Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (630 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The repeating structural units of chromatin, each consisting of approximately 200 base pairs of DNA wound around a protein core. This core is composed of the histones H2A, H2B, H3, and H4.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Nucleosome; Dinucleosomes; Dinucleosome; Polynucleosomes; Polynucleosome.
Where it fits in the MeSH classification
- Broader topics
- Chromatin
Research landscape
PubMed indexes 11,946 records tagged with the MeSH heading “Nucleosomes” (counts retrieved 2026-10-29). 2,378 of them (19.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 3,883 records.
Reviews account for 1,670 records (14.0%) and meta-analyses for 1. Randomized controlled trials number 8 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,965 |
| 2000-2009 | 2,720 |
| 2010-2019 | 3,883 |
| 2020 onward | 2,378 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,670 | 14.0% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 8 | 0.1% |
Method: PubMed query "Nucleosomes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in genetics and genomics
Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| MRE11 liberates cGAS from nucleosome sequestration during tumorigenesis | 2024 | Research article Design not recorded in structured metadata | 128 | cc by PMID 38200309 · DOI · PMC10794148 |
| Histone modifications regulate pioneer transcription factor cooperativity | 2023 | Research article Design not recorded in structured metadata | 113 | cc by PMID 37225990 · DOI · PMC10338341 |
| Structure of native chromatin fibres revealed by Cryo-ET in situ | 2023 | Research article Design not recorded in structured metadata | 94 | cc by PMID 37816746 · DOI · PMC10564948 |
| FACT depletion demonstrates a role for nucleosome organization in TAD formation | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41145704 · DOI · PMC12759068 |
MRE11 liberates cGAS from nucleosome sequestration during tumorigenesis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Oncogene-induced replication stress generates endogenous DNA damage that activates cGAS-STING-mediated signalling and tumour suppression1-3.
- Closing excerpt
- These findings establish MRE11 as a crucial mediator that links DNA damage and cGAS activation, resulting in tumour suppression through ZBP1-dependent necroptosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (173 words)
Oncogene-induced replication stress generates endogenous DNA damage that activates cGAS-STING-mediated signalling and tumour suppression1-3. However, the precise mechanism of cGAS activation by endogenous DNA damage remains enigmatic, particularly given that high-affinity histone acidic patch (AP) binding constitutively inhibits cGAS by sterically hindering its activation by double-stranded DNA (dsDNA)4-10. Here we report that the DNA double-strand break sensor MRE11 suppresses mammary tumorigenesis through a pivotal role in regulating cGAS activation. We demonstrate that binding of the MRE11-RAD50-NBN complex to nucleosome fragments is necessary to displace cGAS from acidic-patch-mediated sequestration, which enables its mobilization and activation by dsDNA. MRE11 is therefore essential for cGAS activation in response to oncogenic stress, cytosolic dsDNA and ionizing radiation. Furthermore, MRE11-dependent cGAS activation promotes ZBP1-RIPK3-MLKL-mediated necroptosis, which is essential to suppress oncogenic proliferation and breast tumorigenesis. Notably, downregulation of ZBP1 in human triple-negative breast cancer is associated with increased genome instability, immune suppression and poor patient prognosis. These findings establish MRE11 as a crucial mediator that links DNA damage and cGAS activation, resulting in tumour suppression through ZBP1-dependent necroptosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38200309 · DOI · PMC10794148
Histone modifications regulate pioneer transcription factor cooperativity [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Pioneer transcription factors have the ability to access DNA in compacted chromatin1.
- Closing excerpt
- Thus, our findings suggest that the epigenetic landscape could regulate OCT4 activity to ensure proper cell programming.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (191 words)
Pioneer transcription factors have the ability to access DNA in compacted chromatin1. Multiple transcription factors can bind together to a regulatory element in a cooperative way, and cooperation between the pioneer transcription factors OCT4 (also known as POU5F1) and SOX2 is important for pluripotency and reprogramming2-4. However, the molecular mechanisms by which pioneer transcription factors function and cooperate on chromatin remain unclear. Here we present cryo-electron microscopy structures of human OCT4 bound to a nucleosome containing human LIN28B or nMATN1 DNA sequences, both of which bear multiple binding sites for OCT4. Our structural and biochemistry data reveal that binding of OCT4 induces changes to the nucleosome structure, repositions the nucleosomal DNA and facilitates cooperative binding of additional OCT4 and of SOX2 to their internal binding sites. The flexible activation domain of OCT4 contacts the N-terminal tail of histone H4, altering its conformation and thus promoting chromatin decompaction. Moreover, the DNA-binding domain of OCT4 engages with the N-terminal tail of histone H3, and post-translational modifications at H3K27 modulate DNA positioning and affect transcription factor cooperativity. Thus, our findings suggest that the epigenetic landscape could regulate OCT4 activity to ensure proper cell programming.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37225990 · DOI · PMC10338341
Structure of native chromatin fibres revealed by Cryo-ET in situ [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The structure of chromatin plays pivotal roles in regulating gene transcription, DNA replication and repair, and chromosome segregation.
