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The yeast cell cycle: positive and negative controls

M Aldea¹, C Casas, C Gallego

¹Departament de Ciències Mèdiques Bàsiques, Facultat de Medicina, Universitat de Lleida.

Microbiologia (Madrid, Spain)

|March 1, 1994

Summary

Yeast cell cycle control at START relies on G1 cyclins activating Cdc28 kinase. A newly identified gene links nutrient availability to G1 cyclin expression, impacting cell cycle progression.

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Area of Science:

Molecular Biology
Cell Cycle Regulation
Yeast Genetics

Background:

Cell cycle progression in Saccharomyces cerevisiae is primarily regulated at the START transition in G1 phase.
Yeast cells assess environmental cues like nutrients and pheromones at START before committing to division.
G1 cyclins are crucial regulators, activating the Cdc28 (p34) protein kinase to control entry into the cell cycle.

Purpose of the Study:

To review the molecular mechanisms governing the START cell cycle point in yeast.
To elucidate the positive and negative regulatory factors influencing START.
To introduce a novel gene connecting nutrient availability to G1 cyclin expression.

Main Methods:

Review of existing literature on yeast cell cycle control.

Related Experiment Videos

Analysis of molecular pathways involving G1 cyclins and Cdc28 kinase.

Description of a newly identified gene and its potential role in nutrient sensing.

Main Results:

START regulation involves the precise accumulation and degradation of G1 cyclins, leading to a peak in Cdc28 kinase activity.
This kinase activity phosphorylates specific substrates, facilitating passage through START.
A novel gene has been identified that links nutrient availability to the expression of G1 cyclins.

Conclusions:

The START transition is a critical checkpoint controlled by cyclin-dependent kinases and regulated by environmental signals.
The newly discovered gene provides a molecular link between nutrient status and cell cycle progression via G1 cyclin regulation.
Further investigation into the Ras-cAMP pathway may reveal additional connections to nutrient-mediated cell cycle control.