Flooding of plants causes an impairment of aerobic metabolism as oxygen diffusion is limited, resulting in the activation of hypoxic responses. The activation of energy-saving and fermentative pathways is directed by transcription factors of the group VII ETHYLENE-RESPONSE FACTOR (ERFVII) family. Despite the eminent role of ERFVIIs in hypoxia signaling, the upstream signals and molecular components which activate the diverse transcriptional pathways during low-oxygen stress are unknown.
Through diverse approaches we demonstrate that a hypoxia-induced reactive oxygen species (ROS) burst occurs, and that it contributes to low-oxygen adaptation. Interestingly, this ROS burst is generated by both mitochondria and plasma membrane-located NADPH-oxidases. In addition, specific NADPH oxidases affect plant survival upon low oxygen stress, and to some extend the expression of ERFVII-regulated genes. Next to the ability to generate ROS, also maintenance of ROS homeostasis has a profound effect on hypoxia tolerance and the initial expression of hypoxia-responsive genes.
Taken together, ROS homeostasis and signaling are important for adaptation towards hypoxic conditions. Moreover, we suggest that different cellular compartments contribute to the hypoxia-induced ROS burst and thereby generate an integrative ROS signal that defines hypoxia stress specificity.