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Related Experiment Videos

Is START a switch?

F Cross1, J McKinney

  • 1Rockefeller University, New York, NY 10021-6399.

Ciba Foundation Symposium
|January 1, 1992
PubMed
Summary
This summary is machine-generated.

In Saccharomyces cerevisiae, CLN1, CLN2, and CLN3 cyclins regulate the cell cycle at START. Their expression activates CDC28 kinase, promoting cell cycle progression and coordinated development.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The cell cycle in Saccharomyces cerevisiae is precisely regulated at a point called START, typically in late G1 phase.
  • Progression through START is crucial for cell cycle commitment and subsequent development.
  • The CLN1, CLN2, and CLN3 gene families encode cyclins essential for this transition.

Purpose of the Study:

  • To elucidate the regulatory mechanisms controlling passage through START in Saccharomyces cerevisiae.
  • To investigate the role of CLN cyclins and CDC28 protein kinase in START regulation.
  • To understand the feedback loops and transcriptional regulation involved in cell cycle commitment.

Main Methods:

  • Utilized inducible promoters to control the expression of CLN1 and CLN3.

Related Experiment Videos

  • Analyzed cyclin-deficient yeast strains arrested in G1 phase.
  • Investigated the transcriptional regulation of CLN1 and CLN2 by cell cycle-dependent regulators SWI4 and SWI6.
  • Examined the role of FAR1 in inhibiting CLN function and its expression dynamics.

    • Main Results:

    • Inducible expression of CLN1 or CLN3 enabled cyclin-deficient G1-arrested cells to traverse START.
    • A model was proposed where CLN proteins activate CDC28 kinase, initiating a positive feedback loop for CLN1 and CLN2 transcription.
    • SWI4 and SWI6 were identified as potential components of this feedback loop.
    • Expression of FAR1, an inhibitor of CLN function, decreased at the time of START, correlating with peak CLN1 and CLN2 mRNA levels.

    Conclusions:

    • The interplay of CLN cyclins, CDC28 kinase, and transcriptional regulators like SWI4/SWI6 sharpens the START transition into an all-or-nothing event.
    • This precise regulation ensures coordinated activation of START-dependent events for timely cell cycle progression.
    • FAR1's regulated expression contributes to the abruptness of the START transition, preventing premature cell cycle commitment.