Sulfur dioxide-induced guard cell death and stomatal closure are attenuated in nitrate/proton antiporter AtCLCa mutants

TL;DR

The study finds that acidification of guard cells helps plants close their stomata in response to sulfur dioxide, with a key role played by a nitrate/proton antiporter.

Contribution

The novel finding is that cytosolic acidification, mediated by the H+/nitrate antiporter AtCLCa, is a key mechanism for sulfur dioxide-induced stomatal closure in Arabidopsis.

Findings

Cytosolic acidification is a credible mechanism for SO2-induced stomatal closure in Arabidopsis.

CLCa mutants, which affect cytosolic pH homeostasis, show reduced sensitivity to SO2-induced stomatal closure.

Auxin and jasmonates are not primary mediators of SO2-induced stomatal closure.

Abstract

Guard cells surrounding the stomata play a crucial role in regulating the entrance of hazardous gases such as SO2 into leaves. Stomatal closure could be a plant response to mitigate SO2 damage, although the mechanism for SO2-induced closure remains controversial. Proposed mediators for SO2-induced stomatal closure include phytohormones, reactive oxygen species, gasotransmitters, and cytosolic acidification. In this study, we investigated the mechanism of stomatal closure in Arabidopsis in response to SO2. Despite an increment in auxin and jasmonates after SO2 exposure, the addition of auxin did not cause stomatal closure and jasmonate-insensitive mutants exhibited SO2-induced stomatal closure suggesting auxin and jasmonates are not mediators leading to the closure. In addition, supplementation of scavenging reagents for reactive oxygen species and gasotransmitters did not inhibit SO2-induced closure. Instead, we found that cytosolic acidification is a credible mechanism for SO2-induced stomatal closure in Arabidopsis. CLCa mutants coding H+/nitrate antiporter, involved in cytosolic pH homeostasis, showed less sensitive stomatal phenotype against SO2. These results suggest that cytosolic pH homeostasis plays a tenable role in SO2 response in guard cells.

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