- Closing excerpt
- This work will inspire future high-resolution investigations on native chromatin structures in situ at both a single-nucleosome level and a population level under many different cellular conditions in health and disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (128 words)
The structure of chromatin plays pivotal roles in regulating gene transcription, DNA replication and repair, and chromosome segregation. This structure, however, remains elusive. Here, using cryo-FIB and cryo-ET, we delineate the 3D architecture of native chromatin fibres in intact interphase human T-lymphoblasts and determine the in situ structures of nucleosomes in different conformations. These chromatin fibres are not structured as uniform 30 nm one-start or two-start filaments but are composed of relaxed, variable zigzag organizations of nucleosomes connected by straight linker DNA. Nucleosomes with little H1 and linker DNA density are distributed randomly without any spatial preference. This work will inspire future high-resolution investigations on native chromatin structures in situ at both a single-nucleosome level and a population level under many different cellular conditions in health and disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37816746 · DOI · PMC10564948
FACT depletion demonstrates a role for nucleosome organization in TAD formation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Mammalian genomes are organized into distinct chromatin structures, which include small-scale nucleosome arrays and large-scale topologically associating domains (TADs).
- Closing excerpt
- FACT depletion therefore allows us to separate the role of nucleosome organization and CTCF binding and to demonstrate that the organization of nucleosomes at TAD boundaries contributes to TAD formation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (138 words)
Mammalian genomes are organized into distinct chromatin structures, which include small-scale nucleosome arrays and large-scale topologically associating domains (TADs). The mechanistic interplay between chromatin structures across scales is poorly understood. Here, we investigate how changes in nucleosome organization impact TAD structure by studying the role of the histone chaperone facilitates chromatin transcription (FACT) in 3D genome organization. We show that FACT depletion perturbs TADs, causing decreased insulation and weaker CTCF loops. These changes in TAD structure cannot be attributed to changes in chromatin occupancy of CTCF or cohesin and occur specifically in transcribed regions of the genome, where we observe perturbed nucleosome organization in the absence of FACT. FACT depletion therefore allows us to separate the role of nucleosome organization and CTCF binding and to demonstrate that the organization of nucleosomes at TAD boundaries contributes to TAD formation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41145704 · DOI · PMC12759068
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article ChIP-seq: advantages and challenges of a maturing technology [5]
- Research article Chromatin accessibility and the regulatory epigenome [6]
- Research article Mechanisms of action and regulation of ATP-dependent chromatin-remodelling complexes [7]
- Research article Lateral Thinking: How Histone Modifications Regulate Gene Expression [8]
- Research article Determinants of nucleosome positioning [9]
- Research article Understanding nucleosome dynamics and their links to gene expression and DNA replication [10]
References
- Cho MG, Kumar RJ, Lin CC, Boyer JA, Shahir JA, Fagan-Solis K, et al.. MRE11 liberates cGAS from nucleosome sequestration during tumorigenesis. . 2024. PMID 38200309 · DOI · PMC10794148
- Sinha KK, Bilokapic S, Du Y, Malik D, Halic M. Histone modifications regulate pioneer transcription factor cooperativity. . 2023. PMID 37225990 · DOI · PMC10338341
- Hou Z, Nightingale F, Zhu Y, MacGregor-Chatwin C, Zhang P. Structure of native chromatin fibres revealed by Cryo-ET in situ. . 2023. PMID 37816746 · DOI · PMC10564948
- Mauksch C, Zhu Y, Velychko T, Sagropoulou S, Aljahani A, Ramasamy S, et al.. FACT depletion demonstrates a role for nucleosome organization in TAD formation. . 2026. PMID 41145704 · DOI · PMC12759068
- Park PJ. ChIP-seq: advantages and challenges of a maturing technology. Nat Rev Genet. 2009. PMID 19736561 · DOI · PMC3191340
- Klemm SL, Shipony Z, Greenleaf WJ. Chromatin accessibility and the regulatory epigenome. Nat Rev Genet. 2019. PMID 30675018 · DOI
- Clapier CR, Iwasa J, Cairns BR, Peterson CL. Mechanisms of action and regulation of ATP-dependent chromatin-remodelling complexes. Nat Rev Mol Cell Biol. 2017. PMID 28512350 · DOI · PMC8127953
- Lawrence M, Daujat S, Schneider R. Lateral Thinking: How Histone Modifications Regulate Gene Expression. Trends Genet. 2016. PMID 26704082 · DOI
- Struhl K, Segal E. Determinants of nucleosome positioning. Nat Struct Mol Biol. 2013. PMID 23463311 · DOI · PMC3740156
- Lai WKM, Pugh BF. Understanding nucleosome dynamics and their links to gene expression and DNA replication. Nat Rev Mol Cell Biol. 2017. PMID 28537572 · DOI · PMC5831138
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.