Stomatal movements are essential for plants to regulate photosynthesis rate, water status, and immunity. Upon stress stimulation, the production of hydrogen peroxide (HO) in the apoplasts and its accumulation within the guard cells are among key determinatives for stomatal closure. The regulatory mechanisms of HO production and transport under plant-pathogen interaction and drought stress response in stomata are important fields of research. Specifically, the regulation of NADPH oxidases and aquaporins appears to be crucial in HO-controlled stomatal closure. In this review, we summarize how the calcium-dependent and calcium-independent mechanisms activate RESPIRATORY BURST OXIDASE HOMOLOG (RBOH)D/F NADPH oxidases and the aquaporin PIP2;1 to induce stomatal closure, and highlight how the HO production is targeted by pathogen toxins and effectors to counteract plant immunity.
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