The activation of the oxidative metabolism in plants under low oxygen conditions has prompted controversial views. The presence of a ROS component in the transcriptome in response to low oxygen has been observed and an overlap with heat stress has been proved. It has been also demonstrated that ROS are produced during both anoxia and heat, but the site of their production remain contentious. Membrane NADPH oxidase and mitochondrial electron transport flow have been indicated as possible ROS generation systems. Both anoxia and heat have been shown to induce the transcription of Heat Shock Factors (HSFs) and Heat Shock Proteins (HSPs), among which HSFA2 and some of its targets. HSFA2 over-expressing plant has been shown to be more tolerant to anoxia, while the knockout hsfa2 lose the capability of wild type plants to cross-acclimate to anoxia through mild heat pre-treatment. The production of ROS seems to be an integral part of the anoxia and heat response, where HSFs likely play a central role in activating the HSP pathway. This mechanism is suggested to result in enhanced plant tolerance to both anoxia and heat.
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