Human BIN3 Complements the F-actin Localization Defects Caused by Loss of Hob3p, the Fission Yeast Homolog of Rvs161p

摘要: Abstract The BAR adaptor proteins encoded by theRVS167 and RVS161 genes fromSaccharomyces cerevisiae form a complex that regulates actin, endocytosis, viability following starvation or osmotic stress. In this study, we identified human homolog ofRVS161, termed BIN3 (bridgingintegrator-3), Schizosaccharomyces pombehomolog of RVS161, hob3+ (homolog Bin3). tissues, the gene was expressed ubiquitously except for brain. S. pombe cells lacking Hob3p were often multinucleate characterized increased amounts calcofluor-stained material mislocalized F-actin. For example, while wild-type localized F-actin to cell ends during interphase,hob3Δ mutants had patches distributed randomly around cell. addition, medial rings rarely found inhob3Δ mutants. Notably, in contrast rvs161Δ mutants, hob3Δ showed no measurable defects endocytosis response stress, yethob3+ complemented osmosensitivity arvs161Δ mutant. failed rescue rvs161Δ, but actin localization completely rescued byBIN3 partially RVS161. These findings suggest regulate localization, like other roles have diverged somewhat evolution.