https://orcid.org/0000-0002-0128-1524
Abstract
A key tricarboxylic acid (TCA) cycle metabolite, malate, accumulates in leaves during dehydration and induces stomatal closure by recruiting cytosolic Ca2+, activating SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1), and promoting reactive oxygen species (ROS). However, the effects of malate on stomatal opening and its underlying molecular mechanisms remain poorly understood. Our study revealed that, among TCA cycle metabolites, malate specifically inhibited light-induced stomatal opening in both grapevine and Arabidopsis. We demonstrated that SLAC1 was required for malate's inhibitory effects. The inhibition by malate was disrupted by Ca2+ signaling inhibitors. Additionally, the malate signal was mediated by G-proteins, which regulate the production of second messengers. ROS production was abolished when G-proteins were inhibited. These findings show that malate efficiently maintains stomatal closure by not only inducing stomatal closure but also inhibiting stomatal opening. The inhibition of stomatal opening by malate is mediated through the activation of SLAC1 and the G-protein signaling cascade.
A proposed working model for malate signaling.
