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 (492 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 complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes interphase, which includes G0 phase; G1 phase; S phase; and G2 phase, and cell division phase.
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: Cell Cycles; Cycle, Cell; Cycles, Cell; Cell Division Cycle; Cell Division Cycles; Cycle, Cell Division; Cycles, Cell Division; Division Cycle, Cell.
Where it fits in the MeSH classification
- Broader topics
- Cell Physiological Phenomena
- Narrower topics
- Cell Cycle Checkpoints; Cell Division; Interphase
- See also
- Cell Cycle Proteins; Genes, cdc
Related concepts
Research landscape
PubMed indexes 359,497 records tagged with the MeSH heading “Cell Cycle” (counts retrieved 2026-10-29). 25,312 of them (7.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 165,592 records.
Reviews account for 32,626 records (9.1%) and meta-analyses for 133. Randomized controlled trials number 561 (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 | 165,592 |
| 2000-2009 | 96,310 |
| 2010-2019 | 72,283 |
| 2020 onward | 25,312 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 32,626 | 9.1% |
| Meta-analyses | 133 | 0.0% |
| Randomized controlled trials | 561 | 0.2% |
Method: PubMed query "Cell Cycle"[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 |
|---|---|---|---|---|
| The penicillin-binding protein PBP1b fortifies the Escherichia coli division site against osmotic rupture | 2026 | Research article Design not recorded in structured metadata | 8 | cc by PMID 42399561 · DOI · PMC13423804 |
| Defective transcription of AAGAG satellite DNA causes sex-ratio meiotic drive in Drosophila | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42034642 · DOI · PMC13320161 |
| ESCRT-III assembles around mis-segregated DNA to protect genome stability | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42458110 · DOI · PMC13468122 |
The penicillin-binding protein PBP1b fortifies the Escherichia coli division site against osmotic rupture [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The divisome apparatus synthesizes septal peptidoglycan (PG) during bacterial division.
- Closing excerpt
- The conservation of aPBPs with extended cytoplasmic N termini suggests that other Gram-negative bacteria may use similar mechanisms for division site reinforcement.
- 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 (155 words)
The divisome apparatus synthesizes septal peptidoglycan (PG) during bacterial division. In Escherichia coli, the class A penicillin-binding protein (aPBP) called PBP1b has been implicated in division, but its role in the process has remained unclear. Here we show using in situ cryo-electron tomography, genetics and other imaging methods that PBP1b is required to produce a wedge-like density of PG at the division site and that loss of this structure weakens the division site, making it hypersusceptible to osmotic lysis. Surprisingly, the activator LpoB needed for general PBP1b function was not required for its role in division. Of the two PBP1b isoforms produced in cells, we show that the one with an extended cytoplasmic N terminus localizes to and functions at the division site, probably via recruitment by the FtsA component of the divisome. The conservation of aPBPs with extended cytoplasmic N termini suggests that other Gram-negative bacteria may use similar mechanisms for division site reinforcement.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42399561 · DOI · PMC13423804
Defective transcription of AAGAG satellite DNA causes sex-ratio meiotic drive in Drosophila [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Male germ cells have complex transcriptomes, with a large fraction of the genome being transcribed.
- Closing excerpt
- We further propose that differential composition and amount of satellite DNA on chromosomes may underlie naturally occurring male meiotic drive.
- 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 (181 words)
Male germ cells have complex transcriptomes, with a large fraction of the genome being transcribed. This includes protein-coding genes (often not translated), non-coding DNA, and repetitive DNA, such as transposons and satellite DNA, which are normally silenced as heterochromatin. The significance of such widespread transcription remains unknown. Here, we show that a heterochromatin protein, HP2, is required for the transcription of AAGAG satellite DNA in Drosophila spermatocytes. HP2 depletion leads to abnormal retention of heterochromatin histone marks (H3K9me3) and spermatid death during sperm DNA packaging, leading to a model that transcription of AAGAG satellite DNA facilitates the remodeling of its heterochromatic nature in preparation for sperm DNA packaging. Strikingly, the severity of the spermatid death correlates with the amount of AAGAG satellite DNA carried by the spermatids, leading to preferential death of Y-chromosome-containing spermatids over X-containing spermatids, and hence sex-ratio meiotic drive phenotype. We propose that widespread spermatocyte transcription may reflect the process of chromatin remodeling to allow sperm DNA packaging. We further propose that differential composition and amount of satellite DNA on chromosomes may underlie naturally occurring male meiotic drive.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42034642 · DOI · PMC13320161
ESCRT-III assembles around mis-segregated DNA to protect genome stability [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Chromosome mis-segregation events that remain unresolved during cytokinesis threaten genome stability.
