Heat waves increase the vulnerability of plants to infectious diseases by compromising their immunity. Short periods of high temperatures suppress the production of a defense hormone in plants called salicylic acid, although the mechanism has remained unclear, until now.
In an article published on June 29, 2022, in the journal Nature, “Increasing the resilience of plant immunity to a warming climate” scientists led by Duke University biologist Sheng-Yang He, PhD, claim to have identified a gene in plant cells that explains why immunity falters with rising heat, and demonstrate optimizing the expression of this gene could restore the production of salicylic acid and bolster immunity in plants against heat waves. The investigators conducted their experiments on the model plant Arabidopsis thaliana. If their findings in this model hold in crops, it would go a long way to ensure food security in a warming world, said He.
Earlier studies from He’s team has shown even brief heat waves can have a dramatic effect on hormone defenses in Arabidopsis, leaving them more prone to infection by the bacterium Pseudomonas syringae. Under normal ambient temperatures, salicylic acid levels increase nearly seven-fold upon infection, but when temperatures rise above 86°F, the plant can no longer produce enough of the defense hormone, and the infection spreads.
“Plants get a lot more infections at warm temperatures because their level of basal immunity is down,” He said. “So we wanted to know, how do plants feel the heat? And can we fix it to make plants heat-resilient?”
Earlier studies from other labs had identified plant proteins called phytochromes that act as thermometers and trigger growth and flowering in spring. He and his colleagues wondered whether phytochromes played a role in suppressing plant immunity as temperatures rise.
To answer this question, He’s team infected mutant plants with continuously active phytochromes and normal plants with P. syringae bacteria and grew them at 73 and 82°F. They found phytochrome mutants, like normal plants, still couldn’t make enough salicylic acid when temperatures rose.
The team spent several years testing other thermoregulatory genes but could not identify any that made plants resilient to infections in hot weather. This led the authors to conclude that suppression of salicylic acid production in Arabidopsis at high temperatures is independent of genes that regulate heat-responsive plant growth and development, such as phytochromeB and early flowering 3.
They then adopted next-generation sequencing to compare gene expression in infected Arabidopsis plants at normal and elevated temperatures and found many genes that were suppressed at high temperatures were regulated by a gene called CBP60g. CBP60g is a master switch that controls many other genes, including genes that produce salicylic acid.
In-depth analysis revealed heat impairs the molecular machinery that decodes CBP60g. The investigators demonstrated, Arabidopsis with continuously active CBP60g maintained adequate levels of salicylic acid and were resilient against bacterial infections even when exposed to heat.
However, constant activation of CBP60g can stunt plant growth. Therefore, the researchers optimized the regulation of the genetic master switch such that it turned on only under attack. He said, “These results could be good news for food supplies made insecure by climate change.”
In addition to Arabidopsis, He’s team found that increased temperatures also decreased salicylic acid defenses in tomato, rapeseed and rice. The team is currently restoring CBP60g gene activity in rapeseed and has seen promising results.
In addition to regulating the production of salicylic acid, CPB60g activity also protects other immunity-related genes against heat. “We were able to make the whole plant immune system more robust at warm temperatures,” He said. “If this is true for crop plants as well, that’s a really big deal because then we have a very powerful weapon.”