Functional interaction between the PKC1 pathway and CDC31 network of SPB duplication genes

The earliest known step in yeast spindle pole body (SPB) duplication requir es Cdc31p and Kar1p, two physically interacting SPB components, and Dsk2p a nd Rad23p, a pair of ubiquitin-like proteins. Components of the PKC1 pathwa y were found to interact with these SPB duplication genes in two independen t genetic screens. Initially, SLG1 and PKC1 were obtained as high-copy supp ressors of dsk2 Delta rad23 Delta and a mutation in MPK1 was synthetically lethal with kar1-Delta 17. Subsequently, we demonstrated extensive genetic interactions between the PKC1 pathway and tho SFB duplication mutants that affect Cdc31p function. The genetic interactions are unlikely to be related to the cell-wall integrity function of thr PKC1 pathway because the SPB mu tants did not exhibit cell-wall defects. Overexpression of multiple PKC1 pa thway components suppressed the G2/M arrest of the SPB duplication mutants and mutations in MPK1 esacerbated the cell cycle arrest of kar1-Delta 17 su ggesting a rule for the PKC1 pathway in SPB duplication. We also found that mutations in SPC110, which encodes a major SPB component, show ed genetic interactions with both CDC31 and PKC1 pathway. In support of the model that PKC1 pathway regulates SFB duplication, one of the phosphorylated forms of Spc110p was absent in pkc1 and mpk1 Delta mutants.