ArticleNature communications2022
Xist exerts gene-specific silencing during XCI maintenance and impacts lineage-specific cell differentiation and proliferation during hematopoiesis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Escape from X-chromosome inactivation: from gene discovery to regulatory mechanisms.Biochemical Society transactions · 2026Review
- Review
- Using combined RNA/DNA short read sequencing to investigate allele-specific expression from the inactive X chromosome in human cells.bioRxiv : the preprint server for biology · 2026Article
- 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
- Escape from X inactivation is directly modulated by Xist noncoding RNA.Nature cell biology · 2026Article
- Long noncoding RNA regulation of immunity.Nature immunology · 2026Review
- Xist in X chromosome inactivation: mechanisms and disease relevance.Cell communication and signaling : CCS · 2025Review
- Prenatal exposure to Zika virus shapes offspring neutrophil function in a sex-specific manner.Nature communications · 2025Article
- XIST Loss Induces Variable Transcriptional Responses Dependent on Cell States.Non-coding RNA · 2025Article
- X inactive-specific transcript regulates mitochondrial function and neuronal differentiation of stem cellsWorld journal of stem cells · 2025Article
- BLIMP1 controls GC B cell expansion and exit through regulating cell cycle progression and key transcription factors BCL6 and IRF4.Cell reports · 2025Article
- Gene reactivation upon erosion of X chromosome inactivation in female hiPSCs is predictable yet variable and persists through differentiation.Stem cell reports · 2025Article
- The Inactive X Chromosome: A Genetic Driver of Female-Biased Rheumatic Autoimmune Disorders?European journal of immunology · 2025Review
- CTCF-mediated insulation and chromatin environment modulate Car5b escape from X inactivation.BMC biology · 2025Article
- Deletion of Xist repeat B disrupts cell cycle and asymmetric cell division through Usp9x hyperactivation in mice.Nucleic acids research · 2025Article
- The role of the LncRNA XIST/miR-15a-5p/MN1 signaling axis in gender disparities in bladder cancer prognosis.Frontiers in immunology · 2025Article
- Loss of XIST lncRNA unlocks stemness and cellular plasticity in ovarian cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sex as a biological variable in ageing: insights and perspectives on the molecular and cellular hallmarks.Open biology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
X chromosome inactivation (XCI) is a dosage compensation phenomenon that occurs in females. Initiation of XCI depends on Xist RNA, which triggers silencing of one of the two X chromosomes, except for XCI escape genes that continue to be biallelically expressed. In the soma XCI is stably maintained with continuous Xist expression. How Xist impacts XCI maintenance remains an open question. Here we conditionally delete Xist in hematopoietic system of mice and report differentiation and cell cycle defects in female hematopoietic stem and progenitor cells (HSPCs). By utilizing female HSPCs and mouse embryonic fibroblasts, we find that X-linked genes show variable tolerance to Xist loss. Specifically, XCI escape genes exhibit preferential transcriptional upregulation, which associates with low H3K27me3 occupancy and high chromatin accessibility that accommodates preexisting binding of transcription factors such as Yin Yang 1 (YY1) at the basal state. We conclude that Xist is necessary for gene-specific silencing during XCI maintenance and impacts lineage-specific cell differentiation and proliferation during hematopoiesis.
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