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Article: A Structural Split in the Human Genome

TitleA Structural Split in the Human Genome
Authors
Issue Date2007
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2007, v. 2 n. 7 How to Cite?
AbstractBackground: Promoter-associated CpG islands (PCIs) mediate methylation-dependent gene silencing, yet tend to co-locate to transcriptionally active genes. To address this paradox, we used data mining to assess the behavior of PCI-positive (PCI+) genes in the human genome. Results: PCI+ genes exhibit a bimodal distribution: (1) a 'housekeeping-like' subset characterized by higher GC content and lower intron length/number, and (2) a 'pseudogene paralog' subset characterized by lower GC content and higher intron length/number (p<0.001). These subsets are functionally distinguishable, with the former gene group characterized by higher expression levels and lower evolutionary rate (p<0.001). PCI-negative (PCI-) genes exhibit higher evolutionary rate and narrower expression breadth than PCI+ genes (p<0.001), consistent with more frequent tissue-specific inactivation. Conclusions: Adaptive evolution of the human genome appears driven in part by declining transcription of a subset of PCI+ genes, predisposing to both CpG→TpA mutation and intron insertion. We propose a model of evolving biological complexity in which environmentally-selected gains or losses of PCI methylation respectively favor positive or negative selection, thus polarizing PCI+ gene structures around a genomic core of ancestral PCI- genes. © 2007 Tang, Epstein.
Persistent Identifierhttp://hdl.handle.net/10722/77484
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, CSMen_HK
dc.contributor.authorEpstein, RJen_HK
dc.date.accessioned2010-09-06T07:32:23Z-
dc.date.available2010-09-06T07:32:23Z-
dc.date.issued2007en_HK
dc.identifier.citationPlos One, 2007, v. 2 n. 7en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77484-
dc.description.abstractBackground: Promoter-associated CpG islands (PCIs) mediate methylation-dependent gene silencing, yet tend to co-locate to transcriptionally active genes. To address this paradox, we used data mining to assess the behavior of PCI-positive (PCI+) genes in the human genome. Results: PCI+ genes exhibit a bimodal distribution: (1) a 'housekeeping-like' subset characterized by higher GC content and lower intron length/number, and (2) a 'pseudogene paralog' subset characterized by lower GC content and higher intron length/number (p<0.001). These subsets are functionally distinguishable, with the former gene group characterized by higher expression levels and lower evolutionary rate (p<0.001). PCI-negative (PCI-) genes exhibit higher evolutionary rate and narrower expression breadth than PCI+ genes (p<0.001), consistent with more frequent tissue-specific inactivation. Conclusions: Adaptive evolution of the human genome appears driven in part by declining transcription of a subset of PCI+ genes, predisposing to both CpG→TpA mutation and intron insertion. We propose a model of evolving biological complexity in which environmentally-selected gains or losses of PCI methylation respectively favor positive or negative selection, thus polarizing PCI+ gene structures around a genomic core of ancestral PCI- genes. © 2007 Tang, Epstein.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong Licenseen_US
dc.subject.meshBase Composition-
dc.subject.meshCpG Islands - genetics-
dc.subject.meshDNA Transposable Elements - genetics-
dc.subject.meshEvolution, Molecular-
dc.subject.meshGenome, Human-
dc.titleA Structural Split in the Human Genomeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=2&issue=7&spage=e603&epage=&date=2007&atitle=A+structural+split+in+the+human+genomeen_HK
dc.identifier.emailEpstein, RJ: repstein@hku.hken_HK
dc.identifier.authorityEpstein, RJ=rp00501en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0000603en_HK
dc.identifier.pmid17622348-
dc.identifier.pmcidPMC1904255-
dc.identifier.scopuseid_2-s2.0-47649083350en_HK
dc.identifier.hkuros131232en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-47649083350&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume2en_HK
dc.identifier.issue7en_HK
dc.identifier.isiWOS:000207452000010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, CSM=35764635500en_HK
dc.identifier.scopusauthoridEpstein, RJ=34975074500en_HK
dc.identifier.citeulike3502168-

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