Abscisic acid-triggered guard cell l-cysteine desulfhydrase function and in situ hydrogen sulfide production contributes to heme oxygenase-modulated stomatal closure

Abstract

Recent studies have demonstrated that hydrogen sulfide (HS) produced through the activity of l-cysteine desulfhydrase (DES1) is an important gaseous signaling molecule in plants that could participate in abscisic acid (ABA)-induced stomatal closure. However, the coupling of the DES1/HS signaling pathways to guard cell movement has not been thoroughly elucidated. The results presented here provide genetic evidence for a physiologically relevant signaling pathway that governs guard cell in situ DES1/HS function in stomatal closure. We discovered that ABA-activated DES1 produces HS in guard cells. The impaired guard cell ABA phenotype of the des1 mutant can be fully complemented when DES1/HS function has been specifically rescued in guard cells and epidermal cells, but not mesophyll cells. This research further characterized DES1/HS function in the regulation of LONG HYPOCOTYL1 (HY1, a member of the heme oxygenase family) signaling. ABA-induced DES1 expression and HS production are hyper-activated in the hy1 mutant, both of which can be fully abolished by the addition of HS scavenger. Impaired guard cell ABA phenotype of des1/hy1 can be restored by HS donors. Taken together, this research indicated that guard cell in situ DES1 function is involved in ABA-induced stomatal closure, which also acts as a pivotal hub in regulating HY1 signaling.