mitochondrial model for premature ageing of somatically cloned mammals
Cloned sheep have recently been discovered to have an unexpectedly advanced biological age. We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cel...
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Veröffentlicht in: | IUBMB life 1999-10, Vol.48 (4), p.369-372 |
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description | Cloned sheep have recently been discovered to have an unexpectedly advanced biological age. We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cells but not to zygotes produced by fertilization in normal sexual reproduction. Each increment of ageing in cloning experiments is therefore predicted to be maternally inherited. The hypothesis suggests practical ways of decreasing the effect. The hypothesis is itself a prediction of the recent proposal that mitochondria of the female germ line function primarily as genetic templates. |
doi_str_mv | 10.1080/152165499306711 |
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We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cells but not to zygotes produced by fertilization in normal sexual reproduction. Each increment of ageing in cloning experiments is therefore predicted to be maternally inherited. The hypothesis suggests practical ways of decreasing the effect. 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We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cells but not to zygotes produced by fertilization in normal sexual reproduction. Each increment of ageing in cloning experiments is therefore predicted to be maternally inherited. The hypothesis suggests practical ways of decreasing the effect. The hypothesis is itself a prediction of the recent proposal that mitochondria of the female germ line function primarily as genetic templates.</description><subject>aging</subject><subject>Aging - genetics</subject><subject>Animals</subject><subject>clones</subject><subject>Cloning, Organism</subject><subject>cytoplasmic inheritance</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Electron Transport - genetics</subject><subject>Female</subject><subject>free radicals</subject><subject>Male</subject><subject>mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Models, Genetic</subject><subject>Mutation</subject><subject>oxidative phosphorylation</subject><subject>Predictive Value of Tests</subject><subject>Sheep</subject><subject>somatic cloning</subject><subject>telomeres</subject><issn>1521-6543</issn><issn>1521-6551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkDFPwzAUhC0EolCY2SATW-izHTv2iCoKSJUYoHPkOC8lKI6LnQz996RKhRBvuafTdzccITcUHigoWFDBqBSZ1hxkTukJuTg4qRSCnv7-GZ-Ryxi_YLwc9DmZUZCcCckvyMo1vbefvqtCY9rE-QrbpPYh2QV0ph8CJmaLTbdNfJ1EP1qNNW27T2zrO6wSZ5wzbbwiZ_UoeH3UOdmsnj6WL-n67fl1-bhOLQPep6zKjMqBS2ScgVVUMpVLASITSDNDWYVWZSYT2pocSswVNxpQoURaClHyObmfenfBfw8Y-8I10WLbmg79EAupuWYa9AguJtAGH2PAutiFxpmwLygUh-mKf9ONidtj9VA6rP7w01YjcDcBtfGF2YYmFpt3BpQD01QrqfgPEg5xKg</recordid><startdate>19991001</startdate><enddate>19991001</enddate><creator>Allen, J.F</creator><creator>Allen, C.A</creator><scope>FBQ</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>7X8</scope></search><sort><creationdate>19991001</creationdate><title>mitochondrial model for premature ageing of somatically cloned mammals</title><author>Allen, J.F ; Allen, C.A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c203t-2d4a87036e2320c816287650545e14a12dec84a459ca70be783a90e8e6e1b55b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>aging</topic><topic>Aging - genetics</topic><topic>Animals</topic><topic>clones</topic><topic>Cloning, Organism</topic><topic>cytoplasmic inheritance</topic><topic>DNA, Mitochondrial - genetics</topic><topic>Electron Transport - genetics</topic><topic>Female</topic><topic>free radicals</topic><topic>Male</topic><topic>mitochondria</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>Models, Genetic</topic><topic>Mutation</topic><topic>oxidative phosphorylation</topic><topic>Predictive Value of Tests</topic><topic>Sheep</topic><topic>somatic cloning</topic><topic>telomeres</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allen, J.F</creatorcontrib><creatorcontrib>Allen, C.A</creatorcontrib><collection>AGRIS</collection><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>IUBMB life</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Allen, J.F</au><au>Allen, C.A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>mitochondrial model for premature ageing of somatically cloned mammals</atitle><jtitle>IUBMB life</jtitle><addtitle>IUBMB Life</addtitle><date>1999-10-01</date><risdate>1999</risdate><volume>48</volume><issue>4</issue><spage>369</spage><epage>372</epage><pages>369-372</pages><issn>1521-6543</issn><eissn>1521-6551</eissn><abstract>Cloned sheep have recently been discovered to have an unexpectedly advanced biological age. We propose that the explanation is a simple consequence of inheritance of acquired, free radical-induced cellular damage with somatic mitochondria that contribute to the mitochondrial population of cloned cells but not to zygotes produced by fertilization in normal sexual reproduction. Each increment of ageing in cloning experiments is therefore predicted to be maternally inherited. The hypothesis suggests practical ways of decreasing the effect. The hypothesis is itself a prediction of the recent proposal that mitochondria of the female germ line function primarily as genetic templates.</abstract><cop>England</cop><pmid>10632563</pmid><doi>10.1080/152165499306711</doi><tpages>4</tpages></addata></record> |
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subjects | aging Aging - genetics Animals clones Cloning, Organism cytoplasmic inheritance DNA, Mitochondrial - genetics Electron Transport - genetics Female free radicals Male mitochondria Mitochondria - genetics Mitochondria - metabolism Models, Genetic Mutation oxidative phosphorylation Predictive Value of Tests Sheep somatic cloning telomeres |
title | mitochondrial model for premature ageing of somatically cloned mammals |
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