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Guard cells shrink in response to drought stress and abscisic acid (ABA) signaling, thereby reducing stomatal aperture. Hydrogen peroxide (H 2 O 2 ) is an important signaling molecule acting to induce stomatal closure. As yet, the molecular basis of control over the level of H 2 O 2  in the guard cells remains largely unknown. Here, the leucine-rich repeat (LRR)—receptor-like kinase (RLK) protein HSL3 has been shown to have the ability to negatively regulate stomatal closure by modulating the level of H 2 O 2  in the guard cells.  HSL3  was markedly up-regulated by treating plants with either ABA or H 2 O 2 , as well as by dehydration. In the loss-of-function  hsl3  mutant, both stomatal closure and the activation of anion currents proved to be hypersensitive to ABA treatment, and the mutant was more tolerant than the wild type to moisture deficit; the overexpression of  HSL3  had the opposite effect. In the  hsl3  mutant, the transcription of NADPH oxidase gene  RbohF  involved in H 2 O 2  production showed marked up-regulation, as well as the level of catalase activity was weakly inducible by ABA, allowing H 2 O 2  to accumulate in the guard cells. HSL3 was concluded to participate in the regulation of the response to moisture deficit through ABA-induced stomatal closure triggered by the accumulation of H 2 O 2  in the guard cells.

The LRR-RLK Protein HSL3 Regulates Stomatal Closure and the Drought Stress Response by Modulating Hydrogen Peroxide Homeostasis