Journal
PLANT CELL
Volume 28, Issue 4, Pages 949-965Publisher
OXFORD UNIV PRESS INC
DOI: 10.1105/tpc.15.01050
Keywords
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Funding
- National Basic Research Program of China (973program) [2012CB114300]
- National Natural Science Foundation of China [31170227]
- Hundred Talents Program of the Chinese Academy of Sciences [2010OHTP06]
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Drought stress induces stomatal closure and inhibits stomatal opening simultaneously. However, the underlying molecular mechanism is still largely unknown. Here, we show that the slow-type (S-type) anion channels SLAC1 and SLAH3 mainly inhibit the inward-rectifying K+ channel KAT1 by protein-protein interaction and consequently prevent stomatal opening in Arabidopsis thaliana. Voltage-clamp results demonstrated that SLAC1 inhibited KAT1 dramatically but did not inhibit KAT2. SLAH3 inhibited KAT1 to a lesser extent than did SLAC1. Both the N and C termini of SLAC1 inhibited KAT1, but the inhibition by the N terminus was stronger. The C terminus was essential for SLAC1-mediated inhibition of KAT1. Furthermore, drought stress strongly upregulated the expression of SLAC1 and SLAH3 in Arabidopsis guard cells, and the overexpression of wildtype and truncated SLAC1 dramatically impaired inward K+ (K-in(+)) currents of guard cells and light-induced stomatal opening. Additionally, the inhibition of KAT1 by SLAC1 and KC1 only partially overlapped, suggesting that SLAC1 and KC1 inhibited K+ in channels via different molecular mechanisms. Taken together, these findings reveal a novel regulatory mechanism for stomatal movement, in which signaling pathways for stomatal closure and opening are directly coupled by protein-protein interaction between SLAC1/SLAH3 and KAT1 in Arabidopsis.
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