The role of mitochondrial H2S in stomatal closure induced by pathogens

PANTALENO, ROSARIO; SCUFFI, DENISE; SCHIEL, PAULA; COSTA, ALEX; GARCÍA-MATA, CARLOS

Mendoza

Congreso; LVIII Annual Meeting of the Argentine Society for Biochemistry and Molecular Biology Research; 2022

SAIB

Stomata are microscopic structures in the epidermis of most land plants, formed by a central poredelimited by pairs of highly specialized cells, the guard cells. Stomatal pores have the key physiological function of exchange gasses between the plant and its environment. Guard cells are able to sense external and internal stimuli and integrate them into a complex signalling network that triggers changes in the cellular volume to control pore size, leading to stomatal aperture or closure. Some bacterial and fungal pathogens use stomatal pores as a natural entrance to infect plants. As a consequence, plants evolved to recognize conserved motifs in pathogens surface, the pathogen associated molecular patterns (PAMPs), and trigger different signalling pathways in order to induce stomatal closure, as a first mechanical barrier to prevent infection. The gasotransmitter hydrogen sulfide (H₂S), a highly reactive molecule, participates in the modulation of different physiological processes including stomatal closure. Although H₂S can be produced in different subcellular compartments, the role of mitochondrial H₂S in plants remains little explored. In this work, we present results obtained in our lab showing that mutants of the mitochondrial enzymatic source, β-cyanoalanine synthase (cas-c1 ) has an impairment on stomatal closure induction and a reduced apoplastic ROS production with respect to wild type plants when treated with the bacterial PAMP flagellin (flg22). Moreover, employing genetically encoded sensors, we observed that guard cells from cas-c1 have altered cytosolic H2O2 levels and glutathione (GSH) oxidative status at basal conditions and in response to flg22. In summary, the results presented in the poster show that the mitochondrial H₂S source CAS-C1 is involved in pathogen-induced stomatal closure.