Stanford, CA—Roots face many challenges in the soil in order to supply the plant with the necessary water and nutrients. New work from Carnegie and Stanford University’s José Dinneny shows that one of these challenges, salinity, can cause root cells to explode if the risk is not properly sensed. The findings, published by Current Biology, could help scientists improve agricultural productivity in saline soils, which occur across the globe and reduce crop yields.
Salts build up in soils from natural causes, such as sea spray, or can be introduced as a consequence of irrigation and poor land management. Salinity has deleterious effects on plant health and limits crop yields, because salt inhibits water uptake and can be toxic for plants.
But Dinneny and his collaborators, including Alice Cheung at the University of Massachusetts Amherst and Carnegie’s Wei Feng, the paper’s lead author, determined a never-before-described effect that salt has on the plant cell wall—a structure that provides strength to the plant cell and determines the rate at which plant tissues can grow.
Animal cells are surrounded by a layer of material on the outside, called the extracellular matrix, which provides structural support and facilitates communication. But the walls that surround plant cells need to resist tremendous pressure that builds up inside them. Plant cell walls must be strong enough to resist pressures two to three times greater than that in a car tire, while also being elastic enough to allow for growth.
When this growth extends a plant root into a saline environment, the root’s first response for self-protection is to shut off growth for several hours.
“After this dormant phase, roots are ready to pick themselves up and start growing again,” explained Dinneny. “We were looking for genetic mutations that disrupted the ability of roots to successfully enter the recovery phase. We found one and the effect of the mutation simply shocked us.”
Dinneny, Cheung, Feng, and their colleagues found that a cell surface receptor—a kind of protein that interacts with molecules on the outside of the cell—called FERONIA is crucial to a plant’s ability to sense salinity’s effects on the wall and prevent a loss of structural integrity.
“Plants with mutations that cause them to be deficient in FERONIA actually violently explode as they start to recover growth, their tissues degenerate, and ultimately they die,” added Feng.
The damage caused by salinity could be partly reversed by adding chemicals to the environment that increased the strength of the wall.
Furthermore, the authors further showed similar defects could be observed in mutants that have disruptions in certain chemical bonds in the structures of their cell walls.
Taken together, these findings indicate that the FERONIA protein directly interacts with the plant cell wall and could be directly sensing some of the damage to the wall caused by salinity.
“What our work suggests is that the very processes that regulate plant cell wall chemistry may be important for sensing and surviving high-salt soil conditions,” Dinneny explained. “This opens up a whole new exciting area of research on salt tolerance mechanisms in plants—it may even be possible to change the chemistry of the cell wall to alter its resistance to salt-induced damage.”
The paper’s other co-authors are: Carnegie’s Heather Cartwright; Daniel Kita, Vinh Doan, Qiaohong Duan, Ming-Che Liu, Jacob Maman, Robert Yvon, and Hen-Ming Wuof the University of Massachusetts; Alexis Peaucelle of AgroParisTech and University of Cambridge; and Leonie Steinhorst, Ina Schmitz-Thom, and Jörg Kudla of the University of Münster.
Image Caption: The top images show a normal root with cells expanding during the growth recovery process during salt stress. The bottom row of images show the mutant deficient in FERONIA, where cells are disappearing due to a loss of cell integrity. Image is courtesy of Wei Feng.
This work was supported by the Sainsbury Laboratory at Cambridge University, the U.S. National Science Foundation, the U.S. National Institutes of Health, the Carnegie Institution for Science Endowment, and the German Research Foundation.