Hypoxia-induced increase in GABA content is essential for restoration of membrane potential and preventing ROS-induced disturbance to ion homeostasis

When plants are exposed to hypoxic conditions,the level of g-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 Ca^(2+)signaling.We show that reduced O_(2) availability affects H+-ATPase pumping activity,leading to membrane depolarization and K+loss via outward-rectifying GORK channels.Hypoxia stress also results in H_(2)O_(2) accumulation in the cell that activates ROS-inducible Ca^(2+)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-Ca^(2+)hub by transcriptional control of RBOH genes thus preventing over-excessive H_(2)O_(2) 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.