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: xsw92@yahoo.com.cn

Abstract
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