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 (708 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, occurring during maturation of the germ cells. Two successive cell nucleus divisions following a single chromosome duplication (S phase) result in daughter cells with half the number of chromosomes as the parent cells.
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: Meioses; M Phase, Meiotic; Meiotic M Phase; Meiotic M Phases; M Phases, Meiotic; Phase, Meiotic M; Phases, Meiotic M.
Where it fits in the MeSH classification
- Broader topics
- Cell Nucleus Division
- Narrower topics
- Anaphase; Meiotic Prophase I; Metaphase; Prometaphase; Prophase; Telophase
- See also
- Maturation-Promoting Factor
Related concepts
- Cell Nucleus
- Germ Cells
- Phase
- Chromosomes
Research landscape
PubMed indexes 32,468 records tagged with the MeSH heading “Meiosis” (counts retrieved 2026-10-29). 3,817 of them (11.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 12,795 records.
Reviews account for 2,949 records (9.1%) and meta-analyses for 9. Randomized controlled trials number 42 (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 | 12,795 |
| 2000-2009 | 8,146 |
| 2010-2019 | 7,710 |
| 2020 onward | 3,817 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,949 | 9.1% |
| Meta-analyses | 9 | 0.0% |
| Randomized controlled trials | 42 | 0.1% |
Method: PubMed query "Meiosis"[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 |
|---|---|---|---|---|
| N6-methyladenosine writer METTL16-mediated alternative splicing and translation control are essential for murine spermatogenesis | 2024 | Research article Design not recorded in structured metadata | 29 | cc by PMID 39030605 · DOI · PMC11264951 |
| Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection | 2025 | Research article Design not recorded in structured metadata | 20 | cc by PMID 40240347 · DOI · PMC12003770 |
| hnRNPC Functions with HuR to Regulate Alternative Splicing in an m6A-Dependent Manner and is Essential for Meiosis | 2025 | Research article Design not recorded in structured metadata | 20 | cc by PMID 39921484 · DOI · PMC11967818 |
| 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 |
N6-methyladenosine writer METTL16-mediated alternative splicing and translation control are essential for murine spermatogenesis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundThe mitosis-to-meiosis switch during spermatogenesis requires dynamic changes in gene expression.
- Closing excerpt
- ConclusionsOur findings support a molecular model wherein the m6A writer METTL16-mediated alternative splicing and translation efficiency regulation are required to control the mitosis-to-meiosis germ cell fate decision in mice, with implications for understanding meiosis-related male fertility disorders.
- 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 (169 words)
BackgroundThe mitosis-to-meiosis switch during spermatogenesis requires dynamic changes in gene expression. However, the regulation of meiotic transcriptional and post-transcriptional machinery during this transition remains elusive.ResultsWe report that methyltransferase-like protein 16 (METTL16), an N6-methyladenosine (m6A) writer, is required for mitosis-to-meiosis transition during spermatogenesis. Germline conditional knockout of Mettl16 in male mice impairs spermatogonial differentiation and meiosis initiation. Mechanistically, METTL16 interacts with splicing factors to regulate the alternative splicing of meiosis-related genes such as Stag3. Ribosome profiling reveals that the translation efficiency of many meiotic genes is dysregulated in METTL16-deficient testes. m6A-sequencing shows that ablation of METTL16 causes upregulation of the m6A-enriched transcripts and downregulation of the m6A-depleted transcripts, similar to Meioc and/or Ythdc2 mutants. Further in vivo and in vitro experiments demonstrate that the methyltransferase activity site (PP185-186AA) of METTL16 is necessary for spermatogenesis.ConclusionsOur findings support a molecular model wherein the m6A writer METTL16-mediated alternative splicing and translation efficiency regulation are required to control the mitosis-to-meiosis germ cell fate decision in mice, with implications for understanding meiosis-related male fertility disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39030605 · DOI · PMC11264951
Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Nucleolytic resection of DNA ends is critical for homologous recombination, but its mechanism is not fully understood, particularly in mammalian meiosis.
- Closing excerpt
- Our results elucidate MRN roles in meiotic DSB end processing and establish the importance of resection for mammalian meiosis.
