UCSD scientists find plant immune response that could aid disease resistance
Researchers at UC San Diego have discovered an “on-off” switch in plant immune responses that could give guidance to botanists on how to improve plants’ disease resistance and increase food stability.
The researchers’ findings, published recently in the academic journal Nature Plants, show that a regulatory mechanism in plants can help turn on an immune response after a pathogenic attack and switch off hours later once the plant determines the threat is gone.
Crucial to these defenses is the timing and duration of immune responses. Humans are equipped with a strong and rapid inflammation response that is essential to ward off disease, but chronic and persistent inflammation can be harmful to health. Similarly, plants feature defenses that are timed for rapid and effective responses against pathogens yet are tightly controlled to avoid threatening the host organism.
Plants are known to mount quick defenses against a variety of threats — from attacking insects to invading pathogens. The intricate immune response mechanisms operate through a complex network that plant biologists have sought to untangle.
Keini Dressano, Alisa Huffaker and their colleagues at UCSD’s Division of Biological Sciences discovered a “switch” in an RNA-binding protein that helps turn on immune responses a few minutes after attack. Hours later, the switch follows with a deactivation “off” signal to avoid self-inflicted damage to the plant.
“These findings have provided new insights into how the complex intricacies of plant immune responses are orchestrated to successfully fight off pathogens, and lay a path forward for improving plant disease resistance to ensure future food stability,” said Huffaker, an assistant professor in the Section of Cell and Developmental Biology.
The novel switch was found in Arabidopsis plants, also known as rockcress, a relative to wild mustard and cabbage plants. To turn immune defenses on, the researchers say, a simple chemical modification of the RNA-binding protein reverses mRNA splicing that normally keeps immune responses deactivated. To turn the immune response off, a second chemical modification of the RNA-binding protein returns mRNA splicing to “normal.”
“This work went beyond simply identifying a new regulator of plant immunity,” Huffaker said. “We discovered specific chemical modifications that control regulatory function, transcriptional targets of the regulator, differential splicing of the targets and precise effects of splicing on both target function and overall plant immune responses and disease resistance.” ◆
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