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Published on: June 16, 2011
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Oxygen and RNA in stress-induced mutation
Raul Correa1, Philip C Thornton1, Susan M Rosenberg1,2,3,4
1Department of Molecular and Human Genetics, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX, 77303, USA.
Current Genetics
|January 3, 2018
Summary
Stress responses can increase mutation rates in bacteria like E. coli, potentially aiding adaptation. This review explores how DNA repair, transcription, and damaged bases contribute to stress-induced mutagenesis.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- Stress responses in organisms can upregulate mutation mechanisms.
- These stress-induced mutation mechanisms differ from those in growing cells.
- They share a common requirement for the induction of stress responses.
Purpose of the Study:
- To review progress in stress-response-dependent mutagenic DNA break repair mechanisms in Escherichia coli.
- To explore the relationship between mutation and transcription under stress.
- To examine the role of damaged bases in stress-induced mutagenesis.
Main Methods:
- Review of existing literature on stress-induced mutagenesis in E. coli.
- Analysis of the connection between mutation and transcription.
- Investigation of mechanisms involving damaged DNA bases and replication.
Main Results:
- Mutation can be linked to transcription, potentially targeting transcribed regions.
- Replication initiated by transcription can lead to mutation.
- Stress-induced mutation requires damaged bases, often caused by endogenous oxygen radicals in starved E. coli.
Conclusions:
- Damaged bases may stall the replisome, facilitating DNA-polymerase exchange.
- This exchange allows low-fidelity DNA polymerases to act, promoting mutation.
- Stress-induced mutagenesis may be a targeted adaptive mechanism in E. coli.
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