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Vol. 18, Issue 6, 2047-2056, June 2007

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Novel sfi1 Alleles Uncover Additional Functions for Sfi1p in Bipolar Spindle Assembly and Function

Victoria E. Anderson^*, John Prudden^*,, Simon Prochnik^*,, Thomas H. Giddings, Jr., and Kevin G. Hardwick^*

*Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom; and Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309

Submitted October 13, 2006; Revised March 12, 2006; Accepted March 19, 2007
Monitoring Editor: Tim Stearns

A variety of spindle and kinetochore defects have been shown to induce a mitotic delay through activation of the spindle checkpoint. With the aim of identifying novel mitotic defects we carried out a mad1 synthetic lethal screen in budding yeast. In this screen, four novel alleles of sfi1 were isolated. SFI1 is an essential gene, previously identified through its interaction with centrin/CDC31 and shown to be required for spindle pole body (SPB) duplication. The new mutations were all found in the C-terminal domain of Sfi1p, which has no known function, but it is well conserved among budding yeasts. Analysis of the novel sfi1 mutants, through a combination of light and electron microscopy, revealed duplicated SPBs <0.3 µm apart. Importantly, these SPBs have completed duplication, but they are not separated, suggesting a possible defect in splitting of the bridge. We discuss possible roles for Sfi1p in this step in bipolar spindle assembly.

Department of Energy Joint Genome Institute, 2800 Mitchell Dr., Walnut Creek, CA 94598.

Address correspondence to: Kevin G. Hardwick (kevin.hardwick{at}ed.ac.uk).

Abbreviations used: EM, electron microscopy; MAD, mitotic arrest defective; NAT, nourseothricin; SPB, spindle pole body.

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