ArticleScientific reports2019
Role of Atg8 in the regulation of vacuolar membrane invagination.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
- Microautophagy: current understanding of its molecular mechanisms and functions.Autophagy reports · 2026Review
- Cooperative Function of Atg8- and TORC1-Mediated Activities in Yeast.Yeast (Chichester, England) · 2025Article
- Establishment of a yeast essential protein conditional-degradation library and screening for autophagy-regulating genes.Autophagy · 2025Article
- Physicochemical properties of the vacuolar membrane and cellular factors determine formation of vacuolar invaginations.Scientific reports · 2023Article
- Article
- Evolutionary diversification of the autophagy-related ubiquitin-like conjugation systems.Autophagy · 2022Article
- The HOPS tethering complex is required to maintain signaling endosome identity and TORC1 activity.The Journal of cell biology · 2022Article
- A High-Copy Suppressor Screen Reveals a Broad Role of Prefoldin-like Bud27 in the TOR Signaling Pathway inGenes · 2022Article
- Membrane recruitment of Atg8 by Hfl1 facilitates turnover of vacuolar membrane proteins in yeast cells approaching stationary phase.BMC biology · 2021Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular heat stress can cause damage, and significant changes, to a variety of cellular structures. When exposed to chronically high temperatures, yeast cells invaginate vacuolar membranes. In this study, we found that the expression of Atg8, an essential autophagy factor, is induced after chronic heat stress. In addition, without Atg8, vacuolar invaginations are induced conspicuously, beginning earlier and invaginating vacuoles more frequently after heat stress. Our results indicate that Atg8's invagination-suppressing functions do not require Atg8 lipidation, in contrast with autophagy, which requires Atg8 lipidation. Genetic analyses of vps24 and vps23 further suggest that full ESCRT machinery is necessary to form vacuolar invaginations irrespective of Atg8. In contrast, through a combined mutation with the vacuole BAR domain protein Ivy1, vacuoles show constitutively enhanced invaginated structures. Finally, we found that the atg8Δivy1Δ mutant is sensitive against agents targeting functions of the vacuole and/or plasma membrane (cell wall). Collectively, our findings revealed that Atg8 maintains vacuolar membrane homeostasis in an autophagy-independent function by coordinating with other cellular factors.
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Registered trials
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