In a growing number of cases, transcription of specific genes is known to be governed by oxidation or reduction of electron carriers with which the gene products interact. The biological function of such control is to activate synthesis of appropriate redox proteins, and to repress synthesis of inappropriate ones, in response to altered availability of specific electron sources and sinks. In prokaryotic systems this control appears to operate by two general classes of mechanism: by two-component regulation involving protein phosphorylation on histidine and aspartate; and by direct oxidation-reduction of gene repressors or activators. For the first class, termed ‘two-component redox regulation’, the term ‘redox sensor’ is proposed for any electron carrier that becomes phosphorylated upon oxidation or reduction and thereby controls phosphorylation of specific response regulators, while the term ‘redox response regulator’ is proposed for the corresponding sequence-specific DNA-binding protein that controls transcription as a result of its phosphorylation by one or more redox sensors. For the second class of redox regulatory mechanism, the terms ‘redox activator protein’ and ‘redox repressor protein’ are proposed for single proteins containing both electron transfer and sequence-specific DNA-binding domains. The structure, function and biological distribution of these components are discussed.
