The SOS Response Regulates Adaptive Mutation
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 ti...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2000-06, Vol.97 (12), p.6646-6651 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | McKenzie, Gregory J. Harris, Reuben S. Lee, Peter L. Rosenberg, Susan M. |
| description | 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. |
| doi_str_mv | 10.1073/pnas.120161797 |
| format | Article |
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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. 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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.</description><subject>Adaptation, Physiological</subject><subject>adaptive mutation</subject><subject>Alleles</subject><subject>Bacteria</subject><subject>Bacterial Proteins - physiology</subject><subject>Biological Sciences</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Escherichia coli</subject><subject>Escherichia coli Proteins</subject><subject>Gene expression regulation</subject><subject>Genetic mutation</subject><subject>Genetic SOS response</subject><subject>Genetics</subject><subject>Mutagenesis</subject><subject>Mutation</subject><subject>PsiB protein</subject><subject>RecA protein</subject><subject>RecF protein</subject><subject>Regulon</subject><subject>Serine Endopeptidases - physiology</subject><subject>Signal Transduction</subject><subject>SOS response</subject><subject>SOS Response (Genetics)</subject><subject>T lymphocytes</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtP3DAUhS3UCqbQLRukasSibJrh2olfUjcItbQSCInH2nLiG8goE6exg-i_r0cBOu0CVr7S_c6xfQ4h-xQWFGR-3Hc2LCgDKqjUcovMKGiaiULDOzIDYDJTBSt2yIcQlgCguYJtskNBMQ1SzsiXm3ucX19ez68w9L4LmIa7sbURw_zE2T42Dzi_GKONje_2yPvatgE_Pp275Pb7t5vTH9n55dnP05PzrOJUxsxxy0sGlpVO10rzyvK6RCecKi1wRFegTIATBatl6dLEOXOMVRyYxYrnu-Tr5NuP5QpdhV0cbGv6oVnZ4bfxtjH_brrm3tz5B0OVUCrJPz_JB_9rxBDNqgkVtq3t0I_BSJrS4gzeBKkUVEyOh_-BSz8OXcrApOhzrSCnCVpMUDX4EAasXx5MwazLMuuyzEtZSfBp85sb-NTOBrAWPq-1TB5GiEIk4OhVwNRj20Z8jIk8mMhliH74exVjQtP8D7NNsV0</recordid><startdate>20000606</startdate><enddate>20000606</enddate><creator>McKenzie, Gregory J.</creator><creator>Harris, Reuben S.</creator><creator>Lee, Peter L.</creator><creator>Rosenberg, Susan M.</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20000606</creationdate><title>The SOS Response Regulates Adaptive Mutation</title><author>McKenzie, Gregory J. ; Harris, Reuben S. ; Lee, Peter L. ; Rosenberg, Susan M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c517t-d5a5b20a2bd9f895ca5fbed6d8ba05eed4e75b2d642f7bdb2d552d22c502aec53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adaptation, Physiological</topic><topic>adaptive mutation</topic><topic>Alleles</topic><topic>Bacteria</topic><topic>Bacterial Proteins - physiology</topic><topic>Biological Sciences</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Escherichia coli</topic><topic>Escherichia coli Proteins</topic><topic>Gene expression regulation</topic><topic>Genetic mutation</topic><topic>Genetic SOS response</topic><topic>Genetics</topic><topic>Mutagenesis</topic><topic>Mutation</topic><topic>PsiB protein</topic><topic>RecA protein</topic><topic>RecF protein</topic><topic>Regulon</topic><topic>Serine Endopeptidases - physiology</topic><topic>Signal Transduction</topic><topic>SOS response</topic><topic>SOS Response (Genetics)</topic><topic>T lymphocytes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McKenzie, Gregory J.</creatorcontrib><creatorcontrib>Harris, Reuben S.</creatorcontrib><creatorcontrib>Lee, Peter L.</creatorcontrib><creatorcontrib>Rosenberg, Susan M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McKenzie, Gregory J.</au><au>Harris, Reuben S.</au><au>Lee, Peter L.</au><au>Rosenberg, Susan M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The SOS Response Regulates Adaptive Mutation</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2000-06-06</date><risdate>2000</risdate><volume>97</volume><issue>12</issue><spage>6646</spage><epage>6651</epage><pages>6646-6651</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>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. 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| subjects | Adaptation, Physiological adaptive mutation Alleles Bacteria Bacterial Proteins - physiology Biological Sciences Deoxyribonucleic acid DNA DNA damage DNA Repair DNA-Binding Proteins - physiology Escherichia coli Escherichia coli Proteins Gene expression regulation Genetic mutation Genetic SOS response Genetics Mutagenesis Mutation PsiB protein RecA protein RecF protein Regulon Serine Endopeptidases - physiology Signal Transduction SOS response SOS Response (Genetics) T lymphocytes |
| title | The SOS Response Regulates Adaptive Mutation |
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