Climate change breaks down the immune system of plants. Can they be restarted?

This story was originally published by WIRED and is reproduced here as part of the Climate office collaboration.

As the weeds disappear, Arabidopsis thaliana is a rather charming specimen. One spring day, you might see it sprouting from the cracks of a parking lot, setting off a small riot of white flowers that give it the common name “mouse cress.” But its round leaves often carry unwanted passengers: among them, a bacterium called Pseudomonas syringae. It sits there looking for a way to enter the plant, usually the stomata through which the leaf absorbs water and carbon dioxide, or through a wound. This is where things get interesting.

Typically, the first warning of invasion comes from receptors that instruct plant cells to release their defenses. Among the most important is a hormone called salicylic acid or SA. It is used not only by arabidopsis, but by many other plants, including field crops, to avoid infections. But imagine that spring day being unusually warm. A few days after a temporary heat wave, you will see that the leaves of the plant turn yellow and wither. His immune system seems to be failing.

For much of the past decade, Sheng-Yang He, a plant biologist at Duke University, has studied why plants’ immune systems fail due to heat. It’s a molecular mystery that involves unpacking dozens of genes to figure out why plants can no longer produce important chemicals, like SA, when temperatures rise just a few degrees. It’s the kind of malfunction that is expected to become much more common for all kinds of plants as the climate changes and heat waves become more intense and frequent. And now in a article published in NatureHis team describes how this immunity can be restored.

There is more than one way that climate change will affect plants. In some cases, increased heat and CO2 levels can speed up photosynthesis, causing them to grow faster. In others, they may shrivel up and die from the stress of overheating. The geography of climate change will also vary considerably, causing crippling drought in some places during other ecosystems are drowning. Overall, such rapid change is not good for organizations that can’t walk fast to new habitats, as animals can. And just like more diseases are expected at overflow in people as the range of pests and pathogens spreads in a warming world, plants will also face new or more aggressive pestilences in their home ecosystems or farmlands. Last week another published study by researchers at the Chinese University of Hong Kong, global crop yields could fall by 20% by 2050 due to the effects of climate change.

But a surprising effect of heat is that changes occur inside the plant immune system itself. Plants lack what’s called adaptive immunity, like cells found in animals who learn by encountering a new microbial enemy and are ready to spring into action when confronted with it again. But they have a whole arsenal of other defenses at their disposal. Every chemical response, like the production of SA, depends on the action of many genes that translate various proteins into others. These steps work well in the normal factory environment, but a bend in the process due to an external factor like heat can derail the whole thing. “We’re talking about millions of years of evolution,” says He, who is also a researcher at the Howard Hughes Medical Institute. “The last 150 years have changed things dramatically, and humans are responsible for that.”

He grew up in a farming community in eastern China, where he remembers the smell of pesticides hanging in the air during the growing season. In elementary school, he joined other children in the fields as part of a “pest control team” that pulled caterpillars from cotton plants. Today, in the lab, much of his work involves doing the exact opposite: inoculating plants with disease-causing bacteria. Its goal is to study the effects of increasing or decreasing the expression of specific plant genes, looking for changes that signal the role they play in its immune response.

Much of this work has been done on hardy arabidopsis – “the plant lab ratas He says. There are a few things that make it the perfect test subject. The first is that the humble weed’s genome is quite short, in part for the reason that it was the first plant to be fully sequenced. Another is the unique way its code can be modified. For most plants, the process is laborious. New genetic material is introduced into a Petri dish, carried by bacteria which slip into the cells of the plant. Once this happens, these modified cells must be grown and turned into new roots and stems. But arabidopsis offers a shortcut. Biologists only have to dip the flowers of the plant in a solution filled with gene-carrying bacteria and the messages will be transmitted directly to the seeds, which can simply be planted. In the laboriously slow field of botany, things go at full speed.

Yet it took years to figure out what all these AS-producing genes were doing under perfect greenhouse conditions. Only then could He’s team start altering the environment to test what’s wrong. Their mission: to find a gene or genes that control the step that blocked the production of SA when it was hot. It took 10 years to find the answer. They modified gene after gene, infecting plants and examining the effects. But no matter what they do, the plants still wilt from the disease. “You wouldn’t believe the number of failed experiments we’ve had,” he says. Major tracks, such as the identification of the laboratory of another heat-sensitive genes that affect flowering and growth, ended in overwhelming disappointment. Generations of graduate students have kept the project going. “My job is mostly to be their cheerleader,” he says.

Eventually, the lab found a winner. The gene was called CBP60g, and it seemed to act as a “master switch” for a number of steps involved in making SA. The process of taking those genetic instructions and producing a protein was choked off by an intermediate molecular step. The key was to circumvent it. The researchers were able to do this, they found, by introducing a new piece of code – a “promoter” taken from a virus – that would force the plant to transcribe the CBP60g 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 the heat.

His team has since started testing the genetic modifications on food crops like rapeseed, a close cousin of Arabidopsis. Genetic similarities aside, it’s 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 managed to reactivate the immune response in the lab, but they need to carry out tests in the field. Other potential candidates include wheat, soybeans and potatoes.

Given the ubiquity of the SA pathway, it’s no surprise that He’s genetic solution works broadly across many plants, says Marc Nishimura, a plant immunity expert at Colorado State University who has no participated in the research. But that’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 all plants, but it gives you a general idea of ​​what’s wrong and how you can fix it,” he says. He considers this a victory for using basic science to decipher plant genes.

But for all of this to work, consumers will have to accept more genetic modification of their diets. The alternative, says Nishimura, is more crop losses and more pesticides to prevent them. “As climate change accelerates, we’re going to be under pressure to learn things in the lab and apply them faster in the field,” he says. “I don’t see how we’re going to do this without greater acceptance of genetically modified plants.”