ArticleJournal of molecular cell biology2019
AFF3-DNA methylation interplay in maintaining the mono-allelic expression pattern of XIST in terminally differentiated cells.
Article in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Variant-specific pathophysiological mechanisms of AFF3 differently influence transcriptome profiles.Genome medicine · 2024Article
- Variant-specific pathophysiological mechanisms of AFF3 differently influence transcriptome profiles.medRxiv : the preprint server for health sciences · 2024Article
- AFF3, a susceptibility factor for autoimmune diseases, is a molecular facilitator of immunoglobulin class switch recombination.Science advances · 2022Article
- Transcription Pause and Escape in Neurodevelopmental Disorders.Frontiers in neuroscience · 2022Review
- Variants in the degron of AFF3 are associated with intellectual disability, mesomelic dysplasia, horseshoe kidney, and epileptic encephalopathy.American journal of human genetics · 2021Article
- AFF3: a new player in maintaining XIST monoallelic expression.Journal of molecular cell biology · 2019Article
- Suppression of the NTS-CPS1 regulatory axis by AFF1 in lung adenocarcinoma cells.The Journal of biological chemistryArticle
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11 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
X chromosome inactivation and genomic imprinting are two classic epigenetic regulatory processes that cause mono-allelic gene expression. In female mammals, mono-allelic expression of the long non-coding RNA gene X-inactive specific transcript (XIST) is essential for initiation of X chromosome inactivation upon differentiation. We have previously demonstrated that the central factor of super elongation complex-like 3 (SEC-L3), AFF3, is enriched at gamete differentially methylated regions (DMRs) of the imprinted loci and regulates the imprinted gene expression. Here, we found that AFF3 can also bind to the DMR downstream of the XIST promoter. Knockdown of AFF3 leads to de-repression of the inactive allele of XIST in terminally differentiated cells. In addition, the binding of AFF3 to the XIST DMR relies on DNA methylation and also regulates DNA methylation level at DMR region. However, the KAP1-H3K9 methylation machineries, which regulate the imprinted loci, might not play major roles in maintaining the mono-allelic expression pattern of XIST in these cells. Thus, our results suggest that the differential mechanisms involved in the XIST DMR and gDMR regulation, which both require AFF3 and DNA methylation.
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