ArticleMolecular cell2026
Precise control of transcription condensates across S phase balances linker histone expression with DNA replication, ensuring genome stability.
Article in Molecular cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- ATR activity regulates DNA replication and RNA polymerase II transcription during S-phase.iScience · 2026Article
- Anoxia tolerant DNA replication is supported by ATR kinase in the annual killifish Austrofundulus limnaeus.Journal of cell science · 2026Article
- Protocol for cell cycle-resolved high-content imaging of transcription condensate dynamics in human cells.STAR protocols · 2026Article
- Large RNA polymerase II condensates are promoter-centric assemblies associated with early stages of transcription at all expressed genes.bioRxiv : the preprint server for biology · 2026Article
- ATR enforcement of the S/G2 checkpoint prevents premature S phase shutdown and genome instability.bioRxiv : the preprint server for biology · 2026Article
- Differential control of both cell cycle-regulated and quantitative histone mRNA expression bybioRxiv : the preprint server for biology · 2026Article
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9 authors.
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Abstract
Transcription condensates are liquid-like compartments where transcription factors, co-activators, and RNA polymerases are selectively enriched and regulate transcription initiation of associated genes. While the principles governing the enrichment of proteins within transcription condensates are being elucidated, mechanisms that coordinate condensate dynamics with other nuclear processes, such as DNA replication, have not been identified. We show in human cells that at the G1/S cell-cycle transition, large transcription condensates form at histone locus bodies (HLBs) in a cyclin-dependent kinase 1 and 2 (CDK1/2)-dependent manner. By mid-S phase, ataxia-telangiectasia and Rad3-related kinase (ATR) accumulates within HLBs and dissolves the associated condensates via its downstream effector, CHK1. Failure to dissolve condensates results in overexpression of linker H1 histones and nucleus-wide DNA damage. Moreover, an imbalance in the different linker histones accentuates DNA damage in ATR-CHK1-deficient cells. Our work reveals how transcription condensates are precisely controlled in the S phase to fine-tune gene activation and safeguard genome stability.
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