ArticleNature communications2022
Regulation of chromatin accessibility by the histone chaperone CAF-1 sustains lineage fidelity.
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 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Stress triggers global histone synthesis in the liver.bioRxiv : the preprint server for biology · 2026Article
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Newly synthesized histones: passive or active players in the regulation of epigenetic inheritance?Nucleic acids research · 2026Review
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- Chromatin Assembly Factor 1 is required for normal structure and function of facultative heterochromatin inbioRxiv : the preprint server for biology · 2026Article
- HIRA-mediated H3.3 deposition preserves hepatocyte cell identity during liver aging.Research square · 2026Article
- Proximal proteomics analysis reveals DNA polymerase δ subunit 3 is a new MCM2 binding partner and promotes parental histones inheritance in mammalian cells.Cell death and differentiation · 2026Article
- Post-replicative chromatin accessibility predicts cell fate change.Stem cell reports · 2026Article
- DNA Adenine Methylation Clock in Brain Aging and Alzheimer's Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Spt7 Deletion Reveals Vulnerabilities inMicroorganisms · 2026Article
- Natural language processing of gene descriptions for overrepresentation analysis with GeneTEA.Genome biology · 2025Article
- Escape of Kdm6a from X Chromosome Is Detrimental to Ischemic Brains via IRF5 Signaling.Translational stroke research · 2025Article
- Reversible proliferative arrest induced by rapid depletion of RNase MRP.Nature communications · 2025Article
- STAT3 Facilitates Super Enhancer Formation to Promote Fibroblast-To-Myofibroblast Differentiation by the Analysis of ATAC-Seq, RNA-Seq and ChIP-Seq.Journal of cellular and molecular medicine · 2025Review
- Histone chaperones coupled to DNA replication and transcription control divergent chromatin elements to maintain cell fate.Genes & development · 2025Article
- Benchmark of chromatin-protein interaction methods in haploid round spermatids.Frontiers in cell and developmental biology · 2025Article
- Manipulating cell fate through reprogramming: approaches and applications.Development (Cambridge, England) · 2024Review
- Escape of Kdm6a from X chromosome is detrimental to ischemic brains via IRF5 signaling.Research square · 2024Article
- CRISPR screen of venetoclax response-associated genes identifies transcription factor ZNF740 as a key functional regulator.Cell death & disease · 2024Article
- Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress.Developmental cell · 2024Article
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Authors and funding
21 authors at 8 institutions in 1 country.
Funding
Abstract
Cell fate commitment is driven by dynamic changes in chromatin architecture and activity of lineage-specific transcription factors (TFs). The chromatin assembly factor-1 (CAF-1) is a histone chaperone that regulates chromatin architecture by facilitating nucleosome assembly during DNA replication. Accumulating evidence supports a substantial role of CAF-1 in cell fate maintenance, but the mechanisms by which CAF-1 restricts lineage choice remain poorly understood. Here, we investigate how CAF-1 influences chromatin dynamics and TF activity during lineage differentiation. We show that CAF-1 suppression triggers rapid differentiation of myeloid stem and progenitor cells into a mixed lineage state. We find that CAF-1 sustains lineage fidelity by controlling chromatin accessibility at specific loci, and limiting the binding of ELF1 TF at newly-accessible diverging regulatory elements. Together, our findings decipher key traits of chromatin accessibility that sustain lineage integrity and point to a powerful strategy for dissecting transcriptional circuits central to cell fate commitment.
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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.