期刊
DEVELOPMENTAL CELL
卷 13, 期 3, 页码 433-445出版社
CELL PRESS
DOI: 10.1016/j.devcel.2007.07.003
关键词
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资金
- NIGMS NIH HHS [R01 GM064386, R01 GM064386-07] Funding Source: Medline
It is critical to elucidate the pathways that mediate spindle assembly and therefore ensure accurate chromosome segregation during cell division. Our studies of a unique allele of the budding yeast IpI1/Aurora protein kinase revealed that it is required for centrosome-mediated spindle assembly in the absence of the BimC motor protein Cin8. In addition, we found that the Ase1 spindle midzone-associated protein is required for bipolar spindle assembly. The cin8 ipl1 and cin8 ase1 double mutant cells exhibit similar defects, and Ase1 overexpression completely restores spindle assembly in cin8 ipi1 strains. Consistent with the possibility that IpI1 regulates Ase1, an ase1 mutant lacking the IpI1 consensus phosphorylation sites cannot assemble spindles in the absence of Cin8. In addition, Ase1 phosphorylation and localization were altered in an ipll mutant. We therefore propose that IpI1/Aurora and ase1 constitute a previously unidentified spindle assembly pathway that becomes essential in the absence of Cin8.
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