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 (585 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
A type of cell nucleus division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species.
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: Mitoses; M Phase, Mitotic; Mitotic M Phase; Mitotic M Phases; M Phases, Mitotic; Phase, Mitotic M; Phases, Mitotic M.
Where it fits in the MeSH classification
- Broader topics
- Cell Nucleus Division
- Narrower topics
- Anaphase; M Phase Cell Cycle Checkpoints; Metaphase; Prometaphase; Prophase; Telophase
- See also
- Mitogens; Mitotic Index; Maturation-Promoting Factor; Antimitotic Agents
Related concepts
- Cell Nucleus
- Chromosomes
Research landscape
PubMed indexes 61,551 records tagged with the MeSH heading “Mitosis” (counts retrieved 2026-10-29). 4,460 of them (7.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 32,755 records.
Reviews account for 5,024 records (8.2%) and meta-analyses for 5. Randomized controlled trials number 52 (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 | 32,755 |
| 2000-2009 | 12,312 |
| 2010-2019 | 12,024 |
| 2020 onward | 4,460 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,024 | 8.2% |
| Meta-analyses | 5 | 0.0% |
| Randomized controlled trials | 52 | 0.1% |
Method: PubMed query "Mitosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
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 |
|---|---|---|---|---|
| Rules of engagement for condensins and cohesins guide mitotic chromosome formation | 2025 | Research article Design not recorded in structured metadata | 73 | cc by PMID 40208986 · DOI · PMC12118822 |
| Dynamics of microcompartment formation at the mitosis-to-G1 transition | 2025 | Research article Design not recorded in structured metadata | 27 | cc by PMID 41107486 · DOI · PMC12700819 |
| MDM2 functions as a timer reporting the length of mitosis | 2025 | Research article Design not recorded in structured metadata | 26 | cc by PMID 39789219 · DOI · PMC11821534 |
| Interphase chromosome conformation is specified by distinct folding programmes inherited through mitotic chromosomes or the cytoplasm | 2026 | Research article Design not recorded in structured metadata | 23 | cc by PMID 41429936 · DOI · PMC12807859 |
Rules of engagement for condensins and cohesins guide mitotic chromosome formation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- We used Hi-C, imaging, proteomics, and polymer modeling to define rules of engagement for SMC (structural maintenance of chromosomes) complexes as cells refold interphase chromatin into rod-shaped mitotic chromosomes.
- Closing excerpt
- The dynamics of Hi-C interactions and chromosome morphology reveal that during prophase, loops are extruded in vivo at ∼1 to 3 kilobases per second by condensins as they form a disordered discontinuous helical scaffold within individual chromatids.
- 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 (133 words)
We used Hi-C, imaging, proteomics, and polymer modeling to define rules of engagement for SMC (structural maintenance of chromosomes) complexes as cells refold interphase chromatin into rod-shaped mitotic chromosomes. First, condensin disassembles interphase chromatin loop organization by evicting or displacing extrusive cohesin. Second, condensin bypasses cohesive cohesins, thereby maintaining sister chromatid cohesion as sisters separate. Studies of mitotic chromosomes formed by cohesin, condensin II, and condensin I alone or in combination lead to refined models of mitotic chromosome conformation. In these models, loops are consecutive and not overlapping, implying that condensins stall upon encountering each other. The dynamics of Hi-C interactions and chromosome morphology reveal that during prophase, loops are extruded in vivo at ∼1 to 3 kilobases per second by condensins as they form a disordered discontinuous helical scaffold within individual chromatids.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40208986 · DOI · PMC12118822
Dynamics of microcompartment formation at the mitosis-to-G1 transition [2]
Abstract reading summary — source excerpts
- Opening excerpt
- As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished.
- Closing excerpt
- Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
- 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 (153 words)
As cells exit mitosis and enter G1, chromosomes decompact and transcription is reestablished. Hi-C studies have indicated that all interphase three-dimensional genome features, including A/B compartments, topologically associating domains and CCCTC-binding factor loops, are lost during mitosis. However, Hi-C is insensitive to features such as microcompartments, nested focal interactions between cis-regulatory elements. Here we apply region capture Micro-C to mouse erythroblasts from mitosis to G1. We unexpectedly observe microcompartments in prometaphase, which strengthen in anaphase and telophase before weakening throughout G1. Microcompartment anchors coincide with transcriptionally spiking promoters during mitosis. Loss of condensin loop extrusion differentially impacts microcompartments and A/B compartments, suggesting that they are partially distinct. Polymer modeling shows that microcompartment formation is favored by chromatin compaction and disfavored by loop extrusion, providing a basis for strong microcompartmentalization in anaphase and telophase. Our results suggest that compaction and homotypic affinity drive microcompartment formation, which may explain transient transcriptional spiking at mitotic exit.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41107486 · DOI · PMC12700819
MDM2 functions as a timer reporting the length of mitosis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Delays in mitosis trigger p53-dependent arrest in G1 of the next cell cycle, thus preventing repeated cycles of chromosome instability and aneuploidy.
