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dc.contributor.authorFrith, Martin C.eng
dc.contributor.authorPonjavic, Jasminaeng
dc.contributor.authorFredman, Davideng
dc.contributor.authorKai, Chikatoshieng
dc.contributor.authorKawai, Juneng
dc.contributor.authorCarninci, Pieroeng
dc.contributor.authorHayashizaki, Yoshihideeng
dc.contributor.authorSandelin, Albineng
dc.date.accessioned2008-08-04T08:19:40Z
dc.date.available2008-08-04T08:19:40Z
dc.date.issued2006-05-06eng
dc.PublishedGenome Research 16: 713-722en
dc.identifier.issn1088-9051en_US
dc.identifier.urihttp://hdl.handle.net/1956/2744
dc.description.abstractAlignments of homologous genomic sequences are widely used to identify functional genetic elements and study their evolution. Most studies tacitly equate homology of functional elements with sequence homology. This assumption is violated by the phenomenon of turnover, in which functionally equivalent elements reside at locations that are nonorthologous at the sequence level. Turnover has been demonstrated previously for transcriptionfactor-binding sites. Here, we show that transcription start sites of equivalent genes do not always reside at equivalent locations in the human and mouse genomes. We also identify two types of partial turnover, illustrating evolutionary pathways that could lead to complete turnover. These findings suggest that the signals encoding transcription start sites are highly flexible and evolvable, and have cautionary implications for the use of sequence-level conservation to detect gene regulatory elements.en_US
dc.language.isoengeng
dc.publisherCold Spring Harbor Laboratory Pressen_US
dc.titleEvolutionary turnover of mammalian transcription start sitesen_US
dc.typePeer reviewed
dc.typeJournal article
dc.identifier.doihttps://doi.org/10.1101/gr.5031006


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