In budding yeast, PKC1 plays an essential role in cell wall integrity and cell proliferation through a bifurcated PKC1/mitogen-activated protein (MAP) kinase pathway. The evidence that KNR4 is a member of the PKC1 pathway and genetically interacts with BCK2, a gene involved together with Cln3-Cdc28 in the G1 to S transition phase of the cell cycle, was as follows. Both KNR4 and BCK2 were isolated as a dosage suppressor of a calcofluor white hypersensitive ( cwh43) mutant. Overexpression of either of the two genes in a wild-type strain led to increased resistance to wall-affecting drugs, while this effect was not obtained in a bck2Delta mutant that overexpressed KNR4. Deletion of KNR4 or BCK2 was synthetically lethal with components of the linear PKC1/MAP kinase pathway. Loss of Knr4 was lethal in combination with loss of Cln3, as was shown for Bck2. A protein interaction between Knr4 and Bck2 was measured using the two-hybrid system, although a direct physical interaction could not be detected by co-immunuprecipation methods. Finally, a genome-wide analysis of cells that overexpress BCK2 or KNR4 indicated that both genes also have effects independent of each other. In particular, the microarray data showed up-regulation of SWI4, which may account for the suppression of the cell lysis of a pkc1 null mutant, due to overexpression of BCK2.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Reference||Annotation Extension|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|