The DOI matches its Crossref record; 83 of the 85 references it cites were found in a registry or an index.
The SOS response regulates adaptive mutation
Open accessAbstract
Upon starvation some Escherichia coli cells undergo a transient, genome-wide hypermutation (called adaptive mutation) that is recombination-dependent and appears to be a response to a stressful environment. Adaptive mutation may reflect an inducible mechanism that generates genetic variability in times of stress. Previously, however, the regulatory components and signal transduction pathways controlling adaptive mutation were unknown. Here we show that adaptive mutation is regulated by the SOS response, a complex, graded response to DNA damage that includes induction of gene products blocking cell division and promoting mutation, recombination, and DNA repair. We find that SOS-induced levels of proteins other than RecA are needed for adaptive mutation. We report a requirement of RecF for efficient adaptive mutation and provide evidence that the role of RecF in mutation is to allow SOS induction. We also report the discovery of an SOS-controlled inhibitor of adaptive mutation, PsiB. These results indicate that adaptive mutation is a tightly regulated response, controlled both positively and negatively by the SOS system.
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“These data support previous work showing that increases in the mutation rate following DNA damage are due to the action of specific repair machinery, rather than the DNA damage itself (57–60).”
From Staphylococcus aureus Adapts to Oxidative Stress by Producing H 2 O 2 -Resistant Small-Colony Variants via the SOS Response (2015) · cites this paper as [59]
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Cites
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Cleavage of the Escherichia coli lexA protein by the recA protease.
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Nature of the SOS-inducing signal in Escherichia coli
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DNA-damaging agents stimulate gene expression at specific loci in Escherichia coli.
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UmuD′ 2 C is an error-prone DNA polymerase, Escherichia coli pol V
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Research works printed but not linked: 2
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Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms
Karatan, E., & Watnick, P. I. (2009) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00041-08 · Cited by 1,099
Mutation as a Stress Response and the Regulation of Evolvability
Galhardo, R. S., Hastings, P. J., & Rosenberg, S. M. (2007) · Critical Reviews in Biochemistry and Molecular Biology · doi:10.1080/10409230701648502 · Cited by 643
Self-citationCell Death in Pseudomonas aeruginosa Biofilm Development
Webb, J. S., Thompson, L. S., James, S., Charlton, T., Tolker‐Nielsen, T., Koch, B. M., Givskov, M., & Kjelleberg, S. J. (2003) · Journal of Bacteriology · doi:10.1128/jb.185.15.4585-4592.2003 · Cited by 600
Stress-Induced Mutagenesis in Bacteria
Bjedov, I., Tenaillon, O., Gérard, B., Souza, V., Denamur, É., Radman, M., Taddéi, F., & Matić, I. (2003) · Science · doi:10.1126/science.1082240 · Cited by 588
Pulingam, T., Parumasivam, T., Gazzali, A. M., Sulaiman, A. M., Chee, J. Y., Lakshmanan, M., Chin, C. F., & Sudesh, K. (2021) · European Journal of Pharmaceutical Sciences · doi:10.1016/j.ejps.2021.106103 · Cited by 591
Metadata
- Authors
- McKenzie, G. J., Harris, R. S., Lee, P. L., & Rosenberg, S. M.
- Affiliations
- University of Alberta (CA)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2000-05-30
- Volume
- 97
- Issue
- 12
- Pages
- 6646-6651
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC18688
- OpenAlex
- W2037722651
- Cited by
- 295
- References
- 85
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 12 · 2023: 16 · 2022: 16 · 2021: 9 · 2020: 8 · 2019: 12 · 2018: 28 · 2017: 6 · 2016: 12 · 2015: 3 · 2014: 6 · 2013: 7 · 2012: 12
- FWCI
- 8.70
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense
- Fondation pour la Recherche Médicale
- National Institutes of Health (5r01ai043917-05)
- National Institute of General Medical Sciences (R01GM053158)
- National Institute of Allergy and Infectious Diseases (R01-AI43917)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Keywords
- adaptive mutation, SOS response, Escherichia coli, starvation, recF, RecA, DNA damage response, signal transduction regulation
- MeSH terms
- LexA Repressor Protein, Adaptation, Physiological, Bacterial Proteins, DNA Repair, DNA-Binding Proteins, Mutation, Serine Endopeptidases, SOS Response, Genetics, Signal Transduction, Regulon, Escherichia coli Proteins
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