ArticleGenome research2019
Dynamic reversal of random X-Chromosome inactivation during iPSC reprogramming.
Article in Genome research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 67 citations in OpenAlex.
- Antisense Oligonucleotide-MediatedAnimals : an open access journal from MDPI · 2026Article
- Autosomal allelic inactivation at loci with variable replication timing and dosage sensitivity.eLife · 2026Article
- Review
- Reprogramming the inactive X chromosome: dynamics and insights from the germline.Biochemical Society transactions · 2026Review
- The role of m6A RNA methylation in the maintenance of X chromosome inactivation and X-to-autosome dosage compensation in early embryonic lineages.Stem cell reports · 2026Article
- Cell Fusion in Reprogramming and Regeneration.Advances in experimental medicine and biology · 2026Review
- Escape from X inactivation is directly modulated by Xist noncoding RNA.Nature cell biology · 2026Article
- TET3 protects theiScience · 2025Article
- X-chromosome upregulation operates on a gene-by-gene basis at RNA and protein levels.Nature communications · 2025Article
- Temporal and regional X-linked gene reactivation in the mouse germline reveals site-specific retention of epigenetic silencing.Nature structural & molecular biology · 2025Article
- Heterozygous females from a rat model for creatine transporter deficiency reveal altered behavioral response to stressors, normal body weight and slight metabolic changes.Frontiers in neuroscience · 2025Article
- Advancing 3D Engineered In Vitro Models for Heart Failure Research: Key Features and Considerations.Bioengineering (Basel, Switzerland) · 2024Review
- Lineage-specific dynamics of loss of X upregulation during inactive-X reactivation.Stem cell reports · 2024Article
- Multifaceted role of CTCF in X-chromosome inactivation.Chromosoma · 2024Review
- Using Organoids to Model Sex Differences in the Human Brain.Biological psychiatry global open science · 2024Review
- The interferon γ pathway enhances pluripotency and X-chromosome reactivation in iPSC reprogramming.Science advances · 2024Article
- X-chromosome inactivation in human iPSCs provides insight into X-regulated gene expression in autosomes.Genome biology · 2024Article
- The compleX balancing act of controlling X-chromosome dosage and how it impacts mammalian germline development.The Biochemical journal · 2023Article
- Large-scale differentiation of iPSC-derived motor neurons from ALS and control subjects.Neuron · 2023Article
- Cohesin controls X chromosome structure remodeling and X-reactivation during mouse iPSC-reprogramming.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction and reversal of chromatin silencing is critical for successful development, tissue homeostasis, and the derivation of induced pluripotent stem cells (iPSCs). X-Chromosome inactivation (XCI) and reactivation (XCR) in female cells represent chromosome-wide transitions between active and inactive chromatin states. Although XCI has long been studied, providing important insights into gene regulation, the dynamics and mechanisms underlying the reversal of stable chromatin silencing of X-linked genes are much less understood. Here, we use allele-specific transcriptomics to study XCR during mouse iPSC reprogramming in order to elucidate the timing and mechanisms of chromosome-wide reversal of gene silencing. We show that XCR is hierarchical, with subsets of genes reactivating early, late, and very late during reprogramming. Early genes are activated before the onset of late pluripotency genes activation. Early genes are located genomically closer to genes that escape XCI, unlike genes reactivating late. Early genes also show increased pluripotency transcription factor (TF) binding. We also reveal that histone deacetylases (HDACs) restrict XCR in reprogramming intermediates and that the severe hypoacetylation state of the inactive X Chromosome (Xi) persists until late reprogramming stages. Altogether, these results reveal the timing of transcriptional activation of monoallelically repressed genes during iPSC reprogramming, and suggest that allelic activation involves the combined action of chromatin topology, pluripotency TFs, and chromatin regulators. These findings are important for our understanding of gene silencing, maintenance of cell identity, reprogramming, and disease.
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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 OpenQuestion graph.