Abstract
Reactive oxygen species (ROS) are a common source of damage to cellular DNA, and have been implicated in mutagenesis and carcinogenesis. In bacteria, their mutagenicity appears to be mediated in part by the mutagenic SOS system and in part by SOS-independent mechanisms. Since acrobically growing log-phase cells (which by definition are well adapted to their environment) would not be especially well served by the near-continuous induction of their potentially mutagenic SOS systems, it may be that several mechanisms are required to ensure that this does not become a major problem. In addition to some well-documented ROS-scavenging and antioxidant defence systems, it is suggested that ROS-mediated cleavage of the LexA repressor may only be able to activate transcription of the mutagenically important SOS genes (e.g. theumuDC genes) ofEscherichia coli if the cells concerned also contain substantial quantities of a transcription activator known as the cAMP/CRP complex. This may be why aerobically incubated stationary-phase bacteria (which ought to contain increased levels of cAMP/CRP as a consequence of their nutritionally deprived status) often turn out to be significantly more mutable than their log-phase counterparts. Thus when bacteria are being selected for some new characteristic under nutritional duress, it may be their spontaneous mutation-generation systems that are responding adaptively, not the mutations that they produce.
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Macphee, D.G. Adaptive mutability in bacteria. J Genet 78, 29–33 (1999). https://doi.org/10.1007/BF02994700
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DOI: https://doi.org/10.1007/BF02994700