The coordination of guard-cell autonomous ABA synthesis and DES1 function in situ regulates plant water deficit responses

INTRODUCTION: Drought stress triggers the synthesis and accumulation of the phytohormone abscisic acid (ABA), which regulates stomatal aperture and hence reducing plant water loss. Hydrogen sulfide (H(2)S), which is produced by the enzyme L-cysteine desulfhydrase 1 (DES1) that catalyzes the desulfuration of L-cysteine in Arabidopsis, also plays a critical role in the regulation of drought-induced stomatal closure. However, little is known about the regulation of DES1 or the crosstalk between H(2)S and ABA signaling in response to dehydration. OBJECTIVES: To demonstrate the potential crosstalk between DES1-dependent H(2)S and ABA signaling in response to dehydration and its regulation mechanism. METHODS: Firstly, by introducing guard cell-specific MYB60 promoter, to produce complementary lines of DES1 or ABA3 into guard cell of des1 or aba3 mutant. And the related genes expression and water loss under ABA, NaHS, or dehydration treatment in these mutant or transgenics lines were determinate. RESULTS: We found that dehydration-induced expression of DES1 is abolished in the abscisic acid deficient 3 (aba3) mutants that are deficient in ABA synthesis. Both the complementation of ABA3 expression in guard cells of the aba3 mutants and ABA treatment rescue the dehydration-induced expression of DES1, as well as the wilting phenotype observed in these mutants. Moreover, the drought-induced expression of ABA synthesis genes was suppressed in des1 mutants. While the addition of ABA or the expression of either ABA3 or DES1 in the guard cells of the aba3/des1 double mutant did not alter the wilting phenotype of these mutants, the wild type phenotype was fully restored by the expression of both ABA3 and DES1, or by the application of NaHS. CONCLUSION: These results demonstrate that the coordinated synthesis of ABA and DES1 expression is required for drought-induced stomatal closure in Arabidopsis.