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 (610 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 fission of a CELL. It includes cytokinesis, when the cytoplasm of a cell is divided, and cell nucleus division.
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: Division, Cell; Divisions, Cell; Cell Divisions; M Phase; M Phases; Phase, M; Phases, M; Cell Division Phase.
Where it fits in the MeSH classification
- Broader topics
- Cell Cycle; Cell Proliferation; Genetic Phenomena
- Narrower topics
- Asymmetric Cell Division; Cell Nucleus Division; Cell Self Renewal; Cytokinesis; Telomere Homeostasis
- See also
- Cell Cycle Proteins; Genes, cdc
Related concepts
- Cytokinesis
- Cytoplasm
- Cell Nucleus Division
Research landscape
PubMed indexes 260,093 records tagged with the MeSH heading “Cell Division” (counts retrieved 2026-10-29). 12,958 of them (5.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 145,523 records.
Reviews account for 22,927 records (8.8%) and meta-analyses for 85. Randomized controlled trials number 469 (0.2%) 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 | 145,523 |
| 2000-2009 | 70,577 |
| 2010-2019 | 31,035 |
| 2020 onward | 12,958 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 22,927 | 8.8% |
| Meta-analyses | 85 | 0.0% |
| Randomized controlled trials | 469 | 0.2% |
Method: PubMed query "Cell Division"[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 |
|---|---|---|---|---|
| Cleavage of mRNAs by a minority of pachytene piRNAs improves sperm fitness | 2026 | Research article Design not recorded in structured metadata | 9 | cc by PMID 41639461 · DOI · PMC13061629 |
| SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41520142 · DOI · PMC13003928 |
| A mechanical ratchet drives unilateral cytokinesis | 2026 | Research article Design not recorded in structured metadata | 7 | cc by PMID 41501469 · DOI · PMC12916326 |
Cleavage of mRNAs by a minority of pachytene piRNAs improves sperm fitness [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Animals use 18-33-nucleotide PIWI-interacting RNAs (piRNAs) to silence transposons in germ cells1-3.
- Closing excerpt
- Together, our findings explain the lack of conservation of most pachytene piRNA sequences and suggest that these 'selfish' small RNAs persist in mammalian evolution because target cleavage by a tiny minority of piRNAs supports male fertility.
- 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 (190 words)
Animals use 18-33-nucleotide PIWI-interacting RNAs (piRNAs) to silence transposons in germ cells1-3. In addition to transposon-silencing piRNAs, placental mammals make pachytene piRNAs4,5, an abundant class of testis-specific small RNAs derived from long noncoding RNA precursors. Although the sites of pachytene piRNA precursor transcription are often conserved among placental mammals, the sequences of the piRNAs themselves are rapidly diverging, even in the human population6. Consequently, the biological function and mechanism of action of pachytene piRNAs remain debated. Here we report that most mouse pachytene piRNAs have no biological function but instead 'selfishly' promote their own production. Our data suggest that pachytene piRNAs direct endonucleolytic cleavage of partially complementary targets and neither activate nor repress mRNA translation. Although many pachytene piRNAs guide cleavage of specific mRNAs, few alter the steady-state abundance of their targets. The minority of pachytene piRNAs that reduce target mRNA abundance enhance sperm fitness, thereby ensuring production of the entire pachytene piRNA repertoire. Together, our findings explain the lack of conservation of most pachytene piRNA sequences and suggest that these 'selfish' small RNAs persist in mammalian evolution because target cleavage by a tiny minority of piRNAs supports male fertility.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41639461 · DOI · PMC13061629
SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundApproximately 10% of cancers achieve replicative immortality through a telomerase-independent mechanism of telomere maintenance, termed Alternative Lengthening of Telomeres (ALT).
- Closing excerpt
- ConclusionsOur findings demonstrate that the molecular processes orchestrating ALT-mediated telomere maintenance constitute a targetable synthetic lethal vulnerability that can be exploited by SMARCAL1 inhibition, thus supporting the future development of small molecule inhibitors of SMARCAL1 as anti-cancer therapeutics.
