Abstract
Mitotic exit and cytokinesis must be tightly coupled to nuclear division both in time and space in order to preserve genome stability and to ensure that daughter cells inherit the right set of chromosomes after cell division. This is achieved in budding yeast through control over a signal transduction cascade, the mitotic exit network (MEN), which is required for mitotic CDK inactivation in telophase and for cytokinesis. Current models of MEN activation emphasize on the bud as the place where most control is exerted. This review focuses on recent data that instead point to the mother cell as being the residence of key regulators of late mitotic events.
Highlights
In polarized cells alignment of the mitotic spindle respective to the polarity axis is crucial for maintaining the correct ploidy from one generation to the
When the spindle is mispositioned (Fig. 2, left side) Tem1 is kept inactive in the mother cell by Bub2/Bfa1 being localized on both spindle pole bodies (SPBs) and by the lack of exposure to Lte1 present in the bud
Transit of one SPB through the bud neck during proper anaphase (Fig. 2, right side) triggers the disappearance of Bub2/Bfa1 from the mother cell SPB through a mechanism involving Bub2 GTPaseactivating proteins (GAPs) activity and kinases localized at the bud neck with the septin ring
Summary
In polarized cells alignment of the mitotic spindle respective to the polarity axis is crucial for maintaining the correct ploidy from one generation to the next. The myc-tagged Bub form described above and devoid of GAP activity persists on both SPBs throughout the cell cycle along with Bfa and Tem, and prevents mitotic exit in a dominant fashion in cells expressing partially crippled Tem, Cdc or Nud1 This suggests that disappearance of Bub2/Bfa from the mother-bound SPB contributes to timely mitotic exit [18]. Perturbing the integrity of the septin ring can either lead to a lethal mitotic exit defect when the MEN is impaired, or cause improper mitotic exit in mutants defective for spindle positioning While the former is in agreement with the septin ring function in allowing the release of Bub2/Bfa from the mother-bound SPB [18], the latter is Lte1dependent and correlates with Lte spreading into the mother cell cytoplasm [39]. It will be interesting in the future to investigate whether and how Dma and Kin regulate each other
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