Related Experiment Video

Updated: Nov 4, 2025

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
08:05

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast

Published on: September 26, 2025

213

Yeast Fin1-PP1 dephosphorylates an Ipl1 substrate, Ndc80, to remove Bub1-Bub3 checkpoint proteins from the

Michael Bokros1,2, Delaney Sherwin1, Marie-Helene Kabbaj1

  • 1Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, Florida, United States of America.

Plos Genetics
|May 25, 2021
PubMed

Insights

The spindle assembly checkpoint (SAC) ensures accurate chromosome segregation. Fin1-protein phosphatase 1 (PP1) at kinetochores removes SAC proteins, preventing errors during cell division.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The spindle assembly checkpoint (SAC) is crucial for preventing anaphase onset until all chromosomes are correctly attached.
  • Cdc14 phosphatase activation after anaphase onset initiates mitotic exit by dephosphorylating cyclin-dependent kinase substrates.

Purpose of the Study:

  • To investigate the role of Fin1-protein phosphatase 1 (PP1) in regulating SAC protein removal from kinetochores during anaphase.
  • To understand how Fin1-PP1 activity influences the localization and function of SAC components like Bub1, Bub3, and Mad1.
  • To elucidate the mechanism by which Fin1-PP1 dephosphorylates Ndc80 and its impact on SAC regulation and cell viability.

Main Methods:

  • Budding yeast (Saccharomyces cerevisiae) as a model organism.
  • Biochemical assays to study protein dephosphorylation and localization.
  • Genetic manipulation to assess the effects of altered protein function on cell viability and chromosome segregation.

Main Results:

  • Fin1-PP1 promotes the kinetochore removal of Bub3, in addition to Bub1, but not Mad1.
  • Kinetochore localization of Bub1-Bub3 during anaphase depends on Aurora B/Ipl1 kinase activity.
  • Fin1-PP1 facilitates Ndc80 dephosphorylation, reducing Bub1-Bub3 kinetochore association.
  • Premature Ndc80 dephosphorylation leads to viability loss under tensionless chromosome attachment conditions.

Conclusions:

  • Timely kinetochore localization of Fin1-PP1 is essential for regulating the functional window of the SAC.
  • This regulation is critical for ensuring faithful chromosome segregation and preventing aneuploidy.
  • The Fin1-PP1/Ndc80/Bub1-Bub3 axis represents a key mechanism for SAC silencing and timely anaphase progression.

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