The role of mitocondrial H2S in stomatal immunity response

PANTALENO, ROSARIO; SCUFFI, DENISE; CARLOS GARCIA-MATA

Santa Fe

Congreso; Reunión Argentina de Fisiología Vegetal; 2021

SAFV

Stomata are microscopic structures responsible for gas exchange regulation between plant and the environment. They are formed by a central pore delimited by pairs of specialized cells, the guard cells (GCs), which sense different stimuli and integrate them into a signalling network that controls pore size. Stomatal pores, as natural openings, are the entry gate for microorganisms and pathogens, therefore, stomatal closure is considered the first mechanical barrier to prevent infection. The signalling molecule hydrogen sulfide (H2S) is a low-weight gas that belongs to the group known as gasotransmitters. H2S is endogenously synthesized in plant mitochondria, by the activity of the enzyme ß-Cyanoalanine Synthase (CAS-C1), which catalyzes the reaction between cysteine and CN⁻ to form ß-Cyanoalanine and H2S (H2Sm). However, the function of H2Sm is mostly unknown.Currently, we are studying the role of mitochondrial H2S in GCs during pathogen induced stomatal closure. Results obtained so far showed that mitochondrial-targeted H2S donors (AP123, AP39 and RT01) induce stomatal closure in a dose-dependent manner, requiring the normal activity of complexes I an IV of mitochondrial electron transport chain (mETC) to trigger this response. On the other hand, treatment of the mutant cas-c1 with the bacterial elicitor flagellin (flg22), showed a lower apoplastic ROS production and an impaired stomatal closure. The latter response was restored with the addition of exogenous H2Sm (AP39). Altogether, data indicates that H2S donors targeted to mitochondria induce stomatal closure needing mETC normal activity, and suggests that H2Sm participates in the flg22-induced stomatal immunity.