Glucose triggers stomatal closure mediated by basal signaling through HXK1 and PYR/RCAR receptors in Arabidopsis.

Abstract

Sugars play important roles in regulating plant growth, development, and stomatal movement. Here, we found that glucose triggered stomatal closure in a dose- and time-dependent manner in Arabidopsis. Pharmacological data showed that glucose-induced stomatal closure was greatly inhibited by catalase [CAT; a reactive oxygen species (ROS) scavenger], diphenyleneiodonium chloride (DPI; an NADPH oxidase inhibitor), lanthanum chloride (LaCl3; a Ca2+ channel blocker), EGTA (a Ca2+ chelator), and two nitrate reductase (NR) inhibitors, tungstate and sodium azide (NaN3), while it was not affected by salicylhydroxamic acid (SHAM; a peroxidase inhibitor). Moreover, glucose induced ROS and nitric oxide (NO) production in guard cells of Arabidopsis. The ROS production was almost completely removed by CAT, strongly restricted by DPI, and was not affected by SHAM. NO production was partially suppressed by tungstate and NaN3, and the levels of NO were significantly reduced in the nia1-1nia2-5 mutant. Additionally, glucose-triggered stomatal closure was significantly impaired in gin1-1, gin2-1, pyr1pyl1pyl2pyl4, abi1-1, ost1, slac1-4, cpk6-1, and nia1-1nia2-5 mutants. Likewise, the reductions in leaf stomatal conductance (gs) and transpiration rate (E) caused by glucose were reversed in the above mutants. These results suggest that glucose-triggered stomatal closure may be dependent on basal signaling through PYR/RCAR receptors and hexokinase1 (HXK1).