Abstract
The seven yeast OSH genes (OSH1-OSH7) encode a family of orthologs of the mammalian oxysterol-binding protein (OSBP). The OSH genes share at least one essential overlapping function, potentially linked to the regulation of secretory trafficking and membrane lipid composition. To investigate the essential roles of the OSH genes, we constructed conditional OSH mutants and analyzed their cellular defects. Elimination of all OSH function altered intracellular sterol-lipid distribution, caused vacuolar fragmentation, and resulted in an accumulation of lipid droplets in the cytoplasm and within vacuolar fragments. Gradual depletion of Osh proteins also caused cell budding defects and abnormal cell wall deposition. In OSH mutant cells endocytosis was severely impaired, but protein transport to the vacuole and the plasma membrane was largely unaffected. Other mutants affecting sterol-lipid function and distribution, namely erg2Delta and arv1Delta, shared similar defects. These findings suggested that OSH genes, through effects on intracellular sterol distribution, establish a plasma membrane lipid composition that promotes endocytosis.
Highlights
Sterol lipids, such as cholesterol and the fungal sterol ergosterol, are essential for plasma membrane integrity and structure
We found that endocytosis was disrupted in OSH mutants and in other previously described mutants that perturb ergosterol distribution within cells
Deletion of all seven yeast OSH genes causes lethality. This inviability can be rescued by expression of any of the individual OSH genes indicating that the OSH genes share at least one essential overlapping function (Beh et al, 2001)
Summary
Sterol lipids, such as cholesterol and the fungal sterol ergosterol, are essential for plasma membrane integrity and structure. Changes in sterol levels and composition have extensive effects on membrane function. Perturbations in cellular ergosterol and sterol lipid levels affect yeast cell fusion during mating (Gaber et al, 1989; Tomeo et al, 1992), vacuolar homotypic membrane fusion (Kato and Wickner, 2001), and secretory transport to the cell surface (Hardwick and Pelham, 1994; Bagnat et al, 2000). Cholesterol is delivered to the plasma membrane by at least two different transport pathways. Pathways for recycling internalized sterols back to the plasma membrane after endocytosis are poorly understood
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