GSNOR1-mediated Guard Cell Signaling In Arabidopsis

NO plays a central role in guard cell signal transduction pathway. Previous works have demonstrated that NO mediated stomaotal movement by regulated directly with other components such as ion channel, cytoskeleton, and transcription factors. NO and its derivatives (nitroso, etc.) can react with cysteine thiol groups of those proteins, to form S-nitrosothiols and thus change their activity. S-nitrosoglutathione, form from NO and Glutathione, is the main donor of nitroso. S-nitrosoglutathione reductase is the enzyme that control the synthesis and metabolism of GSNO and S-nitrosylation. Absence of GSNOR1 increased nitroso levels and nitrosylation. Recent studies suggest that GSNO also involved in stomatal movements, but the details signaling pathway still largely unkonwn.To address the role of GSNOR1 in stomatal movement, I first iolated the homozygous of GSNOR1 T-DNA insertion homozygous mutant. gsnor1 showed lower leaves surface tempreature and higher water loss in nomal conditions. According with this, stomata of gsnor1 was less sensitive to ABA, SNP, GSNO than wild-type plants. But no obvious difference between wild-type and gsnor1 under H₂O₂ application. Interestingly, high levels of GUS expression were detected in the guard cells of pGSNOR1-GUS transgenic plants, and the GUS activity dramatically inhibited by application of ABA or SNP. We also found that Ca²⁺ also involved in the GSNOR1 inhibited ABA induced stomatal closure. By comparation the stmotal movement of gsnor1 with the mutants of regualtion components in ABA signaling, abi1, abi2 and ost1, we found that GSNOR1 is a new component in ABA meidated guard cell signaling network. Our work provide valuable information to further clarify its role in NO signal transduction pathways in the guard cells and lay the foundation for the molecular mechanisms involved in plant stress response.