A New Player in Jasmonate-Mediated Stomatal Closure: The Arabidopsis thaliana Copper Amine Oxidase β

Plant defence responses to adverse environmental conditions include different stress signalling, allowing plant acclimation and survival. Among these responses one of the most common, immediate, and effective is the modulation of the stomatal aperture, which integrates different transduction pathways involving hydrogen peroxide (H2O2), calcium (Ca2+), nitric oxide (NO), phytohormones and other signalling components. The Arabidopsis thaliana copper amine oxidases beta (AtCuAO beta) encodes an apoplastic CuAO expressed in guard cells and root protoxylem tissues which oxidizes polyamines to aminoaldehydes with the production of H2O2 and ammonia. Here, its role in stomatal closure, signalled by the wound-associated phytohormone methyl-jasmonate (MeJA) was explored by pharmacological and genetic approaches. Obtained data show that AtCuAO beta tissue-specific expression is induced by MeJA, especially in stomata guard cells. Interestingly, two Atcuao beta T-DNA insertional mutants are unresponsive to this hormone, showing a compromised MeJA-mediated stomatal closure compared to the wild-type (WT) plants. Coherently, Atcuao beta mutants also show compromised H2O2-production in guard cells upon MeJA treatment. Furthermore, the H2O2 scavenger N,N-1-dimethylthiourea (DMTU) and the CuAO-specific inhibitor 2-bromoethylamine (2-BrEtA) both reversed the MeJA-induced stomatal closure and the H2O2 production in WT plants. Our data suggest that AtCuAO beta is involved in the H2O2 production implicated in MeJA-induced stomatal closure.

Automated summary

Plant defence responses to adverse environmental conditions involve various stress signalling pathways, with the modulation of stomatal aperture being a common and effective response. AtCuAO beta in Arabidopsis thaliana plays a crucial role in stomatal closure induced by MeJA, involving H2O2 production. Mutants of AtCuAO beta show compromised response to MeJA and reduced H2O2 production in guard cells.