Hydrogen Sulfide modulates Flagellin-Induced Stomatal Immunity

Stomata are natural pores through which plants exchange gases with the environment, mainly carbon dioxide and oxygen required for photosynthesis and respiration, as well as water vapor through evapotranspiration. However, they also serve as entry points for microbial pathogens such as Pseudomonas syringae pv. tomato (Pst) bacteria. To prevent microbe invasion, guard cells detect pathogens-associated molecular patterns (PAMPs), including the bacterial peptide flagellin (flg22), triggering stomatal closure. This study identifies hydrogen sulfide (H2S) and its cytosolic source L-CYSTEINE DESULFHIDRASE 1 (DES1), as key players in stomatal immunity. We demonstrate that H2S and DES1 are involved in flg22- and bacterial-induced responses, including stomatal closure and modulation of reactive oxygen species (ROS) production. We have found that knock out mutants in DES1 gene exhibits reduced susceptibility to Pst spray-inoculation and lower apoplastic and cytosolic H2O2 levels in response to flg22. Additionally, H2S independently induces cytosolic H2O2 levels in guard cells without requiring RBOHD activity. All together, these findings establish H2S and its source, DES1, as critical components of the stomatal immune response. One Sentence SummaryH2S and DES1 actively participate in flg22-induced stomatal closure modulating apoplastic and cytosolic ROS production.