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 (590 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 phase of cell nucleus division following prometaphase, in which the chromosomes line up across the equatorial plane of the spindle apparatus prior to separation.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
Related concepts
- Prometaphase
- Chromosomes
- Spindle Apparatus
Research landscape
PubMed indexes 7,609 records tagged with the MeSH heading “Metaphase” (counts retrieved 2026-10-29). 408 of them (5.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,916 records.
Reviews account for 281 records (3.7%) and meta-analyses for 2. Randomized controlled trials number 26 (0.3%) 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 | 3,916 |
| 2000-2009 | 1,946 |
| 2010-2019 | 1,339 |
| 2020 onward | 408 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 281 | 3.7% |
| Meta-analyses | 2 | 0.0% |
| Randomized controlled trials | 26 | 0.3% |
Method: PubMed query "Metaphase"[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 presence of extra chromosomes leads to genomic instability | 2016 | Research article Design not recorded in structured metadata | 265 | cc by PMID 26876972 · DOI · PMC4756715 |
| 3D-CLEM Reveals that a Major Portion of Mitotic Chromosomes Is Not Chromatin | 2016 | Research article Design not recorded in structured metadata | 110 | cc by PMID 27840028 · DOI · PMC5128728 |
| The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores | 2016 | Research article Design not recorded in structured metadata | 71 | cc by PMID 26981768 · DOI · PMC4821802 |
| A chemical-genetic system to rapidly inhibit the PP2A-B56 phosphatase reveals a role at metaphase kinetochores | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 40157924 · DOI · PMC11954910 |
The presence of extra chromosomes leads to genomic instability [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Aneuploidy is a hallmark of cancer and underlies genetic disorders characterized by severe developmental defects, yet the molecular mechanisms explaining its effects on cellular physiology remain elusive.
- Closing excerpt
- Thus, gain of chromosomes triggers replication stress, thereby promoting genomic instability and possibly contributing to tumorigenesis.
- 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)
Aneuploidy is a hallmark of cancer and underlies genetic disorders characterized by severe developmental defects, yet the molecular mechanisms explaining its effects on cellular physiology remain elusive. Here we show, using a series of human cells with defined aneuploid karyotypes, that gain of a single chromosome increases genomic instability. Next-generation sequencing and SNP-array analysis reveal accumulation of chromosomal rearrangements in aneuploids, with break point junction patterns suggestive of replication defects. Trisomic and tetrasomic cells also show increased DNA damage and sensitivity to replication stress. Strikingly, we find that aneuploidy-induced genomic instability can be explained by the reduced expression of the replicative helicase MCM2-7. Accordingly, restoring near-wild-type levels of chromatin-bound MCM helicase partly rescues the genomic instability phenotypes. Thus, gain of chromosomes triggers replication stress, thereby promoting genomic instability and possibly contributing to tumorigenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26876972 · DOI · PMC4756715
3D-CLEM Reveals that a Major Portion of Mitotic Chromosomes Is Not Chromatin [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Recent studies have revealed the importance of Ki-67 and the chromosome periphery in chromosome structure and segregation, but little is known about this elusive chromosome compartment.
- Closing excerpt
- Thus, chromatin makes up a surprisingly small percentage of the total mass of metaphase chromosomes.
- 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)
Recent studies have revealed the importance of Ki-67 and the chromosome periphery in chromosome structure and segregation, but little is known about this elusive chromosome compartment. Here we used correlative light and serial block-face scanning electron microscopy, which we term 3D-CLEM, to model the entire mitotic chromosome complement at ultra-structural resolution. Prophase chromosomes exhibit a highly irregular surface appearance with a volume smaller than metaphase chromosomes. This may be because of the absence of the periphery, which associates with chromosomes only after nucleolar disassembly later in prophase. Indeed, the nucleolar volume almost entirely accounts for the extra volume found in metaphase chromosomes. Analysis of wild-type and Ki-67-depleted chromosomes reveals that the periphery comprises 30%-47% of the entire chromosome volume and more than 33% of the protein mass of isolated mitotic chromosomes determined by quantitative proteomics. Thus, chromatin makes up a surprisingly small percentage of the total mass of metaphase chromosomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27840028 · DOI · PMC5128728
The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The spindle- and kinetochore-associated (Ska) complex is essential for normal anaphase onset in mitosis.
- Closing excerpt
- Microtubule binding by Ska, rather than acting in force production for chromosome movement, may instead serve to promote PP1 recruitment to kinetochores fully attached to spindle microtubules at metaphase.
