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Polo kinase controls cell-cycle-dependent transcription by targeting a coactivator protein

Author

Listed:
  • Zoulfia Darieva

    (University of Manchester, Michael Smith Building)

  • Richard Bulmer

    (Newcastle University)

  • Aline Pic-Taylor

    (Newcastle University
    CP 02372, Final W5 Norte)

  • Kathryn S. Doris

    (Newcastle University)

  • Marco Geymonat

    (National Institute for Medical Research, Mill Hill)

  • Steven G. Sedgwick

    (National Institute for Medical Research, Mill Hill)

  • Brian A. Morgan

    (Newcastle University)

  • Andrew D. Sharrocks

    (University of Manchester, Michael Smith Building)

Abstract

Polo kinases have crucial conserved functions in controlling the eukaryotic cell cycle through orchestrating several events during mitosis1,2. An essential element of cell cycle control is exerted by altering the expression of key regulators3. Here we show an important function for the polo kinase Cdc5p in controlling cell-cycle-dependent gene expression that is crucial for the execution of mitosis in the model eukaryote Saccharomyces cerevisiae. In particular, we find that Cdc5p is temporally recruited to promoters of the cell-cycle-regulated CLB2 gene cluster, where it targets the Mcm1p–Fkh2p–Ndd1p transcription factor complex, through direct phosphorylation of the coactivator protein Ndd1p. This phosphorylation event is required for the normal temporal expression of cell-cycle-regulated genes such as CLB2 and SWI5 in G2/M phases. Furthermore, severe defects in cell division occur in the absence of Cdc5p-mediated phosphorylation of Ndd1p. Thus, polo kinase is required for the production of key mitotic regulators, in addition to previously defined roles in controlling other mitotic events.

Suggested Citation

  • Zoulfia Darieva & Richard Bulmer & Aline Pic-Taylor & Kathryn S. Doris & Marco Geymonat & Steven G. Sedgwick & Brian A. Morgan & Andrew D. Sharrocks, 2006. "Polo kinase controls cell-cycle-dependent transcription by targeting a coactivator protein," Nature, Nature, vol. 444(7118), pages 494-498, November.
  • Handle: RePEc:nat:nature:v:444:y:2006:i:7118:d:10.1038_nature05339
    DOI: 10.1038/nature05339
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