ArticleCell death & disease2014
The histone methyltransferase ESET is required for the survival of spermatogonial stem/progenitor cells in mice.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Molecular mechanisms and translational implications in apoptosis, ferroptosis, pyroptosis, and cuproptosis of spermatogonial stem cells.Cellular and molecular life sciences : CMLS · 2026Review
- PRMT5 inhibition promotes cross-species spermatogonia expansion and suppresses differentiation.Cell regeneration (London, England) · 2026Article
- Epigenetic regulation by DNA methylation, histone modifications and chromatin remodeling complexes in controlling spermatogenesis and their dysfunction with male infertility.Cellular and molecular life sciences : CMLS · 2025Review
- A convenient research strategy for functional verification of epigenetic regulators during spermatogenesis.Asian journal of andrology · 2025Article
- Abnormal H3K27me3 underlies degenerative spermatogonial stem cells in cryptorchid testis.Development (Cambridge, England) · 2025Article
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- The cytoplasmic fraction of the histone lysine methyltransferase Setdb1 is essential for embryonic stem cells.iScience · 2023Article
- Transcriptome-wide Dynamics of mGenomics, proteomics & bioinformatics · 2023Article
- Review
- Multi-Omics Approaches for Revealing the Epigenetic Regulation of Histone H3.1 during Spermatogonial Stem Cell Differentiation In Vitro.International journal of molecular sciences · 2023Article
- METTL21A, a Non-Histone Methyltransferase, Is Dispensable for Spermatogenesis and Male Fertility in Mice.International journal of molecular sciences · 2022Article
- Article
- Identifying regulators of parental imprinting by CRISPR/Cas9 screening in haploid human embryonic stem cells.Nature communications · 2021Article
- Mitochondrial Dynamics Markers and Related Signaling Molecules Are Important Regulators of Spermatozoa Number and Functionality.International journal of molecular sciences · 2021Article
- Epigenetic Regulation of Spermatogonial Stem Cell Homeostasis: From DNA Methylation to Histone Modification.Stem cell reviews and reports · 2021Review
- SETDB1-Mediated Silencing of Retroelements.Viruses · 2020Review
- Histone Post-Translational Modifications and CircRNAs in Mouse and Human Spermatozoa: Potential Epigenetic Marks to Assess Human Sperm Quality.Journal of clinical medicine · 2020Review
- The Histone Methyltransferase SETDB1 Modulates Survival of Spermatogonial Stem/Progenitor Cells Through NADPH Oxidase.Frontiers in genetics · 2020Article
- Distinct H3K9me3 and DNA methylation modifications during mouse spermatogenesis.The Journal of biological chemistry · 2019Article
- SETDB1 Links the Meiotic DNA Damage Response to Sex Chromosome Silencing in Mice.Developmental cell · 2018Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Self-renewal and differentiation of spermatogonial stem cells (SSCs) are the foundation of spermatogenesis throughout a male's life. SSC transplantation will be a valuable solution for young male patients to preserve their fertility. As SSCs in the collected testis tissue from the patients are very limited, it is necessary to expansion the SSCs in vitro. Previous studies suggested that histone methyltransferase ERG-associated protein with SET domain (ESET) represses gene expression and is essential for the maintenance of the pool of embryonic stem cells and neurons. The objective of this study was to determine the role of ESET in SSCs using in vitro cell culture and germ cell transplantation. Cell transplantation assay showed that knockdown of ESET reduced the number of seminiferous tubules with spermatogenesis when compared with that of the control. Knockdown of ESET also upregulated the expression of apoptosis-associated genes (such as P53, Caspase9, Apaf1), whereas inhibited the expression of apoptosis-suppressing genes (such as Bcl2l1, X-linked inhibitor of apoptosis protein). In addition, suppression of ESET led to increase in expression of Caspase9 and activation of Caspase3 (P17) as well as cleavage of poly (ADP-ribose) polymerase. Among the five ESET-targeting genes (Cox4i2, spermatogenesis and oogenesis Specific Basic Helix-Loop-Helix 2, Nobox, Foxn1 and Dazl) examined by ChIP assay, Cox4i2 was found to regulate SSC apoptosis by the rescue experiment. BSP analyses further showed that DNA methylation in the promoter loci of Cox4i2 was influenced by ESET, indicating that ESET also regulated gene expression through DNA methylation in addition to histone methylation. In conclusion, we found that ESET regulated SSC apoptosis by suppressing of Cox4i2 expression through histone H3 lysine 9 tri-methylation and DNA methylation. The results obtained will provide unique insights that would broaden the research on SSC biology and contribute to the treatment of male infertility.
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