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A Novel Role for the GTPase-Activating Protein Bud2 in the Spindle Position Checkpoint

Authors
Journal
PLoS ONE
1932-6203
Publisher
Public Library of Science
Publication Date
Volume
7
Issue
4
Identifiers
DOI: 10.1371/journal.pone.0036127
Keywords
  • Research Article
  • Biology
  • Model Organisms
  • Yeast And Fungal Models
  • Saccharomyces Cerevisiae
  • Molecular Cell Biology
  • Cell Division
  • Mitosis
  • Cellular Structures
  • Cytoskeleton
  • Chromosome Biology
  • Signal Transduction
  • Signaling In Cellular Processes
  • Gtpase Signaling
  • Signaling Cascades
Disciplines
  • Biology

Abstract

The spindle position checkpoint (SPC) ensures correct mitotic spindle position before allowing mitotic exit in the budding yeast Saccharomyces cerevisiae. In a candidate screen for checkpoint genes, we identified bud2Δ as deficient for the SPC. Bud2 is a GTPase activating protein (GAP), and the only known substrate of Bud2 was Rsr1/Bud1, a Ras-like GTPase and a central component of the bud-site-selection pathway. Mutants lacking Rsr1/Bud1 had no checkpoint defect, as did strains lacking and overexpressing Bud5, a guanine-nucleotide exchange factor (GEF) for Rsr1/Bud1. Thus, the checkpoint function of Bud2 is distinct from its role in bud site selection. The catalytic activity of the Bud2 GAP domain was required for the checkpoint, based on the failure of the known catalytic point mutant Bud2R682A to function in the checkpoint. Based on assays of heterozygous diploids, bud2R682A, was dominant for loss of checkpoint but recessive for bud-site-selection failure, further indicating a separation of function. Tem1 is a Ras-like protein and is the critical regulator of mitotic exit, sitting atop the mitotic exit network (MEN). Tem1 is a likely target for Bud2, supported by genetic analyses that exclude other Ras-like proteins.

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