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Cell. 2012 Mar 2;148(5):958-72. doi: 10.1016/j.cell.2012.01.041.

Spindle pole bodies exploit the mitotic exit network in metaphase to drive their age-dependent segregation.

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1
Institute of Biochemistry, Biology Department, ETH Zurich, 8093 Zurich, Switzerland.

Abstract

Like many asymmetrically dividing cells, budding yeast segregates mitotic spindle poles nonrandomly between mother and daughter cells. During metaphase, the spindle positioning protein Kar9 accumulates asymmetrically, localizing specifically to astral microtubules emanating from the old spindle pole body (SPB) and driving its segregation to the bud. Here, we show that the SPB component Nud1/centriolin acts through the mitotic exit network (MEN) to specify asymmetric SPB inheritance. In the absence of MEN signaling, Kar9 asymmetry is unstable and its preference for the old SPB is disrupted. Consistent with this, phosphorylation of Kar9 by the MEN kinases Dbf2 and Dbf20 is not required to break Kar9 symmetry but is instead required to maintain stable association of Kar9 with the old SPB throughout metaphase. We propose that MEN signaling links Kar9 regulation to SPB identity through biasing and stabilizing the age-insensitive, cyclin-B-dependent mechanism of symmetry breaking.

PMID:
22385961
PMCID:
PMC3779431
DOI:
10.1016/j.cell.2012.01.041
[Indexed for MEDLINE]
Free PMC Article
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