Heat waves are not good for people, but they can be just as bad for certain plants. Hot conditions and rising temperatures can affect the immune systems of plants such that they no longer function efficiently. This means that plants are more susceptible to infection by pathogens after heatwaves, even when the extreme temperatures do not last for long.
Scientists have known for decades that above-normal temperatures suppress a plant’s ability to make salicylic acid, a defense hormone that has an important role in the plant’s immune system, stopping pathogens and pests before they get established. The exact mechanism by which this immune system failure occurs, however, was not fully understood. In new research, published in the journal Nature, scientists now say that they understand why rising plant immune system becomes compromised when the temperatures rise too high. They have also proposed a way to reverse the effect and to boost plant defenses against heat. This would help plants to survive better in conditions of global warming, and keep food on tables around the world.
The scientists worked on a small species of cress, Arabidopsis thaliana, which is a flowering plant native to Eurasia and Africa. It is considered a weed and is commonly used in laboratory experiments involving plants. In earlier research, Sheng-Yang He from Duke University, and his graduate student Bethany Huot, found that even brief heat waves had a dramatic effect on the immune system functioning of Arabidopsis plants. The heat left them more prone to infection by a bacterium known as Pseudomonas syringae. Under normal circumstances, when this pathogen infects a plant, the levels of salicylic acid in the leaves increase up to seven-fold, preventing the bacterium from taking hold or spreading. But when the temperature rises above 86oF, the plant cannot make enough of this defense hormone to keep the pathogen in check.
“Plants get a lot more infections at warm temperatures because their level of basal immunity is down,” said Sheng-Yang He. “So we wanted to know, how do rising plant feel the heat? And can we actually fix it to make plants heat-resilient?” Around the same time, a different team of scientists had found that, in plant cells, molecules called phytochromes function as internal thermometers, helping plants sense warmer temperatures in the spring and activate growth and flowering. He and his colleagues wondered whether these same heat-sensing molecules could be involved in compromising the immune system when the heat is on.
To answer this question, the researchers looked at normal plants and mutant plants in which the phytochrome photoreceptors were always active, irrespective of the temperature. The plants were all infected with P. syringae bacteria, and then grown at temperatures of 73oF and 82oF. The researchers found that the phytochrome mutants fared exactly like normal plants: they still couldn’t make enough salicylic acid to fend off infections when temperatures were high. The scientists continued to search for the molecular mechanism behind failed immunity in Arabidopsis rising plant that were exposed to excess heat. Co-first authors Danve Castroverde and Jonghum Kim spent several years doing similar experiments involving various plant genes that could potentially have been involved, but those mutant plants also became more vulnerable to infections during warm spells.
A new approach had to be adopted. Using next-generation sequencing, the researchers compared gene readouts in infected Arabidopsis plants at normal and elevated temperatures. They found that many of the genes that were suppressed at the higher temperatures were regulated by the same molecule, a gene called CBP60g. The CBP60g gene acts like a master switch that controls the activity of many other genes, so anything that downregulates or “turns off” CBP60g will also affect the functioning of those other genes. In fact, the end result is that the plant cells simply don’t make the proteins needed in order to produce salicylic acid, a key substance in the immune response. Further experiments revealed that the cellular machinery needed to start reading out the genetic instructions in the CBP60g gene doesn’t assemble properly when it gets too hot, and that’s why the plant’s immune system can’t do its job anymore. When the researchers used mutant Arabidopsis plants in which the CBP60g gene was constantly “switched on,” the plants were able to produce high levels of salicylic acid and keep bacteria under control, even when they were heat stressed.
Source: This news is originally published by earth