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 (668 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
Euploid male germ cells of an early stage of spermatogenesis, derived from prespermatogonia. With the onset of puberty, spermatogonia at the basement membrane of the seminiferous tubule proliferate by mitotic then meiotic divisions and give rise to the haploid spermatocytes.
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: Spermatogonias; Spermatophores; Spermatophore.
Where it fits in the MeSH classification
- Broader topics
- Spermatozoa
Related concepts
Research landscape
PubMed indexes 5,053 records tagged with the MeSH heading “Spermatogonia” (counts retrieved 2026-10-31). 999 of them (19.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,569 records.
Reviews account for 378 records (7.5%) and meta-analyses for 3. Randomized controlled trials number 6 (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 | 1,461 |
| 2000-2009 | 1,024 |
| 2010-2019 | 1,569 |
| 2020 onward | 999 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 378 | 7.5% |
| Meta-analyses | 3 | 0.1% |
| Randomized controlled trials | 6 | 0.1% |
Method: PubMed query "Spermatogonia"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 adult human testis transcriptional cell atlas | 2018 | Research article Design not recorded in structured metadata | 572 | cc by PMID 30315278 · DOI · PMC6274646 |
| The Dynamic Transcriptional Cell Atlas of Testis Development during Human Puberty | 2020 | Research article Design not recorded in structured metadata | 260 | cc by PMID 31928944 · DOI · PMC7298616 |
| DMRT1 Is Required for Mouse Spermatogonial Stem Cell Maintenance and Replenishment | 2016 | Research article Design not recorded in structured metadata | 109 | cc by PMID 27583450 · DOI · PMC5008761 |
| ZBTB16/PLZF regulates juvenile spermatogonial stem cell development through an extensive transcription factor poising network | 2025 | Research article Design not recorded in structured metadata | 23 | cc by PMID 40033150 · DOI · PMC12263333 |
The adult human testis transcriptional cell atlas [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Human adult spermatogenesis balances spermatogonial stem cell (SSC) self-renewal and differentiation, alongside complex germ cell-niche interactions, to ensure long-term fertility and faithful genome propagation.
- Closing excerpt
- Overall, our datasets describe key transcriptional and epigenetic signatures of the normal adult human testis, and provide new insights into germ cell developmental transitions and plasticity.
- 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)
Human adult spermatogenesis balances spermatogonial stem cell (SSC) self-renewal and differentiation, alongside complex germ cell-niche interactions, to ensure long-term fertility and faithful genome propagation. Here, we performed single-cell RNA sequencing of ~6500 testicular cells from young adults. We found five niche/somatic cell types (Leydig, myoid, Sertoli, endothelial, macrophage), and observed germline-niche interactions and key human-mouse differences. Spermatogenesis, including meiosis, was reconstructed computationally, revealing sequential coding, non-coding, and repeat-element transcriptional signatures. Interestingly, we identified five discrete transcriptional/developmental spermatogonial states, including a novel early SSC state, termed State 0. Epigenetic features and nascent transcription analyses suggested developmental plasticity within spermatogonial States. To understand the origin of State 0, we profiled testicular cells from infants, and identified distinct similarities between adult State 0 and infant SSCs. Overall, our datasets describe key transcriptional and epigenetic signatures of the normal adult human testis, and provide new insights into germ cell developmental transitions and plasticity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30315278 · DOI · PMC6274646
The Dynamic Transcriptional Cell Atlas of Testis Development during Human Puberty [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The human testis undergoes dramatic developmental and structural changes during puberty, including proliferation and maturation of somatic niche cells, and the onset of spermatogenesis.
- Closing excerpt
- Taken together, our transcriptional atlas of the developing human testis provides multiple insights into developmental changes and key factors accompanying male puberty.
- 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 (154 words)
The human testis undergoes dramatic developmental and structural changes during puberty, including proliferation and maturation of somatic niche cells, and the onset of spermatogenesis. To characterize this understudied process, we profiled and analyzed single-cell transcriptomes of ∼10,000 testicular cells from four boys spanning puberty and compared them to those of infants and adults. During puberty, undifferentiated spermatogonia sequentially expand and differentiate prior to the initiation of gametogenesis. Notably, we identify a common pre-pubertal progenitor for Leydig and myoid cells and delineate candidate factors controlling pubertal differentiation. Furthermore, pre-pubertal Sertoli cells exhibit two distinct transcriptional states differing in metabolic profiles before converging to an alternative single mature population during puberty. Roles for testosterone in Sertoli cell maturation, antimicrobial peptide secretion, and spermatogonial differentiation are further highlighted through single-cell analysis of testosterone-suppressed transfemale testes. Taken together, our transcriptional atlas of the developing human testis provides multiple insights into developmental changes and key factors accompanying male puberty.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31928944 · DOI · PMC7298616
DMRT1 Is Required for Mouse Spermatogonial Stem Cell Maintenance and Replenishment [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Male mammals produce sperm for most of postnatal life and therefore require a robust germ line stem cell system, with precise balance between self-renewal and differentiation.
- Closing excerpt
- Our data therefore reveal that Dmrt1 supports SSC maintenance in two ways: allowing SSCs to remain in the stem cell pool under normal conditions; and enabling progenitor cells to help restore the stem cell pool after germ cell depletion.
