Related Experiment Video

Updated: Oct 11, 2026

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
08:13

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

Published on: September 26, 2025

Saccharomyces cerevisiae cdc42p GTPase is involved in preventing the recurrence of bud emergence during the cell

T J Richman1, D I Johnson

  • 1Department of Microbiology and Molecular Genetics and Markey Center for Molecular Genetics, University of Vermont Burlington, Vermont 05405, USA.

Molecular and Cellular Biology
|October 25, 2000
PubMed

Insights

Mutations in Saccharomyces cerevisiae Cdc42p

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The Saccharomyces cerevisiae Cdc42p GTPase is crucial for cell polarity and morphogenesis.
  • It interacts with regulators and effectors via an effector domain.

Purpose of the Study:

  • To investigate the functional impact of specific Cdc42p effector domain mutations.
  • To characterize how these mutations affect protein interactions and cellular processes.

Main Methods:

  • Site-directed mutagenesis to create four Cdc42p effector domain mutants (Y32K, F37A, D38E, Y40C).
  • Analysis of mutant protein interactions with downstream effectors and regulators.
  • Complementation studies using a Deltacdc42 null mutant.
  • Phenotypic analysis including bud morphology, septin ring localization, and morphogenetic checkpoint activation.

Main Results:

  • Each mutant exhibited differential interaction profiles and varying functionality.
  • Cdc42(D38E)p showed reduced interactions with Cla4p and Bem3p.
  • Cdc42(D38E)p complemented the null mutant but displayed partial functionality, including a temperature-dependent multibudded phenotype.
  • Defects in septin ring localization and Swe1p-dependent morphogenetic checkpoint activation were observed in Cdc42(D38E)p.
  • Analysis revealed sequential bud emergence with premature growth termination and single-bud localization of key proteins.

Conclusions:

  • Cdc42p plays a role in preventing the initiation of supernumerary buds during the cell cycle.
  • The Cdc42(D38E)p mutation leads to a post-bud emergence morphogenetic defect, causing growth cessation and machinery reorganization.
  • This suggests Cdc42p's involvement in regulating bud site selection and growth progression.

More Related Videos

Efficient Sporulation of Saccharomyces cerevisiae in a 96 Multiwell Format08:54

Efficient Sporulation of Saccharomyces cerevisiae in a 96 Multiwell Format

Published on: September 17, 2016

Assay for Adhesion and Agar Invasion in S. cerevisiae04:36

Assay for Adhesion and Agar Invasion in S. cerevisiae

Published on: November 8, 2006

Related Concept Videos

Cells Coordinate Growth and Proliferation02:36

Cells Coordinate Growth and Proliferation

Cell size is a significant factor impacting cellular design, function, and fitness. There exists some internal coordination by which cells double their masses before division, thus, achieving homeostasis. Coordination between cell growth and proliferation depends on the checkpoints in between cell cycle phases. Loss of coordination or failure in the checkpoint mechanism can drive the cell to uncontrolled growth and loss of cellular function. Like dividing cells that coordinate cellular growth,...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
The Cell Cycle Control System01:28

The Cell Cycle Control System

The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and function at the cell...