ArticleStem cell reports2026
The role of m6A RNA methylation in the maintenance of X chromosome inactivation and X-to-autosome dosage compensation in early embryonic lineages.
Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammals, while X chromosome inactivation (XCI) balances the dosage of X-linked gene expression between sexes, upregulation of active-X balances the dosage of monoallelic X-linked genes with biallelic autosomal genes (AA). Here, we have investigated the role of m6A RNA methylation in the maintenance of XCI and X-to-autosome (X-to-A) dosage compensation in early embryonic lineages: epiblast stem cells (EpiSCs), trophoblast stem cells (TSCs), and extraembryonic endoderm stem cells (XENs). We find that the depletion of m6A RNA methylation in these cells does not affect the maintenance of inactive-X silencing. Moreover, we show that m6A marks are less enriched on X-linked transcripts than the autosomal transcripts in early embryonic lineages. Notably, we demonstrate that the extent of X-to-A dosage compensation varies with m6A methylation level. Finally, we show that the depletion of m6A partly disrupts X-to-A dosage compensation in a cell-type-specific manner. Together, our study provides significant insight into the role of m6A RNA methylation in dosage compensation.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.