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Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq Dmel]

ABSTRACT: Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq Dmel]

PROVIDER: PRJNA432260 | ENA |

REPOSITORIES: ENA

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Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals

Project description:Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals

| PRJNA432263 | ENA

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RIP-seq]

Project description:Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RIP-seq]

| PRJNA432261 | ENA

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq mouse]

Project description:Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq mouse]

| PRJNA432258 | ENA

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RNA-seq mouse]

Project description:Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RNA-seq mouse]

| PRJNA432262 | ENA

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RIP-seq]

Project description:Haploinsufficiency and aneuploidy are two phenomena, where alteration of gene dosage causes severe cellular defects ultimately resulting in developmental failures and disease. One remarkable exception is the X chromosome, where copy number differences between males and females are buffered through the action of dosage compensation systems. In Drosophila, the Male-Specific Lethal complex (MSLc) mediates two-fold upregulation of the single male X chromosome via Histone H4 lysine 16 acetylation (H4K16ac). 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 its function on the X, targets dosage-sensitive autosomal genes involved in patterning and morphogenesis. We show that the precise regulation of these genes by MSL2 is required for proper development of the fly wing. This set of dosage sensitive genes maintained such regulation during evolution, as MSL2 binds and similarly regulates mouse orthologues via deposition of H4K16ac. We propose that MSL2-mediated H4K16ac is an evolutionarily conserved process mediating gene-by-gene dosage compensation across flies and mammals.

2018-06-29 | GSE109900 | GEO

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [RNA-seq mouse]

2018-06-29 | GSE109899 | GEO

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq Dmel]

2018-06-29 | GSE109898 | GEO

Facultative dosage compensation of developmental genes on autosomes in Drosophila and mammals [ChIP-seq mouse]

2018-06-29 | GSE109897 | GEO

RNA stability controlled by m6A methylation contributes to X-to-autosome dosage compensation in mammals

Project description:In mammals, X-chromosomal genes are expressed from a single copy since males (XY) possess a single X chromosome, while females (XX) undergo X inactivation. To compensate for this reduction in dosage compared to two active copies of autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation. However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that X-chromosomal transcripts are reduced in m6A modifications and more stable compared to their autosomal counterparts. Acute depletion of m6A selectively stabilises autosomal transcripts, resulting in perturbed dosage compensation in mouse embryonic stem cells. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation is partly regulated by epitranscriptomic RNA modifications.

| EGAS00001007112 | EGA

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [miCLIP2]

Project description:In therian mammals, X-chromosomal genes are expressed only from a single active X chromosome, both in males (XY) as well as females (XX). To compensate for this reduction in dosage compared to the evolutionary ancestral state on two autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation (“Ohno’s hypothesis”). However, the existence and mechanism of X-to-autosome dosage compensation are still under debate. Here, we show that dosage compensation is achieved via differential N6-methyladenosine (m6A) RNA modification. X-chromosomal transcripts are reduced in m6A modifications and more stable compared to the autosomal counterparts. Acute depletion of m6A using a small molecule inhibitor differentially affects autosomal and X-chromosomal transcripts across sexes, cell types, tissues and species, resulting in perturbed dosage compensation. We propose that higher stability of X-chromosomal transcripts is directed by lower levels of m6A, indicating that mammalian dosage compensation occurs via epitranscriptomic RNA regulation.

2023-02-14 | GSE203652 | GEO

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