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Vol. 15, No. 23, pp. 3118-3129, December 1, 2001
1 Division of Basic Sciences, Fred Hutchinson Cancer
Research Center, Seattle, Washington 98109, USA;
2 Department of Physiology, University of California, San
Francisco, San Francisco, California 94143, USA
The spindle checkpoint prevents cell cycle progression in cells that
have mitotic spindle defects. Although several spindle defects activate
the spindle checkpoint, the exact nature of the primary signal is
unknown. We have found that the budding yeast member of the Aurora
protein kinase family, Ipl1p, is required to maintain a subset of
spindle checkpoint arrests. Ipl1p is required to maintain the spindle
checkpoint that is induced by overexpression of the protein kinase
Mps1. Inactivating Ipl1p allows cells overexpressing Mps1p to escape
from mitosis and segregate their chromosomes normally. Therefore, the
requirement for Ipl1p in the spindle checkpoint is not a consequence of
kinetochore and/or spindle defects. The requirement for Ipl1p
distinguishes two different activators of the spindle checkpoint: Ipl1p
function is required for the delay triggered by chromosomes whose
kinetochores are not under tension, but is not required for arrest
induced by spindle depolymerization. Ipl1p localizes at or near
kinetochores during mitosis, and we propose that Ipl1p is required to
monitor tension at the kinetochore.
[Key Words: Ipl1/Aurora protein kinase; spindle checkpoint; budding yeast; Mps1 protein kinase; kinetochores; tension]
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