Journal of Cell Science· 2026Q2
GPI lipid remodeling regulates lipophagy in response to glucose deprivation
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- Q2SCImago
- 2026year
Short summary
Mutants lacking GPI lipid remodeling show increased lipid droplets and impaired lipophagy reporter degradation under glucose starvation.
AI-generated from the title and abstract; the full text is not read.
Key points
- GPI lipid remodeling mutants accumulate lipid droplets and neutral lipids under glucose starvation.
- Degradation of the lipophagy reporter Faa4-GFP is reduced in these mutants.
- GPI-anchored proteins localize to vacuoles upon glucose depletion.
- Endocytosis is implicated in lipophagy, potentially supplying remodeled GPI lipids to the vacuole.
AI-generated from the title and abstract; the full text is not read.
Abstract
Lipophagy is an important microautophagic process that degrades lipid droplets (LDs) to mobilize stored lipids as an energy source during nutrient starvation. However, the molecular mechanisms regulating lipophagy in response to nutrient starvation remain poorly understood. We found that budding yeast mutants defective in glycosylphosphatidylinositol (GPI) lipid remodeling exhibited aberrant accumulation of lipid droplets (LDs), neutral lipids, and a reduced degradation of Faa4-GFP, a lipophagy reporter under glucose starvation. Furthermore, we demonstrated that glycosylphosphatidylinositol-anchored proteins (GPI-APs) localize to vacuoles in response to glucose depletion, and that a mutant defective in endocytosis has defects in lipophagy. These results imply that GPI lipid remodeling is required for lipophagy upon glucose starvation, and we propose that endocytosis functions to supply the lipid portion of GPI-APs, remodeled to C26 diacylglycerol, to the vacuolar membrane for lipophagy.
The authors' abstract, as published at the source. Journal of Cell Science, 2026 · DOI ↗
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Field: Biochemistry (Biochemistry, Genetics and Molecular Biology)
BiochemistryBiochemistry, Genetics and Molecular Biology