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  Facultative dosage compensation of developmental genes on autosomes in Drosophila and mouse embryonic stem cells

Valsecchi Keller, C. I., Basilicata, M. F., Semplicio, G., Georgiev, P., Gutierrez, N. M., & Akhtar, A. (2018). Facultative dosage compensation of developmental genes on autosomes in Drosophila and mouse embryonic stem cells. Nature Communications, 9, 3926. doi:10.1038/s41467-018-05642-2.

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 Creators:
Valsecchi Keller, Claudia Isabelle1, Author
Basilicata , M. Felicia1, Author
Semplicio, Giuseppe1, Author
Georgiev, Plamen1, Author
Gutierrez, Noel Marie1, Author
Akhtar, Asifa1, Author              
Affiliations:
1Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243643              

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 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.

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Language(s): eng - English
 Dates: 2018
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41467-018-05642-2
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Title: Nature Communications
  Abbreviation : Nat. Commun.
Source Genre: Journal
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Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 9 Sequence Number: - Start / End Page: 3926 Identifier: ISSN: 2041-1723
CoNE: https://pure.mpg.de/cone/journals/resource/2041-1723