- 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 (250 words)
BackgroundApproximately 10% of cancers achieve replicative immortality through a telomerase-independent mechanism of telomere maintenance, termed Alternative Lengthening of Telomeres (ALT). ALT is particularly prevalent in certain subtypes of malignant gliomas, such as IDH-mutant astrocytoma and pediatric glioblastoma, and frequently co-occurs with ATRX (ATRX chromatin remodeler) inactivating mutations. Although ALT is an adaptive mechanism through which cancer cells achieve proliferative immortality, the elevated levels of replication stress observed in ALT tumors constitute a potential therapeutic vulnerability.MethodsLeveraging CRISPR/Cas9 screening data from the Cancer Dependency Mapping Project, coupled with patient-derived cell lines and xenografts, we identified SMARCAL1 as a novel synthetic lethal vulnerability in ATRX-deficient glioma models that engage ALT. Using complementary molecular assays for DNA damage, telomere maintenance, and telomeric replication stress, we define the mechanisms underlying cytotoxicity induced by SMARCAL1 depletion in ALT-positive glioma cells.ResultsOur data demonstrate the annealing helicase SMARCAL1 is a highly specific synthetical lethal vulnerability in cancers that use ALT. SMARCAL1 localizes to ALT-associated PML (Promyelocytic leukemia protein) bodies in ALT-positive glioma cell lines, including IDH-mutant astrocytomas. SMARCAL1 depletion, via doxycycline-induced RNAi, led to a hyperactivation of the ALT phenotype, high levels of DNA double-strand breaks in G2 phase, and cell death via mitotic catastrophe. In mice bearing intracranial xenografts derived from high-grade IDH-mutant astrocytoma, inducible SMARCAL1 depletion prolonged animal survival.ConclusionsOur findings demonstrate that the molecular processes orchestrating ALT-mediated telomere maintenance constitute a targetable synthetic lethal vulnerability that can be exploited by SMARCAL1 inhibition, thus supporting the future development of small molecule inhibitors of SMARCAL1 as anti-cancer therapeutics.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41520142 · DOI · PMC13003928
A mechanical ratchet drives unilateral cytokinesis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The canonical mechanism that drives cell division comprises the formation and constriction of a contractile actin ring1-3.
- Closing excerpt
- Our study underscores the role of temporal control over cytoplasmic rheology as a key feature that drives unilateral cytokinesis in the absence of a closed actin ring.
- 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 (170 words)
The canonical mechanism that drives cell division comprises the formation and constriction of a contractile actin ring1-3. However, this mechanism is not compatible with the early development of many vertebrates4-9. Yolk-anchored embryos typically cannot form a complete ring during early cleavage divisions, but it remains unclear how a partial circular arc with loose ends can divide the cell. Here, by combining laser ablation of the cytokinetic band with rheological measurements in vivo, we show that stiffening of the bulk cytoplasm, mediated by the interphase microtubule network, stabilizes the contractile band by anchoring it along its length during growth. Conversely, as the cell cycle progresses, the cytoplasm fluidizes, diminishing band-cytoplasmic anchoring and facilitating band ingression. This dynamic interplay between stability and growth versus instability and ingression repeats for several cell cycles until division is complete, resulting in a mechanical ratchet that drives cell division. Our study underscores the role of temporal control over cytoplasmic rheology as a key feature that drives unilateral cytokinesis in the absence of a closed actin ring.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41501469 · DOI · PMC12916326
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 Telomere dysfunction in ageing and age-related diseases [4]
- Research article Association between shortened leukocyte telomere length and cardiometabolic outcomes: systematic review and meta-analysis [5]
- Research article Principles and dynamics of spindle assembly checkpoint signalling [6]
- Research article Meiosis: Dances Between Homologs [7]
- Research article Effect of obesity on telomere length: Systematic review and meta-analysis [8]
- Research article Control of stem cell renewal and fate by YAP and TAZ [9]
References
- Cecchini K, Zamani M, Ajaykumar N, Vega-Badillo J, Bagci A, Bailey S, et al.. Cleavage of mRNAs by a minority of pachytene piRNAs improves sperm fitness. . 2026. PMID 41639461 · DOI · PMC13061629
- Brown A, Strickland LM, Erman EN, Pirozzi CJ, Low JT, Diplas BH, et al.. SMARCAL1 is a targetable synthetic lethal therapeutic vulnerability in ATRX-deficient gliomas that use alternative lengthening of telomeres. . 2026. PMID 41520142 · DOI · PMC13003928
- Kickuth A, Uršič U, Staddon MF, Brugués J. A mechanical ratchet drives unilateral cytokinesis. . 2026. PMID 41501469 · DOI · PMC12916326
- Rossiello F, Jurk D, Passos JF, d'Adda di Fagagna F. Telomere dysfunction in ageing and age-related diseases. Nat Cell Biol. 2022. PMID 35165420 · DOI · PMC8985209
- D'Mello MJ, Ross SA, Briel M, Anand SS, Gerstein H, Paré G. Association between shortened leukocyte telomere length and cardiometabolic outcomes: systematic review and meta-analysis. Circ Cardiovasc Genet. 2015. PMID 25406241 · DOI
- McAinsh AD, Kops GJPL. Principles and dynamics of spindle assembly checkpoint signalling. Nat Rev Mol Cell Biol. 2023. PMID 36964313 · DOI
- Zickler D, Kleckner N. Meiosis: Dances Between Homologs. Annu Rev Genet. 2023. PMID 37788458 · DOI
- Mundstock E, Sarria EE, Zatti H, Mattos Louzada F, Kich Grun L, Herbert Jones M, et al.. Effect of obesity on telomere length: Systematic review and meta-analysis. Obesity (Silver Spring). 2015. PMID 26407932 · DOI
- Driskill JH, Pan D. Control of stem cell renewal and fate by YAP and TAZ. Nat Rev Mol Cell Biol. 2023. PMID 37626124 · 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.