- 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)
The spindle- and kinetochore-associated (Ska) complex is essential for normal anaphase onset in mitosis. The C-terminal domain (CTD) of Ska1 binds microtubules and was proposed to facilitate kinetochore movement on depolymerizing spindle microtubules. Here, we show that Ska complex recruits protein phosphatase 1 (PP1) to kinetochores. This recruitment requires the Ska1 CTD, which binds PP1 in vitro and in human HeLa cells. Ska1 lacking its CTD fused to a PP1-binding peptide or fused directly to PP1 rescues mitotic defects caused by Ska1 depletion. Ska1 fusion to catalytically dead PP1 mutant does not rescue and shows dominant negative effects. Thus, the Ska complex, specifically the Ska1 CTD, recruits PP1 to kinetochores to oppose spindle checkpoint signaling kinases and promote anaphase onset. Microtubule binding by Ska, rather than acting in force production for chromosome movement, may instead serve to promote PP1 recruitment to kinetochores fully attached to spindle microtubules at metaphase.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26981768 · DOI · PMC4821802
A chemical-genetic system to rapidly inhibit the PP2A-B56 phosphatase reveals a role at metaphase kinetochores [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Serine-threonine phosphatases have been challenging to study because of the lack of specific inhibitors.
- Closing excerpt
- The directSLiMs approach can be used to inhibit any other phosphatase, enzyme or protein that uses a critical SLiM-binding interface, providing a powerful strategy to inhibit and characterise proteins once considered "undruggable".
- 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 (158 words)
Serine-threonine phosphatases have been challenging to study because of the lack of specific inhibitors. Their catalytic domains are druggable, but these are shared or very similar between individual phosphatase complexes, precluding their specific inhibition. Instead, phosphatase complexes often achieve specificity by interacting with short linear motifs (SLiMs) in substrates or their binding partners. We develop here a chemical-genetic system to rapidly inhibit these interactions within the PP2A-B56 family. Drug-inducible recruitment of ectopic SLiMs ("directSLiMs") is used to rapidly block the SLiM-binding pocket on the B56 regulatory subunit, thereby displacing endogenous interactors and inhibiting PP2A-B56 activity within seconds. We use this system to characterise PP2A-B56 substrates during mitosis and to identify a role for PP2A-B56 in allowing metaphase kinetochores to properly sense tension and maintain microtubule attachments. The directSLiMs approach can be used to inhibit any other phosphatase, enzyme or protein that uses a critical SLiM-binding interface, providing a powerful strategy to inhibit and characterise proteins once considered "undruggable".
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40157924 · DOI · PMC11954910
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 Splitting the chromosome: cutting the ties that bind sister chromatids [5]
- Research article Mechanisms of Mitotic Spindle Assembly [6]
- Research article The metaphase arrest technique. A critical review [7]
- Research article Structure of the human centromere at metaphase [8]
- Research article Bookmarking genes for activation in condensed mitotic chromosomes [9]
- Research article Effects of cryopreservation on the meiotic spindle of human oocytes [10]
References
- Passerini V, Ozeri-Galai E, de Pagter MS, Donnelly N, Schmalbrock S, Kloosterman WP, et al.. The presence of extra chromosomes leads to genomic instability. . 2016. PMID 26876972 · DOI · PMC4756715
- Booth DG, Beckett AJ, Molina O, Samejima I, Masumoto H, Kouprina N, et al.. 3D-CLEM Reveals that a Major Portion of Mitotic Chromosomes Is Not Chromatin. . 2016. PMID 27840028 · DOI · PMC5128728
- Sivakumar S, Janczyk PŁ, Qu Q, Brautigam CA, Stukenberg PT, Yu H, et al.. The human SKA complex drives the metaphase-anaphase cell cycle transition by recruiting protein phosphatase 1 to kinetochores. . 2016. PMID 26981768 · DOI · PMC4821802
- Allan LA, Corno A, Valverde JM, Toth R, Ly T, Saurin AT. A chemical-genetic system to rapidly inhibit the PP2A-B56 phosphatase reveals a role at metaphase kinetochores. . 2025. PMID 40157924 · DOI · PMC11954910
- Nasmyth K, Peters JM, Uhlmann F. Splitting the chromosome: cutting the ties that bind sister chromatids. Science. 2000. PMID 10827941 · DOI
- Petry S. Mechanisms of Mitotic Spindle Assembly. Annu Rev Biochem. 2016. PMID 27145846 · DOI · PMC5016079
- Wright NA, Appleton DR. The metaphase arrest technique. A critical review. Cell Tissue Kinet. 1980. PMID 6998560 · DOI
- Pluta AF, Cooke CA, Earnshaw WC. Structure of the human centromere at metaphase. Trends Biochem Sci. 1990. PMID 2193435 · DOI
- John S, Workman JL. Bookmarking genes for activation in condensed mitotic chromosomes. Bioessays. 1998. PMID 9619097 · DOI
- Mandelbaum J, Anastasiou O, Lévy R, Guérin JF, de Larouzière V, Antoine JM. Effects of cryopreservation on the meiotic spindle of human oocytes. Eur J Obstet Gynecol Reprod Biol. 2004. PMID 15041125 · 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.