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DNA damage responses and their many interactions with the replication fork
The cellular response to DNA damage is composed of cell cycle checkpoint and DNA repair mechanisms that serve to ensure proper replication of the genome prior to cell division. The function of the DNA damage response during DNA replication in S-phase is critical to this process. Recent evidence has...
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Published in: | Carcinogenesis (New York) 2006-05, Vol.27 (5), p.883-892 |
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description | The cellular response to DNA damage is composed of cell cycle checkpoint and DNA repair mechanisms that serve to ensure proper replication of the genome prior to cell division. The function of the DNA damage response during DNA replication in S-phase is critical to this process. Recent evidence has suggested a number of interrelationships of DNA replication and cellular DNA damage responses. These include S-phase checkpoints which suppress replication initiation or elongation in response to DNA damage. Also, many components of the DNA damage response are required either for the stabilization of, or for restarting, stalled replication forks. Further, translesion synthesis permits DNA replication to proceed in the presence of DNA damage and can be coordinated with subsequent repair by homologous recombination (HR). Finally, cohesion of sister chromatids is established coincident with DNA replication and is required for subsequent DNA repair by homologous recombination. Here we review these processes, all of which occur at, or are related to, the advancing replication fork. We speculate that these multiple interdependencies of DNA replication and DNA damage responses integrate the many steps necessary to ensure accurate duplication of the genome. |
doi_str_mv | 10.1093/carcin/bgi319 |
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The function of the DNA damage response during DNA replication in S-phase is critical to this process. Recent evidence has suggested a number of interrelationships of DNA replication and cellular DNA damage responses. These include S-phase checkpoints which suppress replication initiation or elongation in response to DNA damage. Also, many components of the DNA damage response are required either for the stabilization of, or for restarting, stalled replication forks. Further, translesion synthesis permits DNA replication to proceed in the presence of DNA damage and can be coordinated with subsequent repair by homologous recombination (HR). Finally, cohesion of sister chromatids is established coincident with DNA replication and is required for subsequent DNA repair by homologous recombination. Here we review these processes, all of which occur at, or are related to, the advancing replication fork. 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The function of the DNA damage response during DNA replication in S-phase is critical to this process. Recent evidence has suggested a number of interrelationships of DNA replication and cellular DNA damage responses. These include S-phase checkpoints which suppress replication initiation or elongation in response to DNA damage. Also, many components of the DNA damage response are required either for the stabilization of, or for restarting, stalled replication forks. Further, translesion synthesis permits DNA replication to proceed in the presence of DNA damage and can be coordinated with subsequent repair by homologous recombination (HR). Finally, cohesion of sister chromatids is established coincident with DNA replication and is required for subsequent DNA repair by homologous recombination. Here we review these processes, all of which occur at, or are related to, the advancing replication fork. We speculate that these multiple interdependencies of DNA replication and DNA damage responses integrate the many steps necessary to ensure accurate duplication of the genome.</description><subject>Animals</subject><subject>ataxia telangiectasia mutated</subject><subject>ATM</subject><subject>ATM and Rad3-related</subject><subject>ATR</subject><subject>Biological and medical sciences</subject><subject>BLM</subject><subject>Bloom syndrome</subject><subject>BRCA1 and 2</subject><subject>BReast CAncer genes/proteins 1 and 2</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>DNA Damage</subject><subject>DNA Repair</subject><subject>DNA Replication</subject><subject>double-strand DNA breaks</subject><subject>DSBs</subject><subject>FANCD1 and FANCD2</subject><subject>Fanconi anemia proteins D1 and D2</subject><subject>homologous recombination</subject><subject>Humans</subject><subject>ionizing radiation</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Models, Genetic</subject><subject>NBS</subject><subject>Nijmegen breakage syndrome</subject><subject>Recombination, Genetic</subject><subject>S