ArticlePLoS genetics2014
Aberrant autolysosomal regulation is linked to the induction of embryonic senescence: differential roles of Beclin 1 and p53 in vertebrate Spns1 deficiency.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Crystal structure of Bcl-2 from lymphocystis disease virus 2 in complex with the BH3 domain of zebrafish BaxA.Journal of microbiology (Seoul, Korea) · 2026Article
- Succinate supplementation ameliorates musculoskeletal defects caused by PLOD3 mutations in a BCARD syndrome model.Genome medicine · 2026Article
- SPNS1 is an essential cellular factor for EV-A71 by acting as a transporter of viral pocket factor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular basis of Spns1-mediated lysophospholipid transport from the lysosome.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Spns1-dependent endocardial lysosomal function drives valve morphogenesis through Notch1-signaling.iScience · 2024Article
- Spns1 is an iron transporter essential for megalin-dependent endocytosis.American journal of physiology. Renal physiology · 2024Article
- Autophagy-linked plasma and lysosomal membrane protein PLAC8 is a key host factor for SARS-CoV-2 entry into human cells.The EMBO journal · 2022Article
- Advancements on the Multifaceted Roles of Sphingolipids in Hematological Malignancies.International journal of molecular sciences · 2022Review
- Spns1 is a lysophospholipid transporter mediating lysosomal phospholipid salvage.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Carbofuran affects cellular autophagy and developmental senescence through the impairment of Nrf2 signalling.Journal of cellular and molecular medicine · 2022Article
- Lysosomal Function Impacts the Skeletal Muscle Extracellular Matrix.Journal of developmental biology · 2021Article
- Autophagy coordinates chondrocyte development and early joint formation in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Transgenic fluorescent zebrafish lines that have revolutionized biomedical research.Laboratory animal research · 2021Review
- Identification of autophagy-related genes signature predicts chemotherapeutic and immunotherapeutic efficiency in bladder cancer (BLCA).Journal of cellular and molecular medicine · 2021Article
- Article
- Autophagy in Drosophila and Zebrafish.Advances in experimental medicine and biology · 2021Article
- Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish.Journal of cellular and molecular medicine · 2021Article
- In-Silico Study of Immune System Associated Genes in Case of Type-2 Diabetes With Insulin Action and Resistance, and/or Obesity.Frontiers in endocrinology · 2021Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Spinster (Spin) in Drosophila or Spinster homolog 1 (Spns1) in vertebrates is a putative lysosomal H+-carbohydrate transporter, which functions at a late stage of autophagy. The Spin/Spns1 defect induces aberrant autolysosome formation that leads to embryonic senescence and accelerated aging symptoms, but little is known about the mechanisms leading to the pathogenesis in vivo. Beclin 1 and p53 are two pivotal tumor suppressors that are critically involved in the autophagic process and its regulation. Using zebrafish as a genetic model, we show that Beclin 1 suppression ameliorates Spns1 loss-mediated senescence as well as autophagic impairment, whereas unexpectedly p53 deficit exacerbates both of these characteristics. We demonstrate that 'basal p53' activity plays a certain protective role(s) against the Spns1 defect-induced senescence via suppressing autophagy, lysosomal biogenesis, and subsequent autolysosomal formation and maturation, and that p53 loss can counteract the effect of Beclin 1 suppression to rescue the Spns1 defect. By contrast, in response to DNA damage, 'activated p53' showed an apparent enhancement of the Spns1-deficient phenotype, by inducing both autophagy and apoptosis. Moreover, we found that a chemical and genetic blockage of lysosomal acidification and biogenesis mediated by the vacuolar-type H+-ATPase, as well as of subsequent autophagosome-lysosome fusion, prevents the appearance of the hallmarks caused by the Spns1 deficiency, irrespective of the basal p53 state. Thus, these results provide evidence that Spns1 operates during autophagy and senescence differentially with Beclin 1 and p53.
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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.