ArticleNature cell biology2025
RNA-binding proteins mediate the maturation of chromatin topology during differentiation.
Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Regulation of neuronal transcription by RNA-binding proteins via R-loop dynamics.Neural regeneration research · 2026Article
- SAM68 is a multifunctional post-transcriptional regulator of cardiomyocyte differentiation.Nucleic acids research · 2026Article
- Hnf1aos1 as a Metabolic Coordinator of Hepatic Lipid Homeostasis and Feedback Control.Non-coding RNA · 2026Article
- A comparative analysis of topological domain callers over RNA-associated interactome.BMC bioinformatics · 2026Article
- Chromatin boundary permeability is controlled by CTCF conformational ensembles.bioRxiv : the preprint server for biology · 2026Article
- Mechanobiology of the Nucleolus.Biology of the cell · 2026Review
- From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.Frontiers in aging · 2026Review
- LncRNA CISTR-ACT regulates cell size in human and mouse by guiding FOSL2.Nature communications · 2025Article
- RNA-binding proteins pull in chromatin loops.Nature cell biology · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Topologically associating domains (TADs) and chromatin architectural loops impact promoter-enhancer interactions, with CCCTC-binding factor (CTCF) defining TAD borders and loop anchors. TAD boundaries and loops progressively strengthen upon embryonic stem (ES) cell differentiation, underscoring the importance of chromatin topology in ontogeny. However, the mechanisms driving this process remain unclear. Here we show a widespread increase in CTCF-RNA-binding protein (RBP) interactions upon ES to neural stem (NS) cell differentiation. While dispensable in ES cells, RBPs reinforce CTCF-anchored chromatin topology in NS cells. We identify Pantr1, a non-coding RNA, as a key facilitator of CTCF-RBP interactions, promoting chromatin maturation. Using acute CTCF degradation, we find that, through its insulator function, CTCF helps maintain neuronal gene silencing in NS cells by acting as a barrier to untimely gene activation during development. Altogether, we reveal a fundamental mechanism driving developmentally linked chromatin structural consolidation and the contribution of this process to the control of gene expression in differentiation.
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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.