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. 2013 Mar;54(3):831–842. doi: 10.1194/jlr.M034678

Fig. 7.

Fig. 7.

The SUR4 gene interacts at the genetic level with genes encoding CORVET subunits. (A) BY4741 (wild-type), 5281 (sur4Δ), 4329 (vps3Δ), MRY121 (sur4Δ vps3Δ), 405 (vps8Δ), MRY135 (sur4Δ vps8Δ), 3774 (vps39Δ), MRY136 (sur4Δ vps39Δ), 4015 (vps41Δ), and MRY137 (sur4Δ vps41Δ) cells were grown to stationary phase, serially diluted at 1:10, spotted on YPD plates, grown for 48 h at 30°C or 36°C, and photographed against a dark background. (B) BY4741 (wild-type), 5281 (sur4Δ), MRY235 (vps8Δ vps19Δ), MRY242 (sur4Δ vps8Δ vps19Δ), MRY106 (vps19Δ), and MRY124 (sur4Δ vps19Δ) cells were grown to stationary phase, serially diluted at 1:10, spotted on YPD plates, grown for 48 h at 30°C or 36°C, and photographed against a dark background. (C) Schematic representation of the CORVET and HOPS complexes and interactions between their encoding genes and the SUR4 gene. Deletion of VPS21 or VPS3 causes severe synthetic growth defect when combined with the SUR4 deletion; these genes are illustrated as filled gray circles with thick lines. Simultaneous disruption of genes encoding the Vps21 effectors VPS8 and VPS19 also results in severe synthetic growth defect when combined with the SUR4 deletion; these genes are illustrated as white circles enclosed by thick lines. Two-headed arrows indicate protein-protein interactions between Rab GTPases and proteins involved in vesicle tethering.