ArticlePLoS genetics2021
Rubicon prevents autophagic degradation of GATA4 to promote Sertoli cell function.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Beclin1 Regulates Sertoli Cell Function to Maintain Mouse Spermatogenesis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Targeting programmed cell death in male infertility: pathogenic mechanisms and therapeutic strategies.Molecular biology reports · 2026Review
- scRNA-seq reveals different cell clusters in the testes of Mongolian cattle and EGR1/FOS/JUN regulation in Sertoli cells.Scientific reports · 2026Article
- Effects of Aging on Mammalian Spermatogenesis From a Cellular Perspective.Molecular reproduction and development · 2025Review
- Nor1 and Mitophagy: An Insight into Sertoli Cell Function Regulating Spermatogenesis Using a Transgenic Rat Model.International journal of molecular sciences · 2025Article
- Interplay of Oxidative Stress, Autophagy, and Rubicon in Ovarian Follicle Dynamics: Orchestrating Ovarian Aging.Antioxidants (Basel, Switzerland) · 2025Review
- Rubicon, a Key Molecule for Oxidative Stress-Mediated DNA Damage, in Ovarian Granulosa Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Microenvironment of spermatogonial stem cells: a key factor in the regulation of spermatogenesis.Stem cell research & therapy · 2024Review
- MondoA and AKI and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2024Article
- Mutation of the Thap4 gene causes dwarfism and testicular anomalies in rats and mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Bone Marrow Mesenchymal Stem Cell-Derived Exosomes Ameliorate Aging-Induced BTB Impairment in Porcine Testes by Activating Autophagy and Inhibiting ROS/NLRP3 Inflammasomes via the AMPK/mTOR Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Rubicon can predict prognosis in patients with pancreatic ductal adenocarcinoma after neoadjuvant chemoradiotherapy.International journal of clinical oncology · 2023Article
- Loss of RUBCN/rubicon in adipocytes mediates the upregulation of autophagy to promote the fasting response.Autophagy · 2022Article
- Rubicon in Metabolic Diseases and Ageing.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
23 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy degrades unnecessary proteins or damaged organelles to maintain cellular function. Therefore, autophagy has a preventive role against various diseases including hepatic disorders, neurodegenerative diseases, and cancer. Although autophagy in germ cells or Sertoli cells is known to be required for spermatogenesis and male fertility, it remains poorly understood how autophagy participates in spermatogenesis. We found that systemic knockout mice of Rubicon, a negative regulator of autophagy, exhibited a substantial reduction in testicular weight, spermatogenesis, and male fertility, associated with upregulation of autophagy. Rubicon-null mice also had lower levels of mRNAs of Sertoli cell-related genes in testis. Importantly, Rubicon knockout in Sertoli cells, but not in germ cells, caused a defect in spermatogenesis and germline stem cell maintenance in mice, indicating a critical role of Rubicon in Sertoli cells. In mechanistic terms, genetic loss of Rubicon promoted autophagic degradation of GATA4, a transcription factor that is essential for Sertoli cell function. Furthermore, androgen antagonists caused a significant decrease in the levels of Rubicon and GATA4 in testis, accompanied by elevated autophagy. Collectively, we propose that Rubicon promotes Sertoli cell function by preventing autophagic degradation of GATA4, and that this mechanism could be regulated by androgens.
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Registered trials
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.