Pectin methylesterification in guard cell (GC) walls plays an important role in stomatal development and stomatal response to external stimuli, and pectin methylesterase inhibitors (PMEIs) modulate pectin methylesterification by inhibition… Click to show full abstract
Pectin methylesterification in guard cell (GC) walls plays an important role in stomatal development and stomatal response to external stimuli, and pectin methylesterase inhibitors (PMEIs) modulate pectin methylesterification by inhibition of pectin methylesterase (PME). However, the function of PMEIs has not been reported in stomata. Here, we report the role of Arabidopsis (Arabidopsis thaliana) PECTIN METHYLESTERASE INHIBITOR18 in stomatal dynamic responses to environmental changes. PMEI18 mutation increased pectin demethylesterification and reduced pectin degradation, resulting in increased stomatal pore size, impaired stomatal dynamics, and hypersensitivity to drought stresses. In contrast, overexpression of PMEI18 reduced pectin demethylesterification and increased pectin degradation, causing more rapid stomatal dynamics. PMEI18 interacted with PME31 in plants, and in vitro enzymatic assays demonstrated that PMEI18 directly inhibits the PME activity of PME31 on pectins. Genetic interaction analyses suggested that PMEI18 modulates stomatal dynamics mainly though inhibition of PME31 on pectin methylesterification in cell walls. Our results provide insight into the molecular mechanism of the PMEI18-PME31 module in stomatal dynamics and highlight the role of PMEI18 and PME31 in stomatal dynamics through modulation of pectin methylesterification and distribution in GC walls.
               
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