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Vol. 14, Issue 2, 798-809, February 2003

Direct Evidence for a Critical Role of Myosin II in Budding Yeast Cytokinesis and the Evolvability of New Cytokinetic Mechanisms in the Absence of Myosin II

Nicola Tolliday, Maria Pitcher, and Rong Li^*

Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115

In the budding yeast Saccharomyces cerevisiae, an actomyosin-based contractile ring is present during cytokinesis, as occurs in animal cells. However, the precise requirement for this structure during budding yeast cytokinesis has been controversial. Here we show that deletion of MYO1, the single myosin II gene, is lethal in a commonly used strain background. The terminal phenotype of myo1 is interconnected chains of cells, suggestive of a cytokinesis defect. To further investigate the role of Myo1p in cytokinesis, we conditionally disrupted Myo1 function by using either a dominant negative Myo1p construct or a strain where expression of Myo1p can be shut-off. Both ways of disruption of Myo1 function result in a failure in cytokinesis. Additionally, we show that a myo1 strain previously reported to grow nearly as well as the wild type contains a single genetic suppressor that alleviates the severe cytokinesis defects of myo1. Using fluorescence time-lapse imaging and electron microscopy techniques, we show that cytokinesis in this strain is achieved through formation of multiple aberrant septa. Taken together, these results strongly suggest that the actomyosin ring is crucial for successful cytokinesis in budding yeast, but new cytokinetic mechanisms can evolve through genetic changes when myosin II function is impaired.

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Online version of this article contains video material. Online version is available at www.molbiolcell.org.

^* Corresponding author. E-mail address: rong_li{at}hms.harvard.edu.

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Molecular Biology of the Cell
Vol. 14, 798-809, February 2003
Copyright © 2003 by The American Society for Cell Biology

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