Open AccessOxygen and RNA in stress-induced mutation
Author(s) -
Raúl Correa,
P. C. Thornton,
Susan M. Rosenberg,
P. J. Hastings
Publication year - 2018
Publication title -
current genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.825
H-Index - 81
eISSN - 1432-0983
pISSN - 0172-8083
DOI - 10.1007/s00294-017-0801-9
Subject(s) - biology , mutation , genetics , mutagenesis , suppressor mutation , dna repair , sos response , dna damage , dna replication , transcription (linguistics) , dna , rna polymerase , microbiology and biotechnology , dna polymerase , polymerase , escherichia coli , gene , linguistics , philosophy
Mechanisms of mutation upregulated by stress responses have been described in several organisms from bacteria to human. These mechanisms might accelerate genetic change specifically when cells are maladapted to their environment. Stress-induced mutation mechanisms differ in their genetic requirements from mutation in growing cells, occurring by different mechanisms in different assay systems, but having in common a requirement for the induction of stress-responses. Here, we review progress in two areas relevant to stress-response-dependent mutagenic DNA break repair mechanisms in Escherichia coli. First, we review evidence that relates mutation to transcription. This connection might allow mutagenesis in transcribed regions, including those relevant to any stress being experienced, opening the possibility that mutations could be targeted to regions where mutation might be advantageous under conditions of a specific stress. We review the mechanisms by which replication initiated by transcription can lead to mutation. Second, we review recent findings that, although stress-induced mutation does not require exogenous DNA-damaging agents, it does require the presence of damaged bases in DNA. For starved E. coli, endogenous oxygen radicals cause these altered bases. We postulate that damaged bases stall the replisome, which, we suggest, is required for DNA-polymerase exchange, allowing the action of low-fidelity DNA polymerases that promote mutation.