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Journal of Cell Science, Vol 113, Issue 3 521-532, Copyright © 2000 by Company of Biologists
JOURNAL ARTICLES |
C Schaerer-Brodbeck and H Riezman
Biozentrum of the University of Basel, Klingelbergstrasse 70, CH-4056 Basel, Switzerland.
Analysis of the arc35-1 mutant has revealed previously that this component of the Arp2/3 complex is involved in organization of the actin cytoskeleton. Further characterization uncovered a cell division cycle phenotype with arrest as large-budded cells. Cells with correctly positioned metaphase spindles accumulated at the restrictive temperature. The observed metaphase arrest most likely occurs by activation of the spindle assembly checkpoint, because arc35-1 was synthetically lethal with a deletion of BUB2. Arc35p activity is required late in G(1) for its cell cycle function. Both the actin and microtubule defects of arc35-1 can be suppressed by overexpression of calmodulin. Analysis of a collection of ts cmd1 mutants for their ability to suppress the actin and/or microtubule defect revealed that the two defects observed in arc35-1 are genetically separable. These data suggest that the actin defect is probably not the cause of the microtubule defect.
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