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- W2891321978 abstract "Abstract Haploinsufficiency and aneuploidy are two phenomena, where gene dosage alterations cause severe defects ultimately resulting in developmental failures and disease. One remarkable exception is the X chromosome, where copy number differences between sexes are buffered by dosage compensation systems. In Drosophila , the Male-Specific Lethal complex (MSLc) mediates upregulation of the single male X chromosome. The evolutionary origin and conservation of this process orchestrated by MSL2, the only male-specific protein within the fly MSLc, have remained unclear. Here, we report that MSL2, in addition to regulating the X chromosome, targets autosomal genes involved in patterning and morphogenesis. Precise regulation of these genes by MSL2 is required for proper development. This set of dosage-sensitive genes maintains such regulation during evolution, as MSL2 binds and similarly regulates mouse orthologues via Histone H4 lysine 16 acetylation. We propose that this gene-by-gene dosage compensation mechanism was co-opted during evolution for chromosome-wide regulation of the Drosophila male X." @default.
- W2891321978 created "2018-09-27" @default.
- W2891321978 creator A5004190083 @default.
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- W2891321978 date "2018-09-07" @default.
- W2891321978 modified "2023-10-17" @default.
- W2891321978 title "Facultative dosage compensation of developmental genes on autosomes in Drosophila and mouse embryonic stem cells" @default.
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- W2891321978 doi "https://doi.org/10.1038/s41467-018-05642-2" @default.
- W2891321978 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6128902" @default.
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