A team of IIGB plant cell biologists has discovered how to rewire a plant’s cellular machinery to heighten its response to stress– a finding that can be used to engineer crops to give them a better shot at surviving and displaying increased yield under drought conditions.

The discovery, made in the laboratory of Sean Cutler, an associate professor of plant cell biology in the Botany and Plant Sciences department, brings drought-tolerant crops a step closer to becoming a reality. When plants encounter drought, they naturally produce abscisic acid, a stress hormone that helps them cope with the drought conditions. Specifically, the hormone turns on receptors in the plants, resulting in a suite of beneficial changes that help the plants survive. These changes typically include guard cells closing on leaves to reduce water loss, cessation of plant growth to reduce water consumption and myriad other stress-relieving responses.

Working on Arabidopsis, a model plant used widely in plant biology labs, the Cutler-led research team has now succeeded supercharging the plant’s stress response pathway by modifying the abscisic acid receptors so that they can be turned on at will and stay on.

According to Cutler, each stress hormone receptor is equipped with a lid that operates like a gate. For the receptor to be in the on state, the lid must be closed. Using receptor genes engineered in the laboratory, the group created and tested more than 740 variants of the stress hormone receptor, hunting for the rare variants that caused the lid to be closed for longer periods of time. Next, the research team plans to take this basic science from the lab into the field – a process that could take many years.

Cutler was joined in the research by Assaf Mosquna (a postdoctoral reseacher and the first author of the research paper), Sang-Youl Park and Jorge Lozano-Juste at UCR; and Francis C. Peterson and Brian F. Volkman at the Medical College of Wisconsin.

Citation:
Mosquna A, Peterson FC, Park S-Y, Lozano-Juste J, Volkman BF, and Cutler SR (2011) Potent and selective activation of abscisic acid receptors in vivo by mutational stabilization of their agonist-bound conformation. PNAS 108 (51): 20838-20843