| Successful zygote formation during yeast mating requires cell fusion of the haploid mating partners. To ensure that cells do not lyse while mating, the cell wall is degraded only after cell-cell contact and only in the region of contact. The signals that control cell wall degradation and the machinery that mediates this process are poorly understood. To understand how cell fusion is regulated, mutants defective in cell fusion were identified. Two mutants were defective in the FPS1 gene, which codes for a glycerol facilitator (Luyten et al., 1995). Additional analyses indicated that their defect results from inability to regulate osmotic balance, suggesting that cells monitor their osmotic state before committing to breaking down their cell wall. We also observed that protein kinase C, previously recognized for its role in osmotic regulation (Davenport et al., 1995), negatively regulates cell fusion, further linking osmosensing pathways to regulation of cell fusion. We propose that high intracellular osmolarity activates Pkc1p, which mediates a checkpoint that inhibits cell wall breakdown.;To identify additional genes involved in cell fusion, we looked for genes whose overexpression relieved the defect in cell fusion caused by hyperactive protein kinase C. This strategy led to the identification of two highly similar, novel genes, KEL1 and KEL2, that encode proteins composed of two domains, one containing six kelch repeats, a motif initially described in the Drosophila protein Kelch (Xue and Cooley, 1993), and the other predicted to form coiled coils. Both Kel1p and Kel2p localize to the site where cell fusion occurs during mating and to regions of polarized growth during vegetative growth. Co-immunoprecipitation and two-hybrid analyses indicate that Kel1p and Kel2p physically interact. Despite this association, only kel1... |
