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. 2019 Apr 15;30(9):1069–1084. doi: 10.1091/mbc.E18-06-0365

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© 2019 Sørensen, Holen, et al. “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology.

This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License.

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FIGURE 11: — SPF1 interacts functionally and genetically with SAC1 in maintaining plasma membrane sterol content. (A) Growth of the spf1/sac1 double mutant is slower than that of the single mutants. Three individual spf1/sac1 mutants were tested. Growth was recorded after 1 d at 30°C. (B) Growth of the spf1/sac1 double mutant is more sensitive to caffeine than the combined effect of the single mutants. Overexpression of SPF1 functionally complements the phenotype. (C) Growth of the spf1/sac1 double mutant is impaired compared with the single mutants when sterol synthesis is inhibited. Fenpropimorph (Fenprop.) was added at 0.0605 μg/ml. (D) Deletion of sac1 partially rescues the accumulation of PM sterols in the spf1 mutant. Nystatin was added at 1.25 μg/ml. (E) Deletion of sac1 partially rescues the accumulation of PM sterols in the spf1 mutant. Three individual spf1/sac1 mutants were tested. Mean intensities of filipin staining were quantified (box plot, two-tailed Welch t test, ****p < 0.0001).