- Closing excerpt
- Subsequent p53-dependent p21 accumulation then channels G1 cells into a sustained cell-cycle arrest, whereas abrogation of the response in p53-deficient cells allows them to bypass this crucial defence mechanism.
- 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)
Delays in mitosis trigger p53-dependent arrest in G1 of the next cell cycle, thus preventing repeated cycles of chromosome instability and aneuploidy. Here we show that MDM2, the p53 ubiquitin ligase, is a key component of the timer mechanism triggering G1 arrest in response to prolonged mitosis. This timer function arises due to the attenuation of protein synthesis in mitosis. Because MDM2 has a short half-life and ongoing protein synthesis is therefore necessary to maintain its steady-state concentration, the amount of MDM2 gradually falls during mitosis but normally remains above a critical threshold for p53 regulation at the onset of G1. When mitosis is extended by prolonged spindle assembly checkpoint activation, the amount of MDM2 drops below this threshold, stabilizing p53. Subsequent p53-dependent p21 accumulation then channels G1 cells into a sustained cell-cycle arrest, whereas abrogation of the response in p53-deficient cells allows them to bypass this crucial defence mechanism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39789219 · DOI · PMC11821534
Interphase chromosome conformation is specified by distinct folding programmes inherited through mitotic chromosomes or the cytoplasm [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Identity-specific chromosome conformation must be re-established at each cell division.
- Closing excerpt
- The combined and interdependent action of chromosome-intrinsic and cytoplasmic inherited folding programmes determines the interphase chromatin conformation as cells exit mitosis.
- 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 (149 words)
Identity-specific chromosome conformation must be re-established at each cell division. To uncover how interphase folding is inherited, we developed an approach that segregates chromosome-intrinsic mechanisms from those propagated through the cytoplasm during G1 nuclear reassembly. Inducible degradation of proteins essential for the establishment of nucleocytoplasmic transport during mitotic exit enabled analysis of folding programmes with distinct modes of inheritance. Here we show that genome compartmentalization is driven entirely by chromosome-intrinsic factors. In addition to conventional compartmental segregation, the chromosome-intrinsic folding programme leads to prominent genome-scale microcompartmentalization of mitotically bookmarked cis-regulatory elements. The microcompartment conformation forms transiently during telophase and is subsequently modulated by a second folding programme inherited through the cytoplasm in early G1. This programme includes cohesin-mediated loop extrusion and factors involved in transcription and RNA processing. The combined and interdependent action of chromosome-intrinsic and cytoplasmic inherited folding programmes determines the interphase chromatin conformation as cells exit mitosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41429936 · DOI · PMC12807859
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 Acetyl coenzyme A: a central metabolite and second messenger [5]
- Research article Ki-67: more than a proliferation marker [6]
- Research article Microtubules and Microtubule-Associated Proteins [7]
- Research article Heterochromatin: Guardian of the Genome [8]
- Research article Targeting Mitosis in Cancer: Emerging Strategies [9]
- Research article Microtubule-Targeting Agents: Strategies To Hijack the Cytoskeleton [10]
References
- Samejima K, Gibcus JH, Abraham S, Cisneros-Soberanis F, Samejima I, Beckett AJ, et al.. Rules of engagement for condensins and cohesins guide mitotic chromosome formation. . 2025. PMID 40208986 · DOI · PMC12118822
- Goel VY, Aboreden NG, Jusuf JM, Zhang H, Mori LP, Mirny LA, et al.. Dynamics of microcompartment formation at the mitosis-to-G1 transition. . 2025. PMID 41107486 · DOI · PMC12700819
- Fulcher LJ, Sobajima T, Batley C, Gibbs-Seymour I, Barr FA. MDM2 functions as a timer reporting the length of mitosis. . 2025. PMID 39789219 · DOI · PMC11821534
- Schooley A, Venev SV, Aksenova V, Lehman JW, Navarrete E, Pai AA, et al.. Interphase chromosome conformation is specified by distinct folding programmes inherited through mitotic chromosomes or the cytoplasm. . 2026. PMID 41429936 · DOI · PMC12807859
- Pietrocola F, Galluzzi L, Bravo-San Pedro JM, Madeo F, Kroemer G. Acetyl coenzyme A: a central metabolite and second messenger. Cell Metab. 2015. PMID 26039447 · DOI
- Sun X, Kaufman PD. Ki-67: more than a proliferation marker. Chromosoma. 2018. PMID 29322240 · DOI · PMC5945335
- Goodson HV, Jonasson EM. Microtubules and Microtubule-Associated Proteins. Cold Spring Harb Perspect Biol. 2018. PMID 29858272 · DOI · PMC5983186
- Janssen A, Colmenares SU, Karpen GH. Heterochromatin: Guardian of the Genome. Annu Rev Cell Dev Biol. 2018. PMID 30044650 · DOI
- Dominguez-Brauer C, Thu KL, Mason JM, Blaser H, Bray MR, Mak TW. Targeting Mitosis in Cancer: Emerging Strategies. Mol Cell. 2015. PMID 26590712 · DOI
- Steinmetz MO, Prota AE. Microtubule-Targeting Agents: Strategies To Hijack the Cytoskeleton. Trends Cell Biol. 2018. PMID 29871823 · 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.