Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases
Despite nearly universal conservation through evolution, the precise function of the DinB/pol κ branch of the Y-family of DNA polymerases has remained unclear. Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitran...
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Veröffentlicht in: | Cell cycle (Georgetown, Tex.) Tex.), 2007-04, Vol.6 (7), p.817-822 |
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description | Despite nearly universal conservation through evolution, the precise function of the DinB/pol κ branch of the Y-family of DNA polymerases has remained unclear. Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitrant to DNA repair mechanisms. Like other translesion DNA polymerases, the error frequency of DinB and its orthologs is higher than the DNA polymerases that replicate the majority of the genome. However, recent results suggest that some Y-family polymerases, including DinB and pol κ, bypass certain types of DNA damage with greater proficiency than an undamaged template. Moreover, they do so relatively accurately. The ability to employ this mechanism to manage DNA damage may be especially important for types of DNA modification that elude repair mechanisms. For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms. |
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Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitrant to DNA repair mechanisms. Like other translesion DNA polymerases, the error frequency of DinB and its orthologs is higher than the DNA polymerases that replicate the majority of the genome. However, recent results suggest that some Y-family polymerases, including DinB and pol κ, bypass certain types of DNA damage with greater proficiency than an undamaged template. Moreover, they do so relatively accurately. The ability to employ this mechanism to manage DNA damage may be especially important for types of DNA modification that elude repair mechanisms. For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms.</description><identifier>ISSN: 1538-4101</identifier><identifier>EISSN: 1551-4005</identifier><identifier>DOI: 10.4161/cc.6.7.4065</identifier><identifier>PMID: 17377496</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; Binding ; Biology ; Bioscience ; Calcium ; Cancer ; Cell ; Cycle ; DNA Damage - genetics ; DNA Repair - genetics ; DNA Replication - genetics ; DNA-Directed DNA Polymerase - genetics ; DNA-Directed DNA Polymerase - metabolism ; Evolution, Molecular ; Humans ; Landes ; Models, Molecular ; Organogenesis ; Phylogeny ; Protein Structure, Tertiary - physiology ; Proteins</subject><ispartof>Cell cycle (Georgetown, Tex.), 2007-04, Vol.6 (7), p.817-822</ispartof><rights>Copyright © 2007 Landes Bioscience 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-d71ed8047d5a58d05e9df402cf9244def62b1948c3b0a2b11a9dd37c13229e0c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17377496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jarosz, Daniel F.</creatorcontrib><creatorcontrib>Godoy, Veronica G.</creatorcontrib><creatorcontrib>Walker, Graham C.</creatorcontrib><title>Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases</title><title>Cell cycle (Georgetown, Tex.)</title><addtitle>Cell Cycle</addtitle><description>Despite nearly universal conservation through evolution, the precise function of the DinB/pol κ branch of the Y-family of DNA polymerases has remained unclear. 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For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms.