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.