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Parallel tracking dosage compensation in the early mouse embryo

ABSTRACT: Parallel tracking dosage compensation in the early mouse embryo

PROVIDER: PRJNA707448 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27276600_1.fastq.gz	Fastqsanger.gz
	SRR27276600_2.fastq.gz	Fastqsanger.gz
	SRR27276700_1.fastq.gz	Fastqsanger.gz
	SRR27276700_2.fastq.gz	Fastqsanger.gz
	SRR27276601_1.fastq.gz	Fastqsanger.gz

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Parallel tracking dosage compensation in the early mouse embryo

Project description:We develop So-Smart-seq to interrogate a comprehensive transcriptome inclusive of coding, noncoding, and repetitive element transcription. We reveal that, surprisingly, de novo silencing pertains only to a subset of paternal X (Xp) genes. In contrast, a set of evolutionarily older genes and LINEs demonstrate constitutive Xp silencing, adopt epigenetically distinct signatures, and do not require Xist to initiate silencing. On maternal X (Xm), however, these elements are hyperactivated. Thus, a significant subset of Xp elements appears to be inherited in a “pre-inactive” state. We also find that Xm-hyperactivation is timed to Xp silencing on an individual gene basis, giving rise to heterogeneity in the parallel track of dosage compensation as well. These conclusions have significant implications for the mechanism and evolution of imprinting in early mammals.

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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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