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

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

PROVIDER: PRJNA432263 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6655500_1.fastq.gz	Fastqsanger.gz
	SRR6655500_2.fastq.gz	Fastqsanger.gz
	SRR6655510_1.fastq.gz	Fastqsanger.gz
	SRR6655510_2.fastq.gz	Fastqsanger.gz
	SRR6655520_1.fastq.gz	Fastqsanger.gz

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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]

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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]

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

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

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

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Dosage compensation mass spectrometry in platypus, chicken and mouse

Project description:Gene dosage imbalance of heteromorphic sex chromosomes (XY or ZW) exists between the sexes, and with the autosomes. Mammalian X chromosome inactivation was long thought to imply a critical need for dosage compensation in vertebrates. However, mRNA abundance measurements that demonstrated sex chromosome transcripts are neither balanced between the sexes or with autosomes in monotreme mammals or birds brought sex chromosome dosage compensation into question. This study examines transcriptomic and proteomic levels of dosage compensation in platypus and chicken compared to mouse, a model eutherian species. We analyzed mRNA and protein levels in heart and liver tissues of chicken, mouse and platypus.

2024-07-30 | PXD040182 | Pride

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

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