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.