ArticleMolecular cell2024
Acute multi-level response to defective de novo chromatin assembly in S-phase.
Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed.
- Chromatin Assembly Factor 1 is required for normal structure and function of facultative heterochromatin inbioRxiv : the preprint server for biology · 2026Article
- Cell-cycle-dependent repression of histone gene transcription by histone H4.Nature structural & molecular biology · 2026Article
- Proteome-widebioRxiv : the preprint server for biology · 2025Article
- H2BK120ub and its reader RNF169 sequentially regulate replication fork remodeling and stability.The EMBO journal · 2025Article
- Article
- Always on the Move: Overview on Chromatin Dynamics within Nuclear Processes.Biochemistry · 2025Review
- Histone chaperones coupled to DNA replication and transcription control divergent chromatin elements to maintain cell fate.Genes & development · 2025Article
Corrections and comments
- Erratum issued
- Update of
Authors and funding
23 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term perturbation of de novo chromatin assembly during DNA replication has profound effects on epigenome maintenance and cell fate. The early mechanistic origin of these defects is unknown. Here, we combine acute degradation of chromatin assembly factor 1 (CAF-1), a key player in de novo chromatin assembly, with single-cell genomics, quantitative proteomics, and live microscopy to uncover these initiating mechanisms in human cells. CAF-1 loss immediately slows down DNA replication speed and renders nascent DNA hyper-accessible. A rapid cellular response, distinct from canonical DNA damage signaling, is triggered and lowers histone mRNAs. In turn, histone variants' usage and their modifications are altered, limiting transcriptional fidelity and delaying chromatin maturation within a single S-phase. This multi-level response induces a p53-dependent cell-cycle arrest after mitosis. Our work reveals the immediate consequences of defective de novo chromatin assembly during DNA replication, indicating how at later times the epigenome and cell fate can be altered.
Indexed as
Identifiers
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Registered trials
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