BAIT
CDC5
MSD2, PKX2, polo kinase CDC5, L000000245, YMR001C
Polo-like kinase; controls targeting and activation of Rho1p at cell division site via Rholp guanine nucleotide exchange factors; regulates Spc72p; also functions in adaptation to DNA damage during meiosis; has similarity to Xenopus Plx1 and S. pombe Plo1p; possible Cdc28p substrate
GO Process (6)
GO Function (2)
GO Component (3)
Gene Ontology Biological Process
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
PREY
PPH3
phosphoprotein phosphatase PP4 catalytic subunit PPH3, L000001471, YDR075W
Catalytic subunit of protein phosphatase PP4 complex; Pph3p and Psy2p form active complex, Psy4p may provide substrate specificity; regulates recovery from the DNA damage checkpoint, the gene conversion- and single-strand annealing-mediated pathways of meiotic double-strand break repair and efficient Non-Homologous End-Joining (NHEJ) pathway; involved in activation of Gln3p to alleviate nitrogen catabolite repression; Pph3p and Psy2p localize to foci on meiotic chromosomes
GO Process (7)
GO Function (1)
GO Component (4)
Gene Ontology Biological Process
- double-strand break repair via homologous recombination [IGI]
- negative regulation of DNA damage checkpoint [IMP]
- negative regulation of glucose mediated signaling pathway [IMP]
- positive regulation of double-strand break repair via nonhomologous end joining [IMP]
- positive regulation of nitrogen compound metabolic process [IMP]
- protein dephosphorylation [IDA, IMP]
- signal transduction involved in meiotic recombination checkpoint [IMP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Saccharomyces cerevisiae (S288c)
Dosage Lethality
A genetic interaction is inferred when over expression or increased dosage of one gene causes lethality in a strain that is mutated or deleted for another gene.
Publication
Phosphatase 2A negatively regulates mitotic exit in Saccharomyces cerevisiae.
In budding yeast Saccharomyces cerevisiae, Cdc5 kinase is a component of mitotic exit network (MEN), which inactivates cyclin-dependent kinase (CDK) after chromosome segregation. cdc5-1 mutants arrest at telophase at the nonpermissive temperature due to the failure of CDK inactivation. To identify more negative regulators of MEN, we carried out a genetic screen for genes that are toxic to cdc5-1 mutants ... [more]
Mol. Biol. Cell Jan. 01, 2006; 17(1);80-9 [Pubmed: 16079183]
Throughput
- High Throughput
Ontology Terms
- phenotype: inviable (APO:0000112)
Curated By
- BioGRID