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• W2019202989 abstract "How and why female somatic X-chromosome inactivation (XCI) evolved in mammals remains poorly understood. It has been proposed that XCI is a dosage-compensation mechanism that evolved to equalize expression levels of X-linked genes in females (2X) and males (1X), with a prior twofold increase in expression of X-linked genes in both sexes (Ohno's hypothesis). Whereas the parity of X chromosome expression between the sexes has been clearly demonstrated, tests for the doubling of expression levels globally along the X chromosome have returned contradictory results. However, changes in gene dosage during sex-chromosome evolution are not expected to impact on all genes equally, and should have greater consequences for dosage-sensitive genes. We show that, for genes encoding components of large protein complexes (≥ 7 members)--a class of genes that is expected to be dosage-sensitive--expression of X-linked genes is similar to that of autosomal genes within the complex. These data support Ohno's hypothesis that XCI acts as a dosage-compensation mechanism, and allow us to refine Ohno's model of XCI evolution. We also explore the contribution of dosage-sensitive genes to X aneuploidy phenotypes in humans, such as Turner (X0) and Klinefelter (XXY) syndromes. X aneuploidy in humans is common and is known to have mild effects because most of the supernumerary X genes are inactivated and not affected by aneuploidy. Only genes escaping XCI experience dosage changes in X-aneuploidy patients. We combined data on dosage sensitivity and XCI to compute a list of candidate genes for X-aneuploidy syndromes." @default.
• W2019202989 created "2016-06-24" @default.
• W2019202989 creator A5015489386 @default.
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• W2019202989 date "2012-03-05" @default.
• W2019202989 modified "2023-10-11" @default.
• W2019202989 title "Mammalian X chromosome inactivation evolved as a dosage-compensation mechanism for dosage-sensitive genes on the X chromosome" @default.
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• W2019202989 doi "https://doi.org/10.1073/pnas.1116763109" @default.
• W2019202989 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3325647" @default.
• W2019202989 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22392987" @default.
• W2019202989 hasPublicationYear "2012" @default.
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