- 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 (180 words)
Nucleolytic resection of DNA ends is critical for homologous recombination, but its mechanism is not fully understood, particularly in mammalian meiosis. Here we examine roles of the conserved MRN complex (MRE11, RAD50, and NBS1) through genome-wide analysis of meiotic resection during spermatogenesis in mice with various MRN mutations, including several that cause chromosomal instability in humans. Meiotic DSBs form at elevated levels but remain unresected if Mre11 is conditionally deleted, thus MRN is required for both resection initiation and regulation of DSB numbers. Resection lengths are reduced to varying degrees in MRN hypomorphs or if MRE11 nuclease activity is attenuated in a conditional nuclease-dead Mre11 model. These findings unexpectedly establish that MRN is needed for longer-range extension of resection beyond that carried out by the orthologous proteins in budding yeast meiosis. Finally, resection defects are additively worsened by combining MRN and Exo1 mutations, and mice that are unable to initiate resection or have greatly curtailed resection lengths experience catastrophic spermatogenic failure. Our results elucidate MRN roles in meiotic DSB end processing and establish the importance of resection for mammalian meiosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40240347 · DOI · PMC12003770
hnRNPC Functions with HuR to Regulate Alternative Splicing in an m6A-Dependent Manner and is Essential for Meiosis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- N6-methyladenosine (m6A) and its reader proteins are involved in pre-mRNA processing and play a variety of roles in numerous biological processes.
- Closing excerpt
- Collectively, these findings reveal hnRNPC as a critical factor for meiosis and contribute to a mechanistic understanding of the hnRNPC-HuR interaction in alternative splicing of mRNAs during germ cell development.
- 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 (169 words)
N6-methyladenosine (m6A) and its reader proteins are involved in pre-mRNA processing and play a variety of roles in numerous biological processes. However, much remains to be understood about the regulation of m6A and the function of its specific readers during meiotic processes. Here, this study shows that the potential m6A reader protein hnRNPC is essential for both male and female meiosis in mice. Germ cell-specific knockout of Hnrnpc causes meiotic arrest at pachynema in male mice. Specifically, hnRNPC-deficient males show abnormal meiosis initiation and defective meiotic progression, ultimately leading to meiotic arrest at the pachytene stage. Interestingly, hnRNPC-null females show similar meiotic defects to males. Mechanistically, this study discovers that in male germ cells, hnRNPC works with HuR to directly bind and modulate alternative splicing of meiotic-related genes (e.g., Sycp1, Brca1, and Smc5) in an m6A-dependent manner during spermatogenesis. Collectively, these findings reveal hnRNPC as a critical factor for meiosis and contribute to a mechanistic understanding of the hnRNPC-HuR interaction in alternative splicing of mRNAs during germ cell development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39921484 · DOI · PMC11967818
Cleavage of mRNAs by a minority of pachytene piRNAs improves sperm fitness [4]
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
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 Recombination, Pairing, and Synapsis of Homologs during Meiosis [5]
- Research article Meiotic Recombination: The Essence of Heredity [6]
- Research article Spermatogenesis: The Commitment to Meiosis [7]
- Research article The molecular biology of meiosis in plants [8]
- Research article Oocyte maturation: gamete-somatic cells interactions, meiotic resumption, cytoskeletal dynamics and cytoplasmic reorganization [9]
- Research article Mechanism and regulation of meiotic recombination initiation [10]
References
- Ma Q, Gui Y, Ma X, Zhang B, Xiong W, Yang S, et al.. N6-methyladenosine writer METTL16-mediated alternative splicing and translation control are essential for murine spermatogenesis. . 2024. PMID 39030605 · DOI · PMC11264951
- Kim S, Yamada S, Li T, Canasto-Chibuque C, Kim JH, Marcet-Ortega M, et al.. Mouse MRE11-RAD50-NBS1 is needed to start and extend meiotic DNA end resection. . 2025. PMID 40240347 · DOI · PMC12003770
- Xiong X, Feng S, Ma X, Liu K, Gui Y, Chen B, et al.. hnRNPC Functions with HuR to Regulate Alternative Splicing in an m6A-Dependent Manner and is Essential for Meiosis. . 2025. PMID 39921484 · DOI · PMC11967818
- 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
- Zickler D, Kleckner N. Recombination, Pairing, and Synapsis of Homologs during Meiosis. Cold Spring Harb Perspect Biol. 2015. PMID 25986558 · DOI · PMC4448610
- Hunter N. Meiotic Recombination: The Essence of Heredity. Cold Spring Harb Perspect Biol. 2015. PMID 26511629 · DOI · PMC4665078
- Griswold MD. Spermatogenesis: The Commitment to Meiosis. Physiol Rev. 2016. PMID 26537427 · DOI · PMC4698398
- Mercier R, Mézard C, Jenczewski E, Macaisne N, Grelon M. The molecular biology of meiosis in plants. Annu Rev Plant Biol. 2015. PMID 25494464 · DOI
- Coticchio G, Dal Canto M, Mignini Renzini M, Guglielmo MC, Brambillasca F, Turchi D, et al.. Oocyte maturation: gamete-somatic cells interactions, meiotic resumption, cytoskeletal dynamics and cytoplasmic reorganization. Hum Reprod Update. 2015. PMID 25744083 · DOI
- Lam I, Keeney S. Mechanism and regulation of meiotic recombination initiation. Cold Spring Harb Perspect Biol. 2014. PMID 25324213 · DOI · PMC4292169
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.