ABA-mediated regulation of PME12 influences stomatal density, pore aperture, and heat stress response in Arabidopsis thaliana.

PME12-mutated plants displayed altered stomatal characteristics and susceptibility to ABA-induced closure. Despite changes in PME activity, the mutant exhibited enhanced thermotolerance. These findings suggest a complex interplay between pectin methylesterification, ABA response, and stomatal function, contributing to plant adaptation to heat stress. Pectin, an essential component of plant cell walls, is synthesized in the Golgi apparatus and deposited into the cell wall in a highly methylesterified form. The degree and distribution of methylesterification within homogalacturonan (HGA) domains are crucial in determining its functional properties. Pectin methylesterase (PME) catalyzes the demethylesterification of HGA, which is pivotal for adjusting cell wall properties in response to environmental cues. Our investigation of PME12, a type-I pectin methylesterase in Arabidopsis, reveals its role in abscisic acid (ABA)-mediated stomatal regulation during heat stress, with the pme12 mutant showing increased stomatal density, reduced size, and heightened sensitivity to ABA-induced closure. Additionally, pme12 plants exhibited altered PME activities under heat stress but displayed enhanced thermotolerance. Moreover, our study identified SCRM as a transcriptional regulator positively influencing PME12 expression, linking stomatal development with PME12-mediated pectin methylesterification. These findings suggest that PME12-mediated pectin modification plays a role in coordinating ABA responses and influencing stomatal behavior under heat stress conditions.