Heterotrimeric G protein mediates ethylene‐induced stomatal closure via hydrogen peroxide synthesis in Arabidopsis

• Published in: The Plant journal : for cell and molecular biology 2015-04, Vol.82 (1), p.138-150
• Main Authors: Ge, Xiao‐Min, Cai, Hong‐Li, Lei, Xue, Zhou, Xue, Yue, Ming, He, Jun‐Min
• Format: Article
• Language: English
• Subjects: Arabidopsis; Arabidopsis - genetics; Arabidopsis - physiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Biosynthesis; Botany; Ethylene; ethylene receptor; Ethylenes - pharmacology; Gene Expression Regulation, Plant; gene overexpression; GTP-Binding Protein alpha Subunits - genetics; GTP-Binding Protein alpha Subunits - metabolism; guard cells; Gα subunit; H2O2; heterotrimeric G protein; Hydrogen peroxide; Hydrogen Peroxide - metabolism; leaves; mutants; Mutation; NADPH oxidases; Plant Growth Regulators - pharmacology; Plant Leaves - genetics; Plant Stomata - genetics; Plant Stomata - physiology; Proteins; Receptors, Cell Surface - genetics; Receptors, Cell Surface - metabolism; Signal Transduction; signalling; stomata; stomatal closure; stomatal movement
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1111/tpj.12799

Heterotrimeric G proteins function as key players in hydrogen peroxide (H₂O₂) production in plant cells, but whether G proteins mediate ethylene‐induced H₂O₂production and stomatal closure are not clear. Here, evidences are provided to show the Gα subunit GPA1 as a missing link between ethylene and H₂O₂in guard cell ethylene signalling. In wild‐type leaves, ethylene‐triggered H₂O₂synthesis and stomatal closure were dependent on activation of Gα. GPA1 mutants showed the defect of ethylene‐induced H₂O₂production and stomatal closure, whereas wGα and cGα overexpression lines showed faster stomatal closure and H₂O₂production in response to ethylene. Ethylene‐triggered H₂O₂generation and stomatal closure were impaired in RAN1, ETR1, ERS1 and EIN4 mutants but not impaired in ETR2 and ERS2 mutants. Gα activator and H₂O₂rescued the defect of RAN1 and EIN4 mutants or etr1‐3 in ethylene‐induced H₂O₂production and stomatal closure, but only rescued the defect of ERS1 mutants or etr1‐1 and etr1‐9 in ethylene‐induced H₂O₂production. Stomata of CTR1 mutants showed constitutive H₂O₂production and stomatal closure, but which could be abolished by Gα inhibitor. Stomata of EIN2, EIN3 and ARR2 mutants did not close in responses to ethylene, Gα activator or H₂O₂, but do generate H₂O₂following challenge of ethylene or Gα activator. The data indicate that Gα mediates ethylene‐induced stomatal closure via H₂O₂production, and acts downstream of RAN1, ETR1, ERS1, EIN4 and CTR1 and upstream of EIN2, EIN3 and ARR2. The data also show that ETR1 and ERS1 mediate both ethylene and H₂O₂signalling in guard cells.