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

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.

Pubmed ID: 22385961

Authors

  • Hotz M
  • Leisner C
  • Chen D
  • Manatschal C
  • Wegleiter T
  • Ouellet J
  • Lindstrom D
  • Gottschling DE
  • Vogel J
  • Barral Y

Journal

Cell

Publication Data

March 2, 2012

Associated Grants

  • Agency: NIA NIH HHS, Id: AG023779
  • Agency: Canadian Institutes of Health Research, Id: MOP-64404
  • Agency: NCI NIH HHS, Id: P30 CA015704
  • Agency: NIA NIH HHS, Id: R37 AG023779

Mesh Terms

  • Cell Cycle Proteins
  • Deoxyribonucleases
  • Metaphase
  • Saccharomyces cerevisiae
  • Saccharomyces cerevisiae Proteins
  • Spindle Apparatus
  • tRNA Methyltransferases