作者: William S. Korinek , Erfei Bi , J.Andrew Epp , Lisa Wang , Joyce Ho
DOI: 10.1016/S0960-9822(00)00626-6
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摘要: Abstract Cytokinesis requires the wholesale reorganization of cytoskeleton and secretion to complete division one cell into two. In budding yeast Saccharomyces cerevisiae , IQGAP-related protein Iqg1 (Cyk1) promotes cytokinetic actin ring formation is required for cytokinesis viability [1–3]. As not essential or viability, must act by another mechanism [4]. To uncover this mechanism, a screen high-copy suppressors iqg1 lethal phenotype was performed. CYK3 suppressed requirement IQG1 in without restoration ring, demonstrating that through an actomyosin-ring-independent pathway. encodes novel SH3-domain found association with mother–bud neck. cyk3 null cells had misshapen necks were deficient cytokinesis. strain, rearrangements associated appeared normal, suggesting reflects defect secretory targeting septal synthesis. Deletion either hof1 alone results mild [5–7], but deletion both genes resulted lethality block, overlapping function. Thus, Cyk3 appears be important acts potentially downstream Iqg1.