A role for ethylene signaling and biosynthesis in regulating and accelerating CO2‐ and abscisic acid‐mediated stomatal movements in Arabidopsis

Abstract

Summary Little is known about long‐distance mesophyll‐driven signals that regulate stomatal conductance. Soluble and/or vapor‐phase molecules have been proposed. In this study, the involvement of the gaseous signal ethylene in the modulation of stomatal conductance in Arabidopsis thaliana by CO2/abscisic acid (ABA) was examined. We present a diffusion model which indicates that gaseous signaling molecule/s with a shorter/direct diffusion pathway to guard cells are more probable for rapid mesophyll‐dependent stomatal conductance changes. We, therefore, analyzed different Arabidopsis ethylene‐signaling and biosynthesis mutants for their ethylene production and kinetics of stomatal responses to ABA/[CO2]‐shifts. According to our research, higher [CO2] causes Arabidopsis rosettes to produce more ethylene. An ACC‐synthase octuple mutant with reduced ethylene biosynthesis exhibits dysfunctional CO2‐induced stomatal movements. Ethylene‐insensitive receptor (gain‐of‐function), etr1‐1 and etr2‐1, and signaling, ein2‐5 and ein2‐1, mutants showed intact stomatal responses to [CO2]‐shifts, whereas loss‐of‐function ethylene receptor mutants, including etr2‐3;ein4‐4;ers2‐3, etr1‐6;etr2‐3 and etr1‐6, showed markedly accelerated stomatal responses to [CO2]‐shifts. Further investigation revealed a significantly impaired stomatal closure to ABA in the ACC‐synthase octuple mutant and accelerated stomatal responses in the etr1‐6;etr2‐3, and etr1‐6, but not in the etr2‐3;ein4‐4;ers2‐3 mutants. These findings suggest essential functions of ethylene biosynthesis and signaling components in tuning/accelerating stomatal conductance responses to CO2 and ABA.