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Abstract

When plants are exposed to hypoxic conditions, the level of γ-aminobutyric acid (GABA) in plant tissues increases by several orders of magnitude. The physiological rationale behind this elevation remains largely unanswered. By combining genetic and electrophysiological approach, in this work we show that hypoxia-induced increase in GABA content is essential for restoration of membrane potential and preventing ROS-induced disturbance to cytosolic K+ homeostasis and Ca2+ signaling. We show that reduced O2 availability affects H+-ATPase pumping activity, leading to membrane depolarization and K+ loss via outward-rectifying GORK channels. Hypoxia stress also results in H2O2 accumulation in the cell that activates ROS-inducible Ca2+ uptake channels and triggers self-amplifying “ROS-Ca hub,” further exacerbating K+ loss via non-selective cation channels that results in the loss of the cell's viability. Hypoxia-induced elevation in the GABA level may restore membrane potential by pH-dependent regulation of H+-ATPase and/or by generating more energy through the activation of the GABA shunt pathway and TCA cycle. Elevated GABA can also provide better control of the ROS-Ca2+ hub by transcriptional control of RBOH genes thus preventing over-excessive H2O2 accumulation. Finally, GABA can operate as a ligand directly controlling the open probability and conductance of K+ efflux GORK channels, thus enabling plants adaptation to hypoxic conditions.

Item Type:	Article
Authors/Creators:	Wu, Qi and Su, N and Huang, Xin and Cui, J and Shabala, L and Zhou, M and Yu, M and Shabala, S
Keywords:	hypoxia, GABA, membrane potential, ROS, ion homeostasis, potassium homeostasis, calcium signaling, NADPH oxidase, GORK, H+-ATPase, reactive oxygen species
Journal or Publication Title:	Plant Communications
Publisher:	Cell Press
ISSN:	2590-3462
DOI / ID Number:	https://doi.org/10.1016/j.xplc.2021.100188
Copyright Information:	Copyright 2021 The Author(s). This is an open access article under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Related URLs:	Google Scholar: Shabala, L UTAS Profile: Shabala, L Google Scholar: Zhou, M UTAS Profile: Zhou, M Google Scholar: Shabala, S UTAS Profile: Shabala, S
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