</description><subject>Animals</subject><subject>Binding</subject><subject>Biology</subject><subject>Bioscience</subject><subject>Calcium</subject><subject>Cancer</subject><subject>Cell</subject><subject>Cycle</subject><subject>DNA Damage - genetics</subject><subject>DNA Repair - genetics</subject><subject>DNA Replication - genetics</subject><subject>DNA-Directed DNA Polymerase - genetics</subject><subject>DNA-Directed DNA Polymerase - metabolism</subject><subject>Evolution, Molecular</subject><subject>Humans</subject><subject>Landes</subject><subject>Models, Molecular</subject><subject>Organogenesis</subject><subject>Phylogeny</subject><subject>Protein Structure, Tertiary - physiology</subject><subject>Proteins</subject><issn>1538-4101</issn><issn>1551-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkEFv2zAMRoVhRdNlPe0--LRL4USyZcs-Ju22FgjaHNazIFMUoMG2MtFB4X9fu8m2S08kiMdH4mPsi-ArKUqxBliVK7WSvCw-sCtRFCKVnBcf5z6vUim4WLBPRL85zypVi0u2ECpXStblFdvvY3AePPZDYnqbbACO0QyYbMeDIUqCS_YYydMwE3ePm2SH5ENPSTMmd77fvs32oR07jIaQPrMLZ1rC63Ndsucf33_d3qe7p58Pt5tdClKIIbVKoK24VLYwRWV5gbV1kmfg6kxKi67MGlHLCvKGm6kVprY2VyDyLKuRQ75k307eQwx_jkiD7jwBtq3pMRxJK57LqlBqAm9OIMRAFNHpQ_SdiaMWXM8BagBdaqXnACf661l7bDq0_9lzYhOwPgHTIYvU-EBzeoD_0Eln4uChxb_K8rThexdiZ15CbK0ezNiG6KLpwZPO3_vlFVWijpg</recordid><startdate>20070401</startdate><enddate>20070401</enddate><creator>Jarosz, Daniel F.</creator><creator>Godoy, Veronica G.</creator><creator>Walker, Graham C.</creator><general>Taylor & Francis</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>7X8</scope></search><sort><creationdate>20070401</creationdate><title>Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases</title><author>Jarosz, Daniel F. ; Godoy, Veronica G. ; Walker, Graham C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-d71ed8047d5a58d05e9df402cf9244def62b1948c3b0a2b11a9dd37c13229e0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Binding</topic><topic>Biology</topic><topic>Bioscience</topic><topic>Calcium</topic><topic>Cancer</topic><topic>Cell</topic><topic>Cycle</topic><topic>DNA Damage - genetics</topic><topic>DNA Repair - genetics</topic><topic>DNA Replication - genetics</topic><topic>DNA-Directed DNA Polymerase - genetics</topic><topic>DNA-Directed DNA Polymerase - metabolism</topic><topic>Evolution, Molecular</topic><topic>Humans</topic><topic>Landes</topic><topic>Models, Molecular</topic><topic>Organogenesis</topic><topic>Phylogeny</topic><topic>Protein Structure, Tertiary - physiology</topic><topic>Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jarosz, Daniel F.</creatorcontrib><creatorcontrib>Godoy, Veronica G.</creatorcontrib><creatorcontrib>Walker, Graham C.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cell cycle (Georgetown, Tex.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jarosz, Daniel F.</au><au>Godoy, Veronica G.</au><au>Walker, Graham C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases</atitle><jtitle>Cell cycle (Georgetown, Tex.)</jtitle><addtitle>Cell Cycle</addtitle><date>2007-04-01</date><risdate>2007</risdate><volume>6</volume><issue>7</issue><spage>817</spage><epage>822</epage><pages>817-822</pages><issn>1538-4101</issn><eissn>1551-4005</eissn><abstract>Despite nearly universal conservation through evolution, the precise function of the DinB/pol κ branch of the Y-family of DNA polymerases has remained unclear. Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitrant to DNA repair mechanisms. Like other translesion DNA polymerases, the error frequency of DinB and its orthologs is higher than the DNA polymerases that replicate the majority of the genome. However, recent results suggest that some Y-family polymerases, including DinB and pol κ, bypass certain types of DNA damage with greater proficiency than an undamaged template. Moreover, they do so relatively accurately. The ability to employ this mechanism to manage DNA damage may be especially important for types of DNA modification that elude repair mechanisms. For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>17377496</pmid><doi>10.4161/cc.6.7.4065</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Binding Biology Bioscience Calcium Cancer Cell Cycle DNA Damage - genetics DNA Repair - genetics DNA Replication - genetics DNA-Directed DNA Polymerase - genetics DNA-Directed DNA Polymerase - metabolism Evolution, Molecular Humans Landes Models, Molecular Organogenesis Phylogeny Protein Structure, Tertiary - physiology Proteins |
title | Proficient and Accurate Bypass of Persistent DNA Lesions by DinB DNA Polymerases |
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