Phase</subject><subject>Sister Chromatid Exchange</subject><subject>SMC</subject><subject>structural maintenance of chromosomes</subject><subject>TLS</subject><subject>translesion synthesis</subject><subject>Tumors</subject><subject>ultraviolet irradiation</subject><subject>UVC</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNp90c9rFDEUB_Agil2rR68yCBUvY5N5mZm8Y2nVqrUKKi5ewpv8aNPOjzWZRfvfm2UXFzx4CuT74YW8L2NPBX8lOMKxoWjCeNxdBRB4jy2EbHhZCcXvswUXEkoAkAfsUUo3nIsGanzIDkQjkbeAC_b-7PKksDTQlSuiS6tpTC4VNNpivnYhFgONd0UYZxfJzCGnxa8wX2_CzFd9MLS5LfwUbx-zB5765J7szkP27c3rr6fn5cWnt-9OTy5KIxXOpa0cb-saLXTIDXKJQJXsrBPoO6WQ0HvwznJqQXgB3IpaKdm6RnUepIVD9mI7dxWnn2uXZj2EZFzf0-imddIVb6CRtcrw5X-hkNgo5LXCTJ__Q2-mdRzzN3QlEDjKWmRUbpGJU0rReb2KYaB4pwXXmzL0tgy9LSP7Z7uh625wdq9328_gaAcoGep9pNGEtHdt3k7VtPuHQ5rd7785xVud07bW58sf-vOXD9-Xy7OP-hL-AAaMomQ</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Andreassen, Paul R.</creator><creator>Ho, Gary P.H.</creator><creator>D'Andrea, Alan D.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20060501</creationdate><title>DNA damage responses and their many interactions with the replication fork</title><author>Andreassen, Paul R. ; Ho, Gary P.H. ; D'Andrea, Alan D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-d2e07559d3b90c90493a24bde19fb889a9ff3fed0a731f130d158847e68bf34d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>ataxia telangiectasia mutated</topic><topic>ATM</topic><topic>ATM and Rad3-related</topic><topic>ATR</topic><topic>Biological and medical sciences</topic><topic>BLM</topic><topic>Bloom syndrome</topic><topic>BRCA1 and 2</topic><topic>BReast CAncer genes/proteins 1 and 2</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>DNA Damage</topic><topic>DNA Repair</topic><topic>DNA Replication</topic><topic>double-strand DNA breaks</topic><topic>DSBs</topic><topic>FANCD1 and FANCD2</topic><topic>Fanconi anemia proteins D1 and D2</topic><topic>homologous recombination</topic><topic>Humans</topic><topic>ionizing radiation</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Models, Genetic</topic><topic>NBS</topic><topic>Nijmegen breakage syndrome</topic><topic>Recombination, Genetic</topic><topic>S Phase</topic><topic>Sister Chromatid Exchange</topic><topic>SMC</topic><topic>structural maintenance of chromosomes</topic><topic>TLS</topic><topic>translesion synthesis</topic><topic>Tumors</topic><topic>ultraviolet irradiation</topic><topic>UVC</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andreassen, Paul R.</creatorcontrib><creatorcontrib>Ho, Gary P.H.</creatorcontrib><creatorcontrib>D'Andrea, Alan D.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andreassen, Paul R.</au><au>Ho, Gary P.H.</au><au>D'Andrea, Alan D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA damage responses and their many interactions with the replication fork</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2006-05-01</date><risdate>2006</risdate><volume>27</volume><issue>5</issue><spage>883</spage><epage>892</epage><pages>883-892</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>The cellular response to DNA damage is composed of cell cycle checkpoint and DNA repair mechanisms that serve to ensure proper replication of the genome prior to cell division. The function of the DNA damage response during DNA replication in S-phase is critical to this process. Recent evidence has suggested a number of interrelationships of DNA replication and cellular DNA damage responses. These include S-phase checkpoints which suppress replication initiation or elongation in response to DNA damage. Also, many components of the DNA damage response are required either for the stabilization of, or for restarting, stalled replication forks. Further, translesion synthesis permits DNA replication to proceed in the presence of DNA damage and can be coordinated with subsequent repair by homologous recombination (HR). Finally, cohesion of sister chromatids is established coincident with DNA replication and is required for subsequent DNA repair by homologous recombination. Here we review these processes, all of which occur at, or are related to, the advancing replication fork. 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subjects | Animals ataxia telangiectasia mutated ATM ATM and Rad3-related ATR Biological and medical sciences BLM Bloom syndrome BRCA1 and 2 BReast CAncer genes/proteins 1 and 2 Carcinogenesis, carcinogens and anticarcinogens DNA Damage DNA Repair DNA Replication double-strand DNA breaks DSBs FANCD1 and FANCD2 Fanconi anemia proteins D1 and D2 homologous recombination Humans ionizing radiation Medical sciences Models, Biological Models, Genetic NBS Nijmegen breakage syndrome Recombination, Genetic S Phase Sister Chromatid Exchange SMC structural maintenance of chromosomes TLS translesion synthesis Tumors ultraviolet irradiation UVC |
title | DNA damage responses and their many interactions with the replication fork |
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