Abstract

Plant cells that are exposed to anoxia run into an energy crisis. As a result of this, compartmental transmembrane gradients break down (sooner or later) leading ultimately to cell death. Regulation of intracellular pH and intercompartmental pH signaling may play a critical role in tolerating anoxia for some time. An early consequence of anoxia is a cytoplasmic pH drop which, according to the Davis-Roberts hypothesis, arises from the lactate formation. H+ leakage from the vacuole or H+ arising from nucleotide triphosphate hydrolysis have been also suggested. Research has focused on the assumption that the anoxic cytoplasmic pH change is an “error signal ” to which the cell should respond to avoid cell-damaging acidosis. This view is challenged here. It is argued that pH under anoxia represents a new set point required for the anaerobic metabolism and for gene activation. It is concluded that acidosis does not occur because of H+ leaking through membranes or because of the production of acids, but because of energy shortage which prevents the maintenance of transmembrane gradients; the leveling of the pH gradients and subsequent cytoplasmic acidosis are a consequence thereof.

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