ArticlePLoS genetics2013
H3.3-H4 tetramer splitting events feature cell-type specific enhancers.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed.
- H2A.Z histone variants facilitate HDACi-dependent removal of H3.3K27M mutant protein in pediatric high-grade glioma cells.Cell reports · 2024Article
- Review
- Epigenetic mechanisms to propagate histone acetylation by p300/CBP.Nature communications · 2023Article
- Involvement of the H3.3 Histone Variant in the Epigenetic Regulation of Gene Expression in the Nervous System, in Both Physiological and Pathological Conditions.International journal of molecular sciences · 2023Review
- The patterns and participants of parental histone recycling during DNA replication in Saccharomyces cerevisiae.Science China. Life sciences · 2023Article
- The high mobility group protein HMG20A cooperates with the histone reader PHF14 to modulate TGFβ and Hippo pathways.Nucleic acids research · 2022Article
- Rtt109 promotes nucleosome replacement ahead of the replication fork.Genome research · 2022Article
- The H3.3K27M oncohistone affects replication stress outcome and provokes genomic instability in pediatric glioma.PLoS genetics · 2021Article
- Parental nucleosome segregation and the inheritance of cellular identity.Nature reviews. Genetics · 2021Review
- Decoding the protein composition of whole nucleosomes with Nuc-MS.Nature methods · 2021Article
- Application of Recombination -Induced Tag Exchange (RITE) to study histone dynamics in human cells.Epigenetics · 2020Article
- Histone H3K27 acetylation is dispensable for enhancer activity in mouse embryonic stem cells.Genome biology · 2020Article
- Rpp29 regulates histone H3.3 chromatin assembly through transcriptional mechanisms.The Journal of biological chemistry · 2018Article
- Structure and function of the histone chaperone FACT - Resolving FACTual issues.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Review
- The Art of War: harnessing the epigenome against cancer.F1000Research · 2018Review
- Transcription and Remodeling Produce Asymmetrically Unwrapped Nucleosomal Intermediates.Molecular cell · 2017Article
- The Inherent Asymmetry of DNA Replication.Annual review of cell and developmental biology · 2017Review
- Breaking Symmetry - Asymmetric Histone Inheritance in Stem Cells.Trends in cell biology · 2017Review
- Partially Assembled Nucleosome Structures at Atomic Detail.Biophysical journal · 2017Article
- Histone variants on the move: substrates for chromatin dynamics.Nature reviews. Molecular cell biology · 2017Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Previously, we reported that little canonical (H3.1-H4)(2) tetramers split to form "hybrid" tetramers consisted of old and new H3.1-H(4) dimers, but approximately 10% of (H3.3-H4)2 tetramers split during each cell cycle. In this report, we mapped the H3.3 nucleosome occupancy, the H3.3 nucleosome turnover rate and H3.3 nucleosome splitting events at the genome-wide level. Interestingly, H3.3 nucleosome turnover rate at the transcription starting sites (TSS) of genes with different expression levels display a bimodal distribution rather than a linear correlation towards the transcriptional activity, suggesting genes are either active with high H3.3 nucleosome turnover or inactive with low H3.3 nucleosome turnover. H3.3 nucleosome splitting events are enriched at active genes, which are in fact better markers for active transcription than H3.3 nucleosome occupancy itself. Although both H3.3 nucleosome turnover and splitting events are enriched at active genes, these events only display a moderate positive correlation, suggesting H3.3 nucleosome splitting events are not the mere consequence of H3.3 nucleosome turnover. Surprisingly, H3.3 nucleosomes with high splitting index are remarkably enriched at enhancers in a cell-type specific manner. We propose that the H3.3 nucleosomes at enhancers may be split by an active mechanism to regulate cell-type specific transcription.
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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.