ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2017
Capitalizing on disaster: Establishing chromatin specificity behind the replication fork.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Nascent CUT&Tag captures transcription factor binding after chromatin duplication.bioRxiv : the preprint server for biology · 2025Article
- The eukaryotic replisome intrinsically generates asymmetric daughter chromatin fibers.bioRxiv : the preprint server for biology · 2025Article
- Article
- Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress.Developmental cell · 2024Article
- Nucleosome assembly and disassembly pathways in vitro.PloS one · 2022Article
- Chromatin replication and epigenetic cell memory.Nature cell biology · 2020Review
- Mitotic Inheritance of PRC2-Mediated Silencing: Mechanistic Insights and Developmental Perspectives.Frontiers in plant science · 2020Review
- Asymmetric Histone Inheritance in Asymmetrically Dividing Stem Cells.Trends in genetics : TIG · 2020Review
- Opposing chromatin remodelers control transcription initiation frequency and start site selection.Nature structural & molecular biology · 2019Article
- RSC-Associated Subnucleosomes Define MNase-Sensitive Promoters in Yeast.Molecular cell · 2019Article
- Replication-Coupled Nucleosome Assembly in the Passage of Epigenetic Information and Cell Identity.Trends in biochemical sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Eukaryotic genomes are packaged into nucleosomal chromatin, and genomic activity requires the precise localization of transcription factors, histone modifications and nucleosomes. Classic work described the progressive reassembly and maturation of bulk chromatin behind replication forks. More recent proteomics has detailed the molecular machines that accompany the replicative polymerase to promote rapid histone deposition onto the newly replicated DNA. However, localized chromatin features are transiently obliterated by DNA replication every S phase of the cell cycle. Genomic strategies now observe the rebuilding of locus-specific chromatin features, and reveal surprising delays in transcription factor binding behind replication forks. This implies that transient chromatin disorganization during replication is a central juncture for targeted transcription factor binding within genomes. We propose that transient occlusion of regulatory elements by disorganized nucleosomes during chromatin maturation enforces specificity of factor binding.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.