Mutations in the Saccharomyces cerevisiae kinase Cbk1p lead to a fertility defect that can be suppressed by the absence of Brr1p or Mpt5p (Puf5p), proteins involved in RNA metabolism.

In Saccharomyces cerevisiae the protein kinase Cbk1p is a member of the regulation of Ace2p and cellular morphogenesis (RAM) network that is involved in cell separation after cytokinesis, cell integrity, and cell polarity. In cell separation, the RAM network promotes the daughter cell-specific localization of the transcription factor Ace2p, resulting in the asymmetric transcription of genes whose products are necessary to digest the septum joining the mother and the daughter cell. RAM and SSD1 play a role in the maintenance of cell integrity. In the presence of a wild-type SSD1 gene, deletion of any RAM component causes cell lysis. We show here that some mutations of CBK1 also lead to a reduced fertility and a reduced expression of some of the mating type-specific genes. As polarized growth is an integral part of the mating process, we have isolated suppressors of the fertility defect. Among these, mutations in BRR1 or MPT5 lead to a restoration of fertility and a more-or-less pronounced restoration of polarity; they also show genetic interactions with SSD1. Our experiments reveal a multilayered system controlling aspects of cell separation, cell integrity, mating, and polarized growth.