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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 University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). (Jan Larsson)
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). (Jan Larsson)
2015 (English)In: Genome Biology and Evolution, ISSN 1759-6653, E-ISSN 1759-6653, Vol. 7, no 4, 1039-1052 p.Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
Oxford University Press, 2015. Vol. 7, no 4, 1039-1052 p.
Keyword [en]
dosage compensation, RNA stability, sex chromosomes, RNA half-life, ribosome density
National Category
Genetics Evolutionary Biology
Research subject
Genetics
Identifiers
URN: urn:nbn:se:umu:diva-101245DOI: 10.1093/gbe/evv054ISI: 000355148800010PubMedID: 25786432OAI: oai:DiVA.org:umu-101245DiVA: diva2:798125
Funder
Swedish Research CouncilSwedish Cancer Society
Available from: 2015-03-26 Created: 2015-03-26 Last updated: 2017-12-04Bibliographically approved

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