Nattiwong Pankasem, University of California San Diego
Nattiwong Pankasem
University of California San Diego

Nattiwong Pankasem is a Ph.D. student in the UCSD-Salk Biological Sciences Program at UC San Diego. He earned his Bachelor’s degree in Agricultural Science at the University of Tsukuba, Japan. Nattiwong grew up on a smallholder family farm in Thailand, where he developed an interest in plant biology from an early age. He is fascinated by the plant adaptation to cope with the ever-changing environment. As atmospheric CO2 increases and global warming continues, environmental stresses such as heat waves, water shortages, and high vapor pressure deficit pose a significant challenge to crop production and food security for humanity. Nattiwong is interested in how stomata respond to elevated CO2, high temperatures, and light stimuli. He is working with Dr. Julian Schroeder on finding molecular sensors and advancing the understanding of guard cell functions using the model plant Arabidopsis thaliana with modern genetic tools. 

Title of presentation

Warming temperature triggers stomatal opening by enhancement of photosynthesis and ensuing guard cell CO2 sensing, whereas further temperature elevation open stomata via a different pathway

Authors

Nattiwong Pankasem , Po-Kai Hsu, Peter J. Franks, Yohei Takahashi and Julian I. Schroeder
Cell and Developmental Biology Department, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093-0116, USA.

Abstract

Stomata provide an avenue to optimize photosynthesis and water loss. In light of global warming, stomatal temperature response and the underlying molecular genetic mechanisms remain less studied. We developed a gas-exchange approach for controlling vapor pressure difference (VPD leaf ), allowing a measurement of reversible warming-induced stomatal opening in intact plants. We analyzed stomatal temperature responses of mutants impaired in signaling pathways for blue-light, ABA, brassinosteroid, CO2 , and temperature-sensitive Phytochrome-B (phyB) and EARLY-FLOWERING-3 (ELF3). We confirmed that the phot1/phot2 mutant lacking blue-light photoreceptors showed partially reduced warming-induced stomatal opening. Furthermore, brassinosteroid signaling, ABA-biosynthesis, phyB, and ELF3 were not essential for the stomatal warming response. Strikingly, mutants lacking guard cell CO2 sensing and signaling mechanisms abolished the stomatal warming response. We have recently identified a primary CO2 /bicarbonate sensor in guard cells that mediates CO2 control of stomatal movement. New advances in understanding this stomatal CO2 sensing core will be presented. We further demonstrate that warming rapidly stimulates photosynthesis, resulting in a reduction in intercellular [CO2 ]. We provide genetic and physiological evidence that the stomatal warming response is triggered by increased photosynthesis and stomatal low-CO2 sensing. Additional findings demonstrate that increasing higher temperature functions via a distinct pathway from the above pathway.

My Sessions
Warming temperature triggers stomatal opening by enhancement of photosynthesis and ensuing guard cell CO2 sensing, whereas further temperature elevation open stomata via a different pathway
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Presentation
Session topics
S:4