Mechanisms of stationary phase mutation: a decade of adaptive mutation - PubMed (original) (raw)
Review
Mechanisms of stationary phase mutation: a decade of adaptive mutation
P L Foster. Annu Rev Genet. 1999.
Abstract
A decade of research on adaptive mutation has revealed a plethora of mutagenic mechanisms that may be important in evolution. The DNA synthesis associated with recombination could be an important source of spontaneous mutation in cells that are not proliferating. The movement of insertion elements can be responsive to environmental conditions. Insertion elements not only activate and inactivate genes, they also provide sequence homology that allows large-scale genomic rearrangements. Some conjugative plasmids can recombine with their host's chromosome, and may acquire chromosomal genes that could then spread through the population and even to other species. Finally, a subpopulation of transient hypermutators could be a source of multiple variant alleles, providing a mechanism for rapid evolution under adverse conditions.
Figures
Figure 1
A model for recombination-dependent mutation. Panels A to B, collapse of the replication fork at oriT; panels C to D, RecABCD catalyzed recombination; panel E, restoration of the replication fork; panel F, translocation of the Holliday junction in opposite directions by RuvAB and RecG; panel G, resolution of the Holliday junction by RuvC (not shown). See text for details. Dashed lines are newly synthesized DNA; * at oriT indicates TraI.
Figure 2
Venn diagram illustrating the role of transient mutators in adaptive mutation.
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