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A role for the Pkc1p/Mpk1p kinase cascade in the morphogenesis checkpoint

Nature Cell Biology volume 3, pages 417–420 (2001)Cite this article

Abstract

In many cells the timing of entry into mitosis is controlled by the balance between the activity of inhibitory Wee1-related kinases (Swe1p in budding yeast) and the opposing effect of Cdc25-related phosphatases (Mih1p in budding yeast) that act on the cyclin-dependent kinase Cdc2 (Cdc28p in budding yeast)1. Wee1 and Cdc25 are key elements in the G2 arrest mediated by diverse checkpoint controls2. In budding yeast, a `morphogenesis checkpoint' that involves Swe1p and Mih1p delays mitotic activation of Cdc28p3. Many environmental stresses (such as shifts in temperature or osmolarity) provoke transient depolarization of the actin cytoskeleton, during which bud construction is delayed while cells adapt to environmental conditions. During this delay, the morphogenesis checkpoint halts the cell cycle in G2 phase until actin can repolarize and complete bud construction, thus preventing the generation of binucleate cells4. A similar G2 delay can be triggered by mutations or drugs that specifically impair actin organization5, indicating that it is probably actin disorganization itself, rather than specific environmental stresses, that triggers the delay. The G2 delay involves stabilization of Swe1p in response to various actin perturbations6, although this alone is insufficient to produce a long G2 delay7.

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Figure 1: Checkpoint defect in mpk1Δ cells.
Figure 2: Activation of Mpk1p in response to actin perturbation.
Figure 3: Role of components of the cell-integrity pathway in the morphogenesis checkpoint.
Figure 4: Genetic interaction of MPK1 with cell-cycle control elements.

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Acknowledgements

We thank T. Zyla for help with strain construction, S. Kornbluth for critical reading of the manuscript, and G. Ammerer, R. Ballester, B. Errede, J. Heitman, D. Levin, N. Marini, J. McCusker, J. McMillan, M. Snyder, L. Stolz, K. Irie, K. Matsumoto, D. Stuart and C. Wittenberg for strains, plasmids and oligonucleotides. We also thank J. McMillan, K. Swenson and members of the Lew laboratory for discussions. This work was supported by a grant from the US Public Health Service grant to D.J.L.

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Authors and Affiliations

  1. Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, 27710, North Carolina, USA

    Jacob C. Harrison, Elaine S.G. Bardes & Daniel J. Lew

  2. Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Hongo, Bunkyo-ku, 113-0033, Tokyo, Japan

    Yoshikazu Ohya

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  1. Jacob C. Harrison
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  2. Elaine S.G. Bardes
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  3. Yoshikazu Ohya
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  4. Daniel J. Lew
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Correspondence to Daniel J. Lew.

Supplementary information

Table 1

Yeast strains used in this study. (PDF 36 kb)

Table 2

Oligonucleotides used in this study (PDF 40 kb)

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Harrison, J., Bardes, E., Ohya, Y. et al. A role for the Pkc1p/Mpk1p kinase cascade in the morphogenesis checkpoint . Nat Cell Biol 3, 417–420 (2001). https://doi.org/10.1038/35070104

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