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Proc Natl Acad Sci U S A. 2017 Aug 22;114(34):9200-9205. doi: 10.1073/pnas.1704754114. Epub 2017 Aug 7.

Aquaporins facilitate hydrogen peroxide entry into guard cells to mediate ABA- and pathogen-triggered stomatal closure.

Author information

1
Biochimie et Physiologie Moléculaire des Plantes, Unité Mixte de Recherche 5004, CNRS/Institut National de la Recherche Agronomique/Montpellier SupAgro/Université de Montpellier, F-34060 Montpellier Cedex 2, France.
2
Department of Biology, Nara Institute of Science and Technology, Ikoma, 630-0192, Japan.
3
Laboratoire de Biologie du Développement des Plantes, French Alternative Energies and Atomic Energy Commission (CEA) Cadarache, Unité Mixte de Recherche 7265, CNRS/CEA/Aix-Marseille Université, F-13108 Saint-Paul-lez-Durance, France.
4
Biochimie et Physiologie Moléculaire des Plantes, Unité Mixte de Recherche 5004, CNRS/Institut National de la Recherche Agronomique/Montpellier SupAgro/Université de Montpellier, F-34060 Montpellier Cedex 2, France; lionel.verdoucq@cnrs.fr.

Abstract

Stomatal movements are crucial for the control of plant water status and protection against pathogens. Assays on epidermal peels revealed that, similar to abscisic acid (ABA), pathogen-associated molecular pattern (PAMP) flg22 requires the AtPIP2;1 aquaporin to induce stomatal closure. Flg22 also induced an increase in osmotic water permeability (Pf) of guard cell protoplasts through activation of AtPIP2;1. The use of HyPer, a genetic probe for intracellular hydrogen peroxide (H2O2), revealed that both ABA and flg22 triggered an accumulation of H2O2 in wild-type but not pip2;1 guard cells. Pretreatment of guard cells with flg22 or ABA facilitated the influx of exogenous H2O2 Brassinosteroid insensitive 1-associated receptor kinase 1 (BAK1) and open stomata 1 (OST1)/Snf1-related protein kinase 2.6 (SnRK2.6) were both necessary to flg22-induced Pf and both phosphorylated AtPIP2;1 on Ser121 in vitro. Accumulation of H2O2 and stomatal closure as induced by flg22 was restored in pip2;1 guard cells by a phosphomimetic form (Ser121Asp) but not by a phosphodeficient form (Ser121Ala) of AtPIP2;1. We propose a mechanism whereby phosphorylation of AtPIP2;1 Ser121 by BAK1 and/or OST1 is triggered in response to flg22 to activate its water and H2O2 transport activities. This work establishes a signaling role of plasma membrane aquaporins in guard cells and potentially in other cellular context involving H2O2 signaling.

KEYWORDS:

aquaporin; guard cell signaling; hydrogen peroxide; pathogen; stomatal movement

PMID:
28784763
PMCID:
PMC5576802
DOI:
10.1073/pnas.1704754114
[Indexed for MEDLINE]
Free PMC Article

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