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

Claudia Isabelle Keller Valsecchi, M. Felicia Basilicata, Giuseppe Semplicio, Plamen Georgiev, Noel Marie Gutierrez and Asifa Akhtar ()
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Claudia Isabelle Keller Valsecchi: Max Planck Institute of Immunobiology and Epigenetics
M. Felicia Basilicata: Max Planck Institute of Immunobiology and Epigenetics
Giuseppe Semplicio: Max Planck Institute of Immunobiology and Epigenetics
Plamen Georgiev: Max Planck Institute of Immunobiology and Epigenetics
Noel Marie Gutierrez: Max Planck Institute of Immunobiology and Epigenetics
Asifa Akhtar: Max Planck Institute of Immunobiology and Epigenetics

Nature Communications, 2018, vol. 9, issue 1, 1-14

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.

Date: 2018
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DOI: 10.1038/s41467-018-05642-2

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