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Increased expression of X-linked genes in mammals is associated with a higher stability of transcripts and an increased ribosome density
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). (Jan Larsson)
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). (Jan Larsson)
2015 (engelsk)Inngår i: Genome Biology and Evolution, ISSN 1759-6653, E-ISSN 1759-6653, Vol. 7, nr 4, s. 1039-1052Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Mammalian sex chromosomes evolved from the degeneration of one homolog of a pair of ancestral autosomes, the proto-Y. This resulted in a gene dose imbalance that is believed to be restored (partially or fully) through up-regulation of gene expression from the single active X-chromosome in both sexes by a dosage compensatory mechanism. We analyzed multiple genome-wide RNA stability datasets and found significantly longer average half-lives for X-chromosome transcripts than for autosomal transcripts in various human cell lines, both male and female, and in mice. Analysis of ribosome profiling data shows that ribosome density is higher on X-chromosome transcripts than on autosomal transcripts in both humans and mice, suggesting that the higher stability is causally linked to a higher translation rate. Our results and observations are in accordance with a dosage compensatory upregulation of expressed X-linked genes. We therefore propose that differential mRNA stability and translation rates of the autosomes and sex chromosomes contribute to an evolutionarily conserved dosage compensation mechanism in mammals.

sted, utgiver, år, opplag, sider
Oxford University Press, 2015. Vol. 7, nr 4, s. 1039-1052
Emneord [en]
dosage compensation, RNA stability, sex chromosomes, RNA half-life, ribosome density
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Forskningsprogram
genetik
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URN: urn:nbn:se:umu:diva-101245DOI: 10.1093/gbe/evv054ISI: 000355148800010PubMedID: 25786432OAI: oai:DiVA.org:umu-101245DiVA, id: diva2:798125
Forskningsfinansiär
Swedish Research CouncilSwedish Cancer SocietyTilgjengelig fra: 2015-03-26 Laget: 2015-03-26 Sist oppdatert: 2018-06-07bibliografisk kontrollert

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