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J. Cell Biol.,
Volume 145, Number 7, June 28, 1999 1381-1394
Department of Microbiology and Institute for Cellular and Molecular Biology, The University of Texas, Austin, Texas
78712
The conserved Ipl1 protein kinase is essential
for proper chromosome segregation and thus cell viability in the budding yeast Saccharomyces cerevisiae.
Its human homologue has been implicated in the tumorigenesis of diverse forms of cancer. We show here that sister chromatids that have separated from each
other are not properly segregated to opposite poles of
ipl1-2 cells. Failures in chromosome segregation are often associated with abnormal distribution of the spindle
pole-associated Nuf2-GFP protein, thus suggesting a
link between potential spindle pole defects and chromosome missegregation in ipl1 mutant cells. A small
fraction of ipl1-2 cells also appears to be defective in
nuclear migration or bipolar spindle formation. Ipl1 associates, probably directly, with the novel and essential Sli15 protein in vivo, and both proteins are localized to
the mitotic spindle. Conditional sli15 mutant cells have
cytological phenotypes very similar to those of ipl1
cells, and the ipl1-2 mutation exhibits synthetic lethal
genetic interaction with sli15 mutations. sli15 mutant
phenotype, like ipl1 mutant phenotype, is partially suppressed by perturbations that reduce protein phosphatase 1 function. These genetic and biochemical studies indicate that Sli15 associates with Ipl1 to promote its
function in chromosome segregation.
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