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

Media type: E-Article
Title: RNA stability controlled by m6A methylation contributes to X-to-autosome dosage compensation in mammals
Contributor: Rücklé, Cornelia; Körtel, Nadine; Basilicata, M. Felicia; Busch, Anke; Zhou, You; Hoch-Kraft, Peter; Tretow, Kerstin; Kielisch, Fridolin; Bertin, Marco; Pradhan, Mihika; Musheev, Michael; Schweiger, Susann; Niehrs, Christof; Rausch, Oliver; Zarnack, Kathi; Keller Valsecchi, Claudia Isabelle; König, Julian
imprint: Springer Science and Business Media LLC, 2023
Published in: Nature Structural & Molecular Biology
Language: English
DOI: 10.1038/s41594-023-00997-7
ISSN: 1545-9993; 1545-9985
Keywords: Molecular Biology ; Structural Biology
Origination:
Footnote:
Description: <jats:title>Abstract</jats:title><jats:p>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 with two active copies of autosomes, it has been proposed that genes from the active X chromosome exhibit dosage compensation. However, the existence and mechanisms of X-to-autosome dosage compensation are still under debate. Here we show that X-chromosomal transcripts have fewer m<jats:sup>6</jats:sup>A modifications and are more stable than their autosomal counterparts. Acute depletion of m<jats:sup>6</jats:sup>A selectively stabilizes 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 m<jats:sup>6</jats:sup>A, indicating that mammalian dosage compensation is partly regulated by epitranscriptomic RNA modifications.</jats:p>

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