- Closing excerpt
- Lastly, cells expressing a DNA-binding mutant of CHMP1B exhibit cytokinesis failure and binucleation when ultrafine DNA bridges persist, revealing a mechanism of safeguarding genome stability.
- 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 (156 words)
Chromosome mis-segregation events that remain unresolved during cytokinesis threaten genome stability. Persistent ultrafine DNA bridges engage the Aurora B-dependent abscission checkpoint (termed NoCut), which delays abscission by phosphorylating components of the ESCRT complex. Here we show that NoCut surveillance repurposes human ESCRT-III, the membrane-remodeling complex that seals the reforming nuclear envelope in anaphase. In response to persistent ultrafine DNA bridges, ESCRT-III transfers from the reforming nuclear envelope to the mis-segregated DNA bridge and ESCRT-III complexes protect the DNA from damage, as evidenced by increased DNA damage upon CHMP1B depletion. Complementary in vitro assembly reactions show that the human ESCRT-III proteins CHMP1B and IST1 can copolymerize into double-stranded filaments that encase double-stranded DNA and nucleosomes and prevent nuclease digestion and cGAS recognition, demonstrating that ESCRT-III complexes can directly bind and protect DNA. Lastly, cells expressing a DNA-binding mutant of CHMP1B exhibit cytokinesis failure and binucleation when ultrafine DNA bridges persist, revealing a mechanism of safeguarding genome stability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42458110 · DOI · PMC13468122
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 Incidence of Endocrine Dysfunction Following the Use of Different Immune Checkpoint Inhibitor Regimens: A Systematic Review and Meta-analysis [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 Cyclin-dependent protein kinases and cell cycle regulation in biology and disease [7]
- Research article Telomere Length and All-Cause Mortality: A Meta-analysis [8]
- Research article Meiosis: Dances Between Homologs [9]
References
- Navarro PP, Vettiger A, Hajdu R, Ananda VY, López-Tavares A, Schmid EW, et al.. The penicillin-binding protein PBP1b fortifies the Escherichia coli division site against osmotic rupture. . 2026. PMID 42399561 · DOI · PMC13423804
- Kumon T, Nakamizo-Dojo M, Raz AA, Lannes R, Fingerhut JM, Yamashita YM. Defective transcription of AAGAG satellite DNA causes sex-ratio meiotic drive in Drosophila. . 2026. PMID 42034642 · DOI · PMC13320161
- Glover J, Talledge N, McCullough J, Alian A, Sadler JBA, Kamboj S, et al.. ESCRT-III assembles around mis-segregated DNA to protect genome stability. . 2026. PMID 42458110 · DOI · PMC13468122
- Barroso-Sousa R, Barry WT, Garrido-Castro AC, Hodi FS, Min L, Krop IE, et al.. Incidence of Endocrine Dysfunction Following the Use of Different Immune Checkpoint Inhibitor Regimens: A Systematic Review and Meta-analysis. JAMA Oncol. 2018. PMID 28973656 · DOI · PMC5838579
- 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
- Pellarin I, Dall'Acqua A, Favero A, Segatto I, Rossi V, Crestan N, et al.. Cyclin-dependent protein kinases and cell cycle regulation in biology and disease. Signal Transduct Target Ther. 2025. PMID 39800748 · DOI · PMC11734941
- Wang Q, Zhan Y, Pedersen NL, Fang F, Hägg S. Telomere Length and All-Cause Mortality: A Meta-analysis. Ageing Res Rev. 2018. PMID 30254001 · DOI
- Zickler D, Kleckner N. Meiosis: Dances Between Homologs. Annu Rev Genet. 2023. PMID 37788458 · 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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.