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Howard Hughes Medical Institute, Department of Cell Biology, Vanderbilt University, Nashville, Tennessee 37212
In a screen for second site mutations capable
of reducing the restrictive temperature of the fission
yeast mutant cdc2-D217N, we have isolated a novel
temperature-sensitive mutant, dim1-35. When shifted
to restrictive temperature, dim1-35 mutant cells arrest
before entry into mitosis or proceed through mitosis in the absence of nuclear division, demonstrating an uncoupling of proper DNA segregation from other cell
cycle events. Deletion of dim1 from the Schizosaccharomyces pombe genome produces a lethal G2 arrest
phenotype. Lethality is rescued by overexpression of the mouse dim1 homolog, mdim1. Likewise, deletion of
the Saccharomyces cerevisiae dim1 homolog, CDH1, is
lethal. Both mdim1 and dim1+ are capable of rescuing
lethality in the cdh1::HIS3 mutant. Although dim1-35
displays no striking genetic interactions with various other G2/M or mitotic mutants, dim1-35 cells incubated
at restrictive temperature arrest with low histone H1 kinase activity. Morevoer, dim1-35 displays sensitivity to
the microtubule destabilizing drug, thiabendazole
(TBZ). We conclude that Dim1p plays a fundamental, evolutionarily conserved role as a protein essential for
entry into mitosis as well as for chromosome segregation during mitosis. Based on TBZ sensitivity and failed
chromosome segregation in dim1-35, we further speculate that Dim1p may play a role in mitotic spindle formation and/or function.
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