- 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 (182 words)
Male mammals produce sperm for most of postnatal life and therefore require a robust germ line stem cell system, with precise balance between self-renewal and differentiation. Prior work established doublesex- and mab-3-related transcription factor 1 (Dmrt1) as a conserved transcriptional regulator of male sexual differentiation. Here we investigate the role of Dmrt1 in mouse spermatogonial stem cell (SSC) homeostasis. We find that Dmrt1 maintains SSCs during steady state spermatogenesis, where it regulates expression of Plzf, another transcription factor required for SSC maintenance. We also find that Dmrt1 is required for recovery of spermatogenesis after germ cell depletion. Committed progenitor cells expressing Ngn3 normally do not contribute to SSCs marked by the Id4-Gfp transgene, but do so when spermatogonia are chemically depleted using busulfan. Removal of Dmrt1 from Ngn3-positive germ cells blocks the replenishment of Id4-GFP-positive SSCs and recovery of spermatogenesis after busulfan treatment. Our data therefore reveal that Dmrt1 supports SSC maintenance in two ways: allowing SSCs to remain in the stem cell pool under normal conditions; and enabling progenitor cells to help restore the stem cell pool after germ cell depletion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27583450 · DOI · PMC5008761
ZBTB16/PLZF regulates juvenile spermatogonial stem cell development through an extensive transcription factor poising network [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Spermatogonial stem cells balance self-renewal with differentiation and spermatogenesis to ensure continuous sperm production.
- Closing excerpt
- Overall, ZBTB16 promotes uSPG cell-cycle progression and colocalizes with SALL4, SOX3, CTCF and RNAPol2 to help establish an extensive and interactive chromatin poising network.
- 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 (183 words)
Spermatogonial stem cells balance self-renewal with differentiation and spermatogenesis to ensure continuous sperm production. Here, we identify roles for the transcription factor zinc finger and BTB domain-containing protein 16 (ZBTB16; also known as promyelocytic leukemia zinc finger (PLZF)) in juvenile mouse undifferentiated spermatogonia (uSPG) in promoting self-renewal and cell-cycle progression to maintain uSPG and transit-amplifying states. Notably, ZBTB16, Spalt-like transcription factor 4 (SALL4) and SRY-box transcription factor 3 (SOX3) colocalize at over 12,000 promoters regulating uSPG and meiosis. These regions largely share broad histone 3 methylation and acetylation (H3K4me3 and H3K27ac), DNA hypomethylation, RNA polymerase II (RNAPol2) and often CCCTC-binding factor (CTCF). Hi-C analyses show robust three-dimensional physical interactions among these cobound promoters, suggesting the existence of a transcription factor and higher-order active chromatin interaction network within uSPG that poises meiotic promoters for subsequent activation. Conversely, these factors do not notably occupy germline-specific promoters driving spermiogenesis, which instead lack promoter-promoter physical interactions and bear DNA hypermethylation, even when active. Overall, ZBTB16 promotes uSPG cell-cycle progression and colocalizes with SALL4, SOX3, CTCF and RNAPol2 to help establish an extensive and interactive chromatin poising network.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40033150 · DOI · PMC12263333
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 Regulation of spermatogonial stem cell self-renewal in mammals [5]
- Research article All you wanted to know about spermatogonia but were afraid to ask [6]
- Research article Proliferation and differentiation of spermatogonial stem cells [7]
- Research article Spermatogonial stem cell regulation and spermatogenesis [8]
- Research article Germline stem cell transplantation and transgenesis [9]
- Research article Paternal age effect mutations and selfish spermatogonial selection: causes and consequences for human disease [10]
References
- Guo J, Grow EJ, Mlcochova H, Maher GJ, Lindskog C, Nie X, et al.. The adult human testis transcriptional cell atlas. . 2018. PMID 30315278 · DOI · PMC6274646
- Guo J, Nie X, Giebler M, Mlcochova H, Wang Y, Grow EJ, et al.. The Dynamic Transcriptional Cell Atlas of Testis Development during Human Puberty. . 2020. PMID 31928944 · DOI · PMC7298616
- Zhang T, Oatley J, Bardwell VJ, Zarkower D. DMRT1 Is Required for Mouse Spermatogonial Stem Cell Maintenance and Replenishment. . 2016. PMID 27583450 · DOI · PMC5008761
- Yi C, Kitamura Y, Maezawa S, Namekawa SH, Cairns BR. ZBTB16/PLZF regulates juvenile spermatogonial stem cell development through an extensive transcription factor poising network. . 2025. PMID 40033150 · DOI · PMC12263333
- Oatley JM, Brinster RL. Regulation of spermatogonial stem cell self-renewal in mammals. Annu Rev Cell Dev Biol. 2008. PMID 18588486 · DOI · PMC4066667
- de Rooij DG, Russell LD. All you wanted to know about spermatogonia but were afraid to ask. J Androl. 2000. PMID 11105904
- de Rooij DG. Proliferation and differentiation of spermatogonial stem cells. Reproduction. 2001. PMID 11226060 · DOI
- Phillips BT, Gassei K, Orwig KE. Spermatogonial stem cell regulation and spermatogenesis. Philos Trans R Soc Lond B Biol Sci. 2010. PMID 20403877 · DOI · PMC2871929
- Brinster RL. Germline stem cell transplantation and transgenesis. Science. 2002. PMID 12077400 · DOI · PMC4881847
- Goriely A, Wilkie AO. Paternal age effect mutations and selfish spermatogonial selection: causes and consequences for human disease. Am J Hum Genet. 2012. PMID 22325359 · DOI · PMC3276674
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 2026-10-31.
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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.