ArticlePLoS genetics2013
The Wilms tumor gene, Wt1, is critical for mouse spermatogenesis via regulation of sertoli cell polarity and is associated with non-obstructive azoospermia in humans.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 137 citations in OpenAlex.
- Long-term culture and significant expansion of human Sertoli cells whilst maintaining stable global phenotype and AKT and SMAD1/5 activation.Cell communication and signaling : CCS · 2015Trial
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- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- WT1 pathogenic variant in azoospermic infertile men with an isolated undescended testis.Clinical and experimental reproductive medicine · 2025Article
- Single-cell RNA sequencing uncovers abnormal Sertoli-cell elevation and testicular niche impairment in the transfemales's testis.Cell & bioscience · 2025Article
- Establishment, identification, and transcriptome analysis of a Sertoli cell line from ovoviviparous black rockfish Sebastes schlegelii.Fish physiology and biochemistry · 2025Article
- Inactivation of JNK signalling results in polarity loss and cell senescence of Sertoli cell.Cell proliferation · 2025Article
- Sertoli cells as a hub in testicular development and male reproductive.Frontiers in cell and developmental biology · 2025Review
- A Study ofGenes · 2024Article
- Microenvironment of spermatogonial stem cells: a key factor in the regulation of spermatogenesis.Stem cell research & therapy · 2024Review
- Blood-testis barrier: a review on regulators in maintaining cell junction integrity between Sertoli cells.Cell and tissue research · 2024Review
- A Comparative Analysis of Orexins in the Physio-Pathological Processes of the Male Genital Tract: New Challenges? A Review.Veterinary sciences · 2024Review
- Multigenerational paternal obesity enhances the susceptibility to male subfertility in offspring via Wt1 N6-methyladenosine modification.Nature communications · 2024Article
- Inhibition ofCells · 2024Article
- Characterization of Two Gonadal Genes, zar1 and wt1b, in Hermaphroditic Fish Asian Seabass (Animals : an open access journal from MDPI · 2024Article
- Unveiling the roles of Sertoli cells lineage differentiation in reproductive development and disorders: a review.Frontiers in endocrinology · 2024Review
- Non-invasive biomarkers for sperm retrieval in non-obstructive patients: a comprehensive review.Frontiers in endocrinology · 2024Review
- High cholesterol diet-induced testicular dysfunction in rats.Hormones (Athens, Greece) · 2023Article
- Article
- Analysis of Notch1 signaling in mammalian sperm development.BMC research notes · 2023Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 9 institutions in 2 countries.
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Abstract
Azoospermia is one of the major reproductive disorders which cause male infertility in humans; however, the etiology of this disease is largely unknown. In the present study, six missense mutations of WT1 gene were detected in 529 human patients with non-obstructive azoospermia (NOA), indicating a strong association between WT1 mutation and NOA. The Wilms tumor gene, Wt1, is specifically expressed in Sertoli cells (SCs) which support spermatogenesis. To examine the functions of this gene in spermatogenesis, Wt1 was deleted in adult testis using Wt1(flox) and Cre-ER(TM) mice strains. We found that inactivation of Wt1 resulted in massive germ cell death and only SCs were present in most of the seminiferous tubules which was very similar to NOA in humans. In investigating the potential mechanism for this, histological studies revealed that the blood-testis barrier (BTB) was disrupted in Wt1 deficient testes. In vitro studies demonstrated that Wt1 was essential for cell polarity maintenance in SCs. Further studies found that the expression of cell polarity associated genes (Par6b and E-cadherin) and Wnt signaling genes (Wnt4, Wnt11) were downregulated in Wt1 deficient SCs, and that the expression of Par6b and E-cadherin was regulated by Wnt4. Our findings suggest that Wt1 is important in spermatogenesis by regulating the polarity of SCs via Wnt signaling pathway and that WT1 mutation is one of the genetic causes of NOA in humans.
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