Research Article

Current Genetics

, Volume 41, Issue 5, pp 323-332

First online:

KNR4 is a member of the PKC1 signalling pathway and genetically interacts with BCK2, a gene involved in cell cycle progression in Saccharomyces cerevisiae

  • Helene Martin-YkenAffiliated withCentre de Bioingenierie Gilbert Durand, UMR-CNRS 5504, UR-INRA 792, 31077 Toulouse, France
  • , Adilia DagkessamanskaiaAffiliated withCentre de Bioingenierie Gilbert Durand, UMR-CNRS 5504, UR-INRA 792, 31077 Toulouse, France
  • , Driss TalibiAffiliated withEurogentec SA, Seraing, Belgium
  • , Jean FrancoisAffiliated withDépartement de Génie Biochimique et Alimentaire, INSA 135, Avenue de Rangueil, 31077 Toulouse Cedex 04, France

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Abstract.

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 bck2Δ 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.

KNR4 BCK2 MAP kinase Cell cycle