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

ABSTRACT: RNA stability controlled by m6A methylation provides X to autosome compensation in mammals

PROVIDER: PRJNA841679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19368300.fastq.gz	Fastqsanger.gz
	SRR19368700.fastq.gz	Fastqsanger.gz
	SRR19368301.fastq.gz	Fastqsanger.gz
	SRR19368701.fastq.gz	Fastqsanger.gz
	SRR19368302.fastq.gz	Fastqsanger.gz

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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.

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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.

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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