of botany, that’s going at warp speed.
Still, it took years to figure out what all those SA-producing genes were doing in perfect greenhouse conditions. Only then could His team begin tinkering with the environment to test what was going wrong. Their mission: to find the gene (or genes) that controlled whatever step stopped the production of SA when it got hot. It took 10 years to find the answer. They modified gene by gene, infecting plants and seeing the effects. But no matter what they did, the plants still wilted from the disease. “You wouldn’t believe how many failed experiments we’ve had,” He says. Major leads, such as someone else’s laboratory identification of heat-responsive genes that affect flowering and growth, ended in abject disappointment. Generations of graduate students continued the project. “My job is mostly to be their cheerleader,” he says.
In the end, the laboratory found a winner. The gene is named CBP60g, and appeared to act as a “master switch” for a number of steps involved in making SA. The process of taking those genetic instructions and making proteins was choked by an intermediate molecular step. The key was to get around it. The researchers could do this, they discovered, by introducing a new piece of code—a “promoter” taken from a virus—that would force the plant to transcribe CBP60g and return to the SA assembly line. There was another obvious benefit: The change also seemed to help restore lesser-understood disease-resistance genes that had been repressed by the heat.
His team has since begun testing gene modifications on food crops such as canola, a close relative of Arabidopsis. Aside from the genetic similarities, it’s a good plant to work with, he says, because it grows in cold climates where the plant is more likely to be affected by rising temperatures. So far, the team has had success rewiring the immune response in the lab, but they need to do field tests. Other potential candidates are wheat, soybeans and potatoes.
Given the ubiquity of the SA pathway, it’s not surprising that He’s genetic repair would work broadly across many plants, says Marc Nishimura, a plant immunity expert at Colorado State University who was not involved in the research. But it’s just one of many climate-sensitive immune pathways that biologists need to explore. And there are variables other than heat waves that will affect plant immunity, he points out, such as increased humidity or sustained heat that lasts throughout the growing season. “It may not be the perfect solution for every plant, but it gives you a general idea of what goes wrong and how you can fix it,” he says. He considers using basic science to decipher plant genes a victory.
But for any of this to work, consumers will have to accept more genetic tampering 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 lab and transfer them to the field more quickly,” he says. “I don’t see how we’re going to do that without greater acceptance of genetically modified plants.”