Evidence map›Paper›PMID 26545815›Full record

ArticleGenes & development2015

Transcription and imprinting dynamics in developing postnatal male germline stem cells.

Saher Sue Hammoud, Diana H P Low, Chongil Yi, Chee Leng Lee, Jon M Oatley, Christopher J Payne, Douglas T Carrell, Ernesto Guccione, Bradley R Cairns

Abstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Quantitative CUT&Tag for Epigenomic Profiling of Mouse Germ Cells.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  6. The Biology and Regulation of Spermatogonial Stem Cells in the Niche.Advances in experimental medicine and biology · 2025
    Review
  7. Review
  8. Epigenetic priming in the male germline.Current opinion in genetics & development · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Saher Sue HammoudHoward Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Oncological Sciences, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Human Genetics, University of Michigan, Ann Arbor, Michigan 48109, USA;
Diana H P LowDivision of Cancer Genetics and Therapeutics, Institute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology, and Research), Singapore 138673, Singapore;
Chongil YiHoward Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Oncological Sciences, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA;
Chee Leng LeeDivision of Cancer Genetics and Therapeutics, Institute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology, and Research), Singapore 138673, Singapore;
Jon M OatleyCenter for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164, USA;
Christopher J PayneDepartment of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA; Department of Obstetrics and Gynecology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA; Human Molecular Genetics Program, Ann and Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois 60614, USA;
Douglas T CarrellDepartment of Surgery (Urology), University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Obstetrics and Gynecology, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA;
Ernesto GuccioneDivision of Cancer Genetics and Therapeutics, Institute of Molecular and Cell Biology (IMCB), A*STAR (Agency for Science, Technology, and Research), Singapore 138673, Singapore; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore.
Bradley R CairnsHoward Hughes Medical Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Department of Oncological Sciences, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA;

Funding

Control Spermatogonial Stem Cell Fate Decisions by bHLH Transcription RegulatorsR01HD061665 · NICHD · WASHINGTON STATE UNIVERSITY · PI OATLEY, JON M · 2009 to 2019
$3.1M
Howard Hughes Medical InstituteNCI NIH HHS CA24014NICHD NIH HHS R01 HD061665
6 · The paper itself

Abstract

Postnatal spermatogonial stem cells (SSCs) progress through proliferative and developmental stages to populate the testicular niche prior to productive spermatogenesis. To better understand, we conducted extensive genomic profiling at multiple postnatal stages on subpopulations enriched for particular markers (THY1, KIT, OCT4, ID4, or GFRa1). Overall, our profiles suggest three broad populations of spermatogonia in juveniles: (1) epithelial-like spermatogonia (THY1(+); high OCT4, ID4, and GFRa1), (2) more abundant mesenchymal-like spermatogonia (THY1(+); moderate OCT4 and ID4; high mesenchymal markers), and (3) (in older juveniles) abundant spermatogonia committing to gametogenesis (high KIT(+)). Epithelial-like spermatogonia displayed the expected imprinting patterns, but, surprisingly, mesenchymal-like spermatogonia lacked imprinting specifically at paternally imprinted loci but fully restored imprinting prior to puberty. Furthermore, mesenchymal-like spermatogonia also displayed developmentally linked DNA demethylation at meiotic genes and also at certain monoallelic neural genes (e.g., protocadherins and olfactory receptors). We also reveal novel candidate receptor-ligand networks involving SSCs and the developing niche. Taken together, neonates/juveniles contain heterogeneous epithelial-like or mesenchymal-like spermatogonial populations, with the latter displaying extensive DNA methylation/chromatin dynamics. We speculate that this plasticity helps SSCs proliferate and migrate within the developing seminiferous tubule, with proper niche interaction and membrane attachment reverting mesenchymal-like spermatogonial subtype cells back to an epithelial-like state with normal imprinting profiles.

Indexed as

Cell DifferentiationGene Expression Regulation, DevelopmentalAdult Stem CellsAnimalsCadherinsCells, CulturedDNA MethylationEpigenomicsGametogenesisGene Expression ProfilingGenomic ImprintingMaleMiceReceptors, OdorantSignal TransductionThy-1 AntigensCadherinsReceptors, OdorantThy-1 AntigensTranscription FactorsDNA methylationgermlineimprintingmonoallelicspermatogoniastem cells

Identifiers

PMID26545815
PMCPMC4647563

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.