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: 3 complete abstracts (392 words), 9 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 material of chromosomes. It is a complex of DNA; histones; and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell.
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: Chromatins.
Where it fits in the MeSH classification
- Broader topics
- Chromosome Structures; Nucleoproteins
- Narrower topics
- Euchromatin; Heterochromatin; Nucleosomes
Related concepts
- Chromosomes
- Histones
- Chromosomal Proteins
- Non-Histone
Research landscape
PubMed indexes 68,535 records tagged with the MeSH heading “Chromatin” (counts retrieved 2026-10-29). 15,430 of them (22.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 20,372 records.
Reviews account for 10,255 records (15.0%) and meta-analyses for 37. Randomized controlled trials number 28 (0.0%) 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 | 20,372 |
| 2000-2009 | 13,512 |
| 2010-2019 | 19,221 |
| 2020 onward | 15,430 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 10,255 | 15.0% |
| Meta-analyses | 37 | 0.1% |
| Randomized controlled trials | 28 | 0.0% |
Method: PubMed query "Chromatin"[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 |
|---|---|---|---|---|
| Unstructured transcription factor interactions enable emergent specificity | 2026 | Research article Design not recorded in structured metadata | 13 | cc by PMID 41855276 · DOI · PMC13581189 |
| Molecular architecture of heterochromatin at the nuclear periphery of primary human cells | 2026 | Research article Design not recorded in structured metadata | 11 | cc by PMID 42399220 · DOI · PMC13332202 |
| Single-cell chromatin state transitions during epigenetic memory formation | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 42490451 · DOI · PMC13394403 |
Unstructured transcription factor interactions enable emergent specificity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- How intrinsically disordered regions (IDRs) shape chromatin binding and nuclear organization of transcription factors (TFs) remains unclear.
- Closing excerpt
- These findings suggest that TF specificity emerges on chromatin when ensembles of diverse, unstructured interactions are scaffolded by transient DNA contacts.
- 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 (121 words)
How intrinsically disordered regions (IDRs) shape chromatin binding and nuclear organization of transcription factors (TFs) remains unclear. We used proximity-assisted photoactivation (PAPA), a single-molecule protein-protein interaction sensor, to investigate how IDRs might influence TF interactions with each other and with chromatin in live cells. We found that the Sp1 DNA binding domain (DBD) interacted poorly with chromatin and did not colocalize with Sp1. Weak interaction of the isolated IDR with full-length Sp1 was enhanced by fusion to various unrelated DBDs. Live imaging of Drosophila polytene chromosomes confirmed that an IDR could confer sharp locus specificity on an otherwise nonspecific DBD. These findings suggest that TF specificity emerges on chromatin when ensembles of diverse, unstructured interactions are scaffolded by transient DNA contacts.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41855276 · DOI · PMC13581189
Molecular architecture of heterochromatin at the nuclear periphery of primary human cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- In eukaryotes, meters of DNA are packaged into micrometer scale nuclei.
- Closing excerpt
- In situ structural biology thus reveals the molecular chromatin organization inside cells and sets the stage for 3D genomics.
- 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 (121 words)
In eukaryotes, meters of DNA are packaged into micrometer scale nuclei. Nucleosomes, as the major organizational unit, have been extensively studied in vitro, yet the elaborate 3D structure of chromatin inside cells and its distinct oligo-nucleosome arrangements remain poorly resolved. Here, we combine cryo-electron tomography with template matching, subtomogram averaging and molecular simulations to visualize nucleosomes and chromatin structure inside human cells. We confidently assign individual nucleosomes and report their in-situ structure at secondary structure resolution. By predicting the paths of linker DNA, we identify oligo-nucleosome arrangements and uncover higher-order chromatin structures in situ, including a 37-nm wide, elongated but non-fibrous arrangement. In situ structural biology thus reveals the molecular chromatin organization inside cells and sets the stage for 3D genomics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42399220 · DOI · PMC13332202
Single-cell chromatin state transitions during epigenetic memory formation [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Repressive chromatin modifications compact chromatin and mediate heritable gene silencing, but how structural changes quantitatively relate to epigenetic memory remains unclear.
- Closing excerpt
- Similar compaction is observed at endogenous loci during differentiation and fate commitment, suggesting that spatial organization may be predictive of epigenetic memory in other systems.
- 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 (150 words)
Repressive chromatin modifications compact chromatin and mediate heritable gene silencing, but how structural changes quantitatively relate to epigenetic memory remains unclear. Using targeted recruitment of the KRAB repressor to induce H3K9me3 at a reporter gene, combined with single-molecule 3D chromatin imaging, we show that irreversible silencing is associated with large-scale chromatin compaction across tens of kilobases. In contrast, histone deacetylation produces reversible silencing without such compaction. Despite substantial single-cell heterogeneity, average compaction at the end of silencing quantitatively predicts epigenetic memory weeks after KRAB removal. Here, memory arises not through stable H3K9me3 domains but rather through a dynamic handoff in which H3K9me3 is gradually lost and replaced by DNA methylation. Stochastic simulations recapitulating these dynamics suggest that compaction enhances read-write feedback to promote this transition. Similar compaction is observed at endogenous loci during differentiation and fate commitment, suggesting that spatial organization may be predictive of epigenetic memory in other systems.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42490451 · DOI · PMC13394403
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 Genome control by SMC complexes [4]
- Research article Pioneer factors: roles and their regulation in development [5]
- Research article Chromatin accessibility: methods, mechanisms, and biological insights [6]
- Research article Energy-driven genome regulation by ATP-dependent chromatin remodellers [7]
- Research article Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application [8]
- Research article Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases [9]
References
- Abidi AA, Cattoglio C, Tang NN, Fan VB, Dailey GM, Hay AD, et al.. Unstructured transcription factor interactions enable emergent specificity. . 2026. PMID 41855276 · DOI · PMC13581189
- Kreysing JP, Cruz-León S, Betz J, Penzo C, Majtner T, Schreiber M, et al.. Molecular architecture of heterochromatin at the nuclear periphery of primary human cells. . 2026. PMID 42399220 · DOI · PMC13332202
- Fujimori T, Thurm AR, Gaudin S, Rios-Martinez C, Doughty BR, Hinks MM, et al.. Single-cell chromatin state transitions during epigenetic memory formation. . 2026. PMID 42490451 · DOI · PMC13394403
- Hoencamp C, Rowland BD. Genome control by SMC complexes. Nat Rev Mol Cell Biol. 2023. PMID 37231112 · DOI
- Barral A, Zaret KS. Pioneer factors: roles and their regulation in development. Trends Genet. 2024. PMID 37940484 · DOI · PMC10873006
- Mansisidor AR, Risca VI. Chromatin accessibility: methods, mechanisms, and biological insights. Nucleus. 2022. PMID 36404679 · DOI · PMC9683059
- Eustermann S, Patel AB, Hopfner KP, He Y, Korber P. Energy-driven genome regulation by ATP-dependent chromatin remodellers. Nat Rev Mol Cell Biol. 2024. PMID 38081975 · DOI · PMC12303036
- Chen Y, Liang R, Li Y, Jiang L, Ma D, Luo Q, et al.. Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application. Signal Transduct Target Ther. 2024. PMID 39627201 · DOI · PMC11615378
- Wu Z, Qu J, Liu GH. Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases. Nat Rev Mol Cell Biol. 2024. PMID 39363000 · DOI
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.