ArticleNature structural & molecular biology2023
Replication dynamics identifies the folding principles of the inactive X chromosome.
Article in Nature structural & molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Cell-cycle-resolved Hi-C reveals unexpected plasticity of A/B compartments across interphase.eLife · 2026Article
- DNA methylation and lncRNA control asynchronous DNA replication at specific imprinted gene domains.Nature communications · 2026Article
- Lyonization of X-chromosome: New insights.Journal of genetics · 2026Review
- scRepli-RamDA-seq: a multi-omics technology enabling the analysis of gene expression dynamics during S-phase.Nature communications · 2025Article
- Article
- A critical role for X-chromosome architecture in mammalian X-chromosome dosage compensation.Current opinion in genetics & development · 2024Review
- Establishment and maintenance of random monoallelic expression.Development (Cambridge, England) · 2024Review
- Transcription and replication meet the silent X chromosome territory.Nature structural & molecular biology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome-wide late replication is an enigmatic hallmark of the inactive X chromosome (Xi). How it is established and what it represents remains obscure. By single-cell DNA replication sequencing, here we show that the entire Xi is reorganized to replicate rapidly and uniformly in late S-phase during X-chromosome inactivation (XCI), reflecting its relatively uniform structure revealed by 4C-seq. Despite this uniformity, only a subset of the Xi became earlier replicating in SmcHD1-mutant cells. In the mutant, these domains protruded out of the Xi core, contacted each other and became transcriptionally reactivated. 4C-seq suggested that they constituted the outermost layer of the Xi even before XCI and were rich in escape genes. We propose that this default positioning forms the basis for their inherent heterochromatin instability in cells lacking the Xi-binding protein SmcHD1 or exhibiting XCI escape. These observations underscore the importance of 3D genome organization for heterochromatin stability and gene regulation.
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