Central function of slow anion channel (SLAC1) in guard cell CO2 signaling
Shaowu Xue 1*, Julian I. Schroeder 2
1Institute of Molecular Science, Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan 030006, China.
2Division of Biological Sciences, University of California, San Diego.
*Corresponding Author： Tel/Fax: (86)351-7017194; E-mail: firstname.lastname@example.org
The continuing rise in atmospheric CO2 causes closing of stomatal pores and regulates stomatal development, and thus globally regulates plant water loss, CO2 influx and water use efficiency. But this CO2 response and early signal transduction mechanisms that trigger CO2-induced stomatal movements have remained unexplored. Here we demonstrate that bicarbonate functions as a small-molecule activator of SLAC1 anion channels in guard cells. Elevated intracellular [HCO3-]i with low [CO2] and [H+] activated S-type anion currents, whereas low [HCO3-]i at high [CO2] and [H+] did not. Bicarbonate enhanced the intracellular Ca2+ sensitivity of S-type anion channel activation in wild type and ht1-2 mutant guard cells. ht1-2 mutant guard cells exhibited enhanced bicarbonate sensitivity of S-type anion channel activation. Interestingly, OST1 loss-of-function alleles showed strongly impaired CO2-induced stomatal closing and HCO3-activation of anion channels. Moreover, PYR/RCAR ABA receptor mutant slowed but did not abolish CO2/HCO3- signaling, redefining the convergence point of CO2 and ABA signaling. Together, bicarbonate collaborates with Ca2+ to activate SLAC1 in guard cell CO2 signaling. S.X. was supported by the Shanxi Scholarship Council of China (2011-012), Shanxi Technology Foundation for Selected Overseas Scholar and Natural Science Foundation of Shanxi Province (2012011006-4).
Key Words: bicarbonate; Ca2+; SLAC1; CO2 signaling; guard cell