Climate change has already caused changes in the distribution of species in many parts of the world. When heat waves strike, they affect not only people but also the plants we rely on for food. This is because when temperatures rise too high, certain plant defences fail, making plants more vulnerable to pathogens and insect pests.
Scientists claim to have discovered a specific protein in plant cells that explains why immunity deteriorates as the temperature rises. They've also discovered a way to reverse the loss and strengthen plant defences against heat. The findings, published recently in the journal Nature, were discovered in Arabidopsis thaliana, a spindly plant with white flowers that serves as the "lab rat" of plant research. If the same results are replicated in crops, it will be good news for food security in a warming world, according to Duke University biologist and corresponding author Sheng-Yang He.
Research Findings:
Scientists have known for decades that high temperatures suppress a plant's ability to produce salicylic acid, a defence hormone that activates the plant's immune system and stops invaders before they cause too much damage. However, the molecular basis of this immune breakdown was not well understood.
He and his then-graduate student Bethany Huot discovered in the mid-2010s that even brief heat waves can have a dramatic effect on hormone defences in Arabidopsis plants, making them more susceptible to infection by the bacterium Pseudomonas syringae.
When this pathogen attacks, the levels of salicylic acid in a plant's leaves increase sevenfold to prevent bacteria from spreading. However, when temperatures rise above 86 degrees for just two days – not even in the triple digits – plants can no longer produce enough defense hormone to keep infection at bay.
"Plants get a lot more infections at warm temperatures because their basal immunity level is lower," he explained. "So we wanted to know how plants react to heat. And can we actually fix it so that plants can withstand heat?"
Around the same time, another team discovered that phytochromes, molecules found in plant cells, act as internal thermometers, allowing plants to sense warmer temperatures in the spring and activate growth and flowering. So he and his colleagues wondered: could these same heat-sensing molecules be what's weakening the immune system when it warms up, and be the key to restoring it?
To find out, the researchers infected normal plants and mutant plants with phytochromes that were always active regardless of temperature with P. syringae bacteria and grew them at 73 & 82 degrees Fahrenheit to see how they fared. However, the phytochrome mutants behaved exactly like normal plants: they couldn't produce enough salicylic acid to fight infections when temperatures rose.
Danve Castroverde and Jonghum Kim, co-first authors, spent several years conducting similar experiments with other gene suspects, and the mutant plants became ill during hot spells as well. So they tried a new strategy. They compared gene readouts in infected Arabidopsis plants grown at normal and elevated temperatures using next-generation sequencing. Many of the genes that were suppressed at high temperatures were found to be regulated by the same molecule, a gene called CBP60g.
Because the CBP60g gene functions as a master switch that controls other genes, anything that downregulates or "turns off" CBP60g means that many other genes are turned off as well — they don't make the proteins that allow a plant cell to build up salicylic acid. Further research revealed that when it gets too hot, the cellular machinery required to begin reading out the genetic instructions in the CBP60g gene does not assemble properly, causing the plant's immune system to fail.
The researchers demonstrated that mutant Arabidopsis plants with their CBP60g gene constantly "on" were able to keep their defence hormone levels high and bacteria at bay, even when subjected to heat stress. The researchers then discovered a way to engineer heat-resistant plants that activated the CBP60g master switch only when under attack, without stunting their growth – an important step if the findings are to help protect plant defences without negatively impacting crop yields.
At the same time, population growth is increasing global food demand. Forecasts indicate that food production will need to increase by 60% to feed the estimated 10 billion people expected on Earth by 2050. He believes that the real test for future food security will be whether their strategy for protecting immunity in Arabidopsis plants works in crops as well.
The researchers discovered that high temperatures not only weakened salicylic acid defences in Arabidopsis plants, but also had a similar effect on crop plants like tomato, rapeseed and rice.
So far, follow-up experiments to restore CBP60g gene activity in rapeseed have yielded the same promising results. He claims that genes with similar DNA sequences can be found across plants. In Arabidopsis, protecting the CPB60g master switch from heat not only restored genes involved in the production of salicylic acid, but also protected other defense-related genes from warmer temperatures.
"We were able to strengthen the entire plant immune system at warm temperatures," he said. "If this holds true for crop plants as well, it's a huge deal because we'll have a very powerful weapon." He's team collaborated with colleagues from Yale University, the University of California, Berkeley, and China's Tao Chen Huazhong Agricultural University on this project. Based on this work, a patent application has been filed.
The Natural Sciences and Engineering Research Council of Canada, the Korean Research Foundation Postdoctoral Fellowship, the National Institutes of Health T32 Predoctoral Fellowship, the Howard Hughes Medical Institute Exceptional Research Opportunities Fellowship, the MSU Plant Resilience Institute, and the Duke Science and Technology Initiative all contributed to this study.
(Source: Duke University)
