Stomata in a state of emergency: H2O2 is the target locked

Stomatal movements are essential for plants to regulate photosynthesis rate, water status, and immunity. Upon stress stimulation, the production of hydrogen peroxide (H2O2) in the apoplasts and its accumulation within the guard cells are among key determinatives for stomatal closure. The regulatory mechanisms of H2O2 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 H2O2-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 H2O2 production is targeted by pathogen toxins and effectors to counteract plant immunity.

Automated summary

This review summarizes the activation of NADPH oxidases and aquaporins in stomatal closure through calcium-dependent and calcium-independent mechanisms, and highlights how pathogen toxins and effectors target H2O2 production to counteract plant immunity.