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

Abstract

Guard cells shrink in response to drought stress and abscisic acid (ABA) signaling, thereby reducing stomatal aperture. Hydrogen peroxide (H₂O₂) is an important signaling molecule acting to induce stomatal closure. As yet, the molecular basis of control over the level of H₂O₂ 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 H₂O₂ in the guard cells. <i>HSL3</i> was markedly up-regulated by treating plants with either ABA or H₂O₂, as well as by dehydration. In the loss-of-function <i>hsl3</i> 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 <i>HSL3</i> had the opposite effect. In the <i>hsl3</i> mutant, the transcription of NADPH oxidase gene <i>RbohF</i> involved in H₂O₂ production showed marked up-regulation, as well as the level of catalase activity was weakly inducible by ABA, allowing H₂O₂ 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 H₂O₂ in the guard cells.