Dominant mutant alleles of yeast protein kinase gene CDC15 suppress the lte1 defect in termination of M phase and genetically interact with CDC14.

LTE1 encodes a homolog of GDP-GTP exchange factors for the Ras superfamily and is required at low temperatures for cell cycle progression at the stage of the termination of M phase in Saccharomyces cerevisiae. We isolated extragenic suppressors which suppress the cold sensitivity of lte1 cells and confer a temperature-sensitive ...
phenotype on cells. Cells mutant for the suppressor alone were arrested at telophase at non-permissive temperatures and the terminal phenotype was almost identical to that of lte1 cells at non-permissive temperatures. Genetic analysis revealed that the suppressor is allelic to CDC15, which encodes a protein kinase. The cdc15 mutations thus isolated were recessive with regard to the temperature-sensitive phenotype and were dominant with respect to suppression of lte1. We isolated CDC14 as a low-copy-number suppressor of cdc15-rlt1. CDC14 encodes a phosphotyrosine phosphatase (PTPase) and is essential for termination of M phase. An extra copy of CDC14 suppressed the temperature sensitivity of cdc15-rlt1 cells, but not that of cdc15-1 cells. In addition, some residues that are essential for the CDC14 PTPase activity were found to be non-essential for the suppression. These results strongly indicate that Cdc14 possesses dual functions; PTPase activity is needed for one function but not for the other. We postulate that the cooperative action of Cdc14 and Cdc15 plays an essential role in the termination of M phase.
Mesh Terms:
Alleles, Amino Acid Sequence, Base Sequence, Binding Sites, Cell Cycle Proteins, DNA Primers, Fungal Proteins, GTP-Binding Proteins, Gene Expression Regulation, Fungal, Genes, Dominant, Guanine Nucleotide Exchange Factors, Mitosis, Molecular Sequence Data, Phenotype, Protein Kinases, Protein Tyrosine Phosphatases, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Sequence Homology, Amino Acid, Suppression, Genetic
Mol. Gen. Genet.
Date: May. 23, 1996
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