CONICET | Buscador de Institutos y Recursos Humanos

Stomata are microscopic structures in the epidermis of most land plants, formed by a central pore delimited by pairs of highlyspecialized cells, the guard cells. Stomatal pores have the key physiological function of exchange gasses between the plant and itsenvironment. Guard cells are able to sense external and internal stimuli and integrate them into a complex signalling network thattriggers 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 torecognize conserved motifs in pathogens surface, the pathogen-associated molecular patterns (PAMPs), and trigger differentsignalling pathways in order to induce stomatal closure, as a first mechanical barrier to prevent infection. The gasotransmitterhydrogen sulfide (H₂S), a highly reactive molecule, participates in the modulation of different physiological processes includingstomatal closure. Although H₂S can be produced in different subcellular compartments, the role of mitochondrial H₂S in plantsremains little explored. In this work, we present results obtained in our lab showing that mutants of the mitochondrial enzymaticsource, β-cyanoalanine synthase (cas-c1) has an impairment on stomatal closure induction and a reduced apoplastic ROSproduction with respect to wild type plants when treated with the bacterial PAMP flagellin (flg22). Moreover, employinggenetically-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 themitochondrial H₂S source CAS-C1 is involved in pathogen-induced stomatal closure.