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RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [SLAM-seq]

ABSTRACT: RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [SLAM-seq]

PROVIDER: PRJNA841674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19368300.fastq.gz	Fastqsanger.gz
	SRR19368301.fastq.gz	Fastqsanger.gz
	SRR19368302.fastq.gz	Fastqsanger.gz
	SRR19368303.fastq.gz	Fastqsanger.gz
	SRR19368304.fastq.gz	Fastqsanger.gz

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RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [SLAM-seq]

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 | GSE203648 | GEO

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

2023-02-14 | GSE203652 | GEO

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

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RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [DNA-seq]

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

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

| PRJNA841679 | ENA

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

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

| PRJNA841682 | ENA

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

Project description:RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [RNA-seq]

| PRJNA841670 | ENA

RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [DNA-seq]

Project description:RNA stability controlled by m6A methylation provides X to autosome compensation in mammals [DNA-seq]

| PRJNA841660 | ENA

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

Dynamicdosage compensation of transposable elementsin mammals

Project description:In mammals, X-linked dosage compensation involves two processes: X-inactivation to balance X chromosome dosage between males and females, and X-hyperactivation to achieve X-autosome balance. Transposable elements (TEs) are repetitive mobile DNA sequences and major sources of X chromosome dosage. Current studies in X-linked dosage compensation mainly focus on genes, with TEs still remaining elusive. Here we use “So-Smart-Seq” to comprehensively determine the allelic dynamics of TEs in the context of imprinted and random X-chromosome inactivation (XCI). We find that chromosomal loci and genetic backgrounds significantly impact TE silencing, and reveal putative roles of SINEs in shaping 3D chromatin architectures. We show remarkable difference in TE silencing between two forms of XCI and discover that X-hyperactivation is absent in TEs. Our data provide deep insight for TE studies and greatly contribute to complete understanding of X-chromosome wide dosage compensation.

2025-02-12 | GSE275192 | GEO

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