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Sct1 functions in partnership with Cdc10 in a transcription complex that activates cell cycle START and inhibits

M Caligiuri1, D Beach

  • 1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724.

Cell
|February 26, 1993
PubMed

Insights

A newly identified fission yeast gene, sct1, is crucial for cell cycle progression at START. Loss of sct1 function arