ArticleGenetics2019
Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast.
Article in Genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 41 citations in OpenAlex.
- In vivo anti-aging effects of naringin, a bioflavonoid: insights from the budding yeast Saccharomyces cerevisiae as a model organism.Biogerontology · 2025Article
- Fission yeast Bsd1 is required for ER stress response in Ire1 independent manner.Molecular biology reports · 2024Article
- Effects of COCurrent opinion in microbiology · 2024Review
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- Extension ofmBio · 2022Article
- Loss of tolerance to multiple environmental stresses due to limitation of structural diversity of complex sphingolipids.Molecular biology of the cell · 2022Article
- Involvement of Sec71 and Ubp2 in tunicamycin-induced ER stress response in the fission yeast.Molecular biology reports · 2022Article
- Protein kinases Elm1 and Sak1 of Saccharomyces cerevisiae exerted different functions under high-glucose and heat shock stresses.Applied microbiology and biotechnology · 2022Article
- Review
- Investigating the Antifungal Mechanism of Action of Polygodial by Phenotypic Screening inInternational journal of molecular sciences · 2021Article
- Effect of overexpression of SNF1 on the transcriptional and metabolic landscape of baker's yeast under freezing stress.Microbial cell factories · 2021Article
- Tricalbins Are Required for Non-vesicular Ceramide Transport at ER-Golgi Contacts and Modulate Lipid Droplet Biogenesis.iScience · 2020Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduced ribosome biogenesis in response to environmental conditions is a key feature of cell adaptation to stress. For example, ribosomal genes are transcriptionally repressed when cells are exposed to tunicamycin, a protein glycosylation inhibitor that induces endoplasmic reticulum stress and blocks vesicular trafficking in the secretory pathway. Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9. Target of rapamycin complex 1 (TORC1), an upstream activator of Sch9, is also required. This pathway links ribosome biogenesis to alterations in membrane lipid composition under tunicamycin-induced stress conditions. Our results suggest that sphingolipid/Pkh1/2-TORC1/Sch9 signaling is an important determinant for adaptation to tunicamycin-induced stress.
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