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

Recent studies have demonstrated that hydrogen sulfide (H 2 S) 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/H 2 S 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/H 2 S function in stomatal closure. We discovered that ABA‐activated DES1 produces H 2 S in guard cells. The impaired guard cell ABA phenotype of the des1 mutant can be fully complemented when DES1/H 2 S function has been specifically rescued in guard cells and epidermal cells, but not mesophyll cells. This research further characterized DES1/H 2 S function in the regulation of LONG HYPOCOTYL1 (HY1, a member of the heme oxygenase family) signaling. ABA‐induced DES1 expression and H 2 S production are hyper‐activated in the hy1 mutant, both of which can be fully abolished by the addition of H 2 S scavenger. Impaired guard cell ABA phenotype of des1/hy1 can be restored by H 2 S 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.