Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B
Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and agi...
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| Veröffentlicht in: | Oncogene 2002-12, Vol.21 (57), p.8675-8682 |
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| creator | STEVNSNER, Tinna NYAGA, Simon DE SOUZA-PINTO, Nadja C VAN DER HORST, Gijsbertus T. J GORGELS, Theo G. M. F HOGUE, Barbara A THORSLUND, Tina BOHR, Vilhelm A |
| description | Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. 8-oxoG is repaired efficiently in mammalian mitochondrial DNA by enzymes in the base excision repair pathway, including the 8-oxoguanine glycosylase (OGG1), which incizes the lesion in the first step of repair. Cockayne syndrome (CS) is a segmental premature aging syndrome in humans that has two complementation groups, CSA and CSB. Previous studies showed that CSB-deficient cells have reduced capacity to repair 8-oxoG. This study examines the role of the CSB gene in regulating repair of 8-oxoG in mitochondrial DNA in human and mouse cells. 8-oxoG repair was measured in liver cells from CSB deficient mice and in human CS-B cells carrying expression vectors for wild type or mutant forms of the human CSB gene. For the first time we report that CSB stimulates repair of 8-oxoG in mammalian mitochondrial DNA. Furthermore, evidence is presented to support the hypothesis that wild type CSB regulates expression of OGG1. |
| doi_str_mv | 10.1038/sj.onc.1205994 |
| format | Article |
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J ; GORGELS, Theo G. M. F ; HOGUE, Barbara A ; THORSLUND, Tina ; BOHR, Vilhelm A</creator><creatorcontrib>STEVNSNER, Tinna ; NYAGA, Simon ; DE SOUZA-PINTO, Nadja C ; VAN DER HORST, Gijsbertus T. J ; GORGELS, Theo G. M. F ; HOGUE, Barbara A ; THORSLUND, Tina ; BOHR, Vilhelm A</creatorcontrib><description>Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. 8-oxoG is repaired efficiently in mammalian mitochondrial DNA by enzymes in the base excision repair pathway, including the 8-oxoguanine glycosylase (OGG1), which incizes the lesion in the first step of repair. Cockayne syndrome (CS) is a segmental premature aging syndrome in humans that has two complementation groups, CSA and CSB. Previous studies showed that CSB-deficient cells have reduced capacity to repair 8-oxoG. This study examines the role of the CSB gene in regulating repair of 8-oxoG in mitochondrial DNA in human and mouse cells. 8-oxoG repair was measured in liver cells from CSB deficient mice and in human CS-B cells carrying expression vectors for wild type or mutant forms of the human CSB gene. For the first time we report that CSB stimulates repair of 8-oxoG in mammalian mitochondrial DNA. Furthermore, evidence is presented to support the hypothesis that wild type CSB regulates expression of OGG1.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1205994</identifier><identifier>PMID: 12483520</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing</publisher><subject>8-Hydroxyguanine ; Active oxygen ; Aging ; Amino Acid Sequence ; Animals ; Base excision repair ; Base Sequence ; Biological and medical sciences ; Cell Line, Transformed ; Cockayne syndrome ; Cockayne Syndrome - genetics ; Complementation ; CSB gene ; Degenerative diseases ; DNA damage ; DNA glycosylase ; DNA Helicases - genetics ; DNA Primers ; DNA Repair ; DNA Repair Enzymes ; DNA, Mitochondrial - genetics ; DNA-Formamidopyrimidine Glycosylase ; Expression vectors ; Fundamental and applied biological sciences. Psychology ; Genetic aspects ; Gerontology ; Guanine - analogs & derivatives ; Guanine - metabolism ; Hepatocytes ; Humans ; Lymphocytes B ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondrial DNA ; Molecular and cellular biology ; Molecular genetics ; Mutagenesis. Repair ; N-Glycosyl Hydrolases - metabolism ; OGG1 protein ; Physiological aspects ; Poly-ADP-Ribose Binding Proteins ; Proteins ; Reactive oxygen species ; Risk factors</subject><ispartof>Oncogene, 2002-12, Vol.21 (57), p.8675-8682</ispartof><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2002 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 12, 2002</rights><rights>Macmillan Publishers Limited 2002.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-9b65653754ff661cb796283844367128ab44962f259bfb817e5253c84830f71b3</citedby><cites>FETCH-LOGICAL-c509t-9b65653754ff661cb796283844367128ab44962f259bfb817e5253c84830f71b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14622730$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12483520$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STEVNSNER, Tinna</creatorcontrib><creatorcontrib>NYAGA, Simon</creatorcontrib><creatorcontrib>DE SOUZA-PINTO, Nadja C</creatorcontrib><creatorcontrib>VAN DER HORST, Gijsbertus T. J</creatorcontrib><creatorcontrib>GORGELS, Theo G. M. F</creatorcontrib><creatorcontrib>HOGUE, Barbara A</creatorcontrib><creatorcontrib>THORSLUND, Tina</creatorcontrib><creatorcontrib>BOHR, Vilhelm A</creatorcontrib><title>Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. 8-oxoG is repaired efficiently in mammalian mitochondrial DNA by enzymes in the base excision repair pathway, including the 8-oxoguanine glycosylase (OGG1), which incizes the lesion in the first step of repair. Cockayne syndrome (CS) is a segmental premature aging syndrome in humans that has two complementation groups, CSA and CSB. Previous studies showed that CSB-deficient cells have reduced capacity to repair 8-oxoG. This study examines the role of the CSB gene in regulating repair of 8-oxoG in mitochondrial DNA in human and mouse cells. 8-oxoG repair was measured in liver cells from CSB deficient mice and in human CS-B cells carrying expression vectors for wild type or mutant forms of the human CSB gene. For the first time we report that CSB stimulates repair of 8-oxoG in mammalian mitochondrial DNA. Furthermore, evidence is presented to support the hypothesis that wild type CSB regulates expression of OGG1.</description><subject>8-Hydroxyguanine</subject><subject>Active oxygen</subject><subject>Aging</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Base excision repair</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Cell Line, Transformed</subject><subject>Cockayne syndrome</subject><subject>Cockayne Syndrome - genetics</subject><subject>Complementation</subject><subject>CSB gene</subject><subject>Degenerative diseases</subject><subject>DNA damage</subject><subject>DNA glycosylase</subject><subject>DNA Helicases - genetics</subject><subject>DNA Primers</subject><subject>DNA Repair</subject><subject>DNA Repair Enzymes</subject><subject>DNA, Mitochondrial - genetics</subject><subject>DNA-Formamidopyrimidine Glycosylase</subject><subject>Expression vectors</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic aspects</subject><subject>Gerontology</subject><subject>Guanine - analogs & derivatives</subject><subject>Guanine - metabolism</subject><subject>Hepatocytes</subject><subject>Humans</subject><subject>Lymphocytes B</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutagenesis. Repair</subject><subject>N-Glycosyl Hydrolases - metabolism</subject><subject>OGG1 protein</subject><subject>Physiological aspects</subject><subject>Poly-ADP-Ribose Binding Proteins</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Risk factors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kc1vEzEQxS1ERUPhyhFZII6b2uOv9bGN-JLacoGz5XXs4JC1g70rkf8eV6yUS9EcRhr_3puRH0JvKFlTwvrrul_n5NYUiNCaP0MrypXshND8OVoRLUingcElelnrnhCiNIEX6JIC75kAskIP93HK7mdO2xLtARd_tLHgHHDf5T95N9sUk8ex4q0P0UWfJhwT3mT3y57aQz01YR493pU8H_HtK3QR7KH610u_Qj8-ffy--dLdffv8dXNz1zlB9NTpQQopmBI8BCmpG5SW0LOecyYVhd4OnLdJAKGHMPRUeQGCub5dTYKiA7tC7__5Hkv-Pfs6mX2eS2orDUhOGche80a9-y8FhHJQBM5WO3vwJqaQp2LdGKszN0AISKrg0Wr9BNVq68focmq_0-ZPCVzJtRYfzLHE0ZaTocQ8Rmfq3rTozBJdE7xdjp2H0W_P-JJVAz4sgK3OHkKxycV65rgEUIywv2AgnTE</recordid><startdate>20021212</startdate><enddate>20021212</enddate><creator>STEVNSNER, Tinna</creator><creator>NYAGA, Simon</creator><creator>DE SOUZA-PINTO, Nadja C</creator><creator>VAN DER HORST, Gijsbertus T. 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Psychology</topic><topic>Genetic aspects</topic><topic>Gerontology</topic><topic>Guanine - analogs & derivatives</topic><topic>Guanine - metabolism</topic><topic>Hepatocytes</topic><topic>Humans</topic><topic>Lymphocytes B</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondrial DNA</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutagenesis. Repair</topic><topic>N-Glycosyl Hydrolases - metabolism</topic><topic>OGG1 protein</topic><topic>Physiological aspects</topic><topic>Poly-ADP-Ribose Binding Proteins</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STEVNSNER, Tinna</creatorcontrib><creatorcontrib>NYAGA, Simon</creatorcontrib><creatorcontrib>DE SOUZA-PINTO, Nadja C</creatorcontrib><creatorcontrib>VAN DER HORST, Gijsbertus T. 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J</au><au>GORGELS, Theo G. M. F</au><au>HOGUE, Barbara A</au><au>THORSLUND, Tina</au><au>BOHR, Vilhelm A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B</atitle><jtitle>Oncogene</jtitle><addtitle>Oncogene</addtitle><date>2002-12-12</date><risdate>2002</risdate><volume>21</volume><issue>57</issue><spage>8675</spage><epage>8682</epage><pages>8675-8682</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Reactive oxygen species, which are prevalent in mitochondria, cause oxidative DNA damage including the mutagenic DNA lesion 7,8-dihydroxyguanine (8-oxoG). Oxidative damage to mitochondrial DNA has been implicated as a causative factor in a wide variety of degenerative diseases, and in cancer and aging. 8-oxoG is repaired efficiently in mammalian mitochondrial DNA by enzymes in the base excision repair pathway, including the 8-oxoguanine glycosylase (OGG1), which incizes the lesion in the first step of repair. Cockayne syndrome (CS) is a segmental premature aging syndrome in humans that has two complementation groups, CSA and CSB. Previous studies showed that CSB-deficient cells have reduced capacity to repair 8-oxoG. This study examines the role of the CSB gene in regulating repair of 8-oxoG in mitochondrial DNA in human and mouse cells. 8-oxoG repair was measured in liver cells from CSB deficient mice and in human CS-B cells carrying expression vectors for wild type or mutant forms of the human CSB gene. For the first time we report that CSB stimulates repair of 8-oxoG in mammalian mitochondrial DNA. Furthermore, evidence is presented to support the hypothesis that wild type CSB regulates expression of OGG1.</abstract><cop>Basingstoke</cop><pub>Nature Publishing</pub><pmid>12483520</pmid><doi>10.1038/sj.onc.1205994</doi><tpages>8</tpages></addata></record> |
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| subjects | 8-Hydroxyguanine Active oxygen Aging Amino Acid Sequence Animals Base excision repair Base Sequence Biological and medical sciences Cell Line, Transformed Cockayne syndrome Cockayne Syndrome - genetics Complementation CSB gene Degenerative diseases DNA damage DNA glycosylase DNA Helicases - genetics DNA Primers DNA Repair DNA Repair Enzymes DNA, Mitochondrial - genetics DNA-Formamidopyrimidine Glycosylase Expression vectors Fundamental and applied biological sciences. Psychology Genetic aspects Gerontology Guanine - analogs & derivatives Guanine - metabolism Hepatocytes Humans Lymphocytes B Mice Mice, Inbred C57BL Mitochondria Mitochondrial DNA Molecular and cellular biology Molecular genetics Mutagenesis. Repair N-Glycosyl Hydrolases - metabolism OGG1 protein Physiological aspects Poly-ADP-Ribose Binding Proteins Proteins Reactive oxygen species Risk factors |
| title | Mitochondrial repair of 8-oxoguanine is deficient in Cockayne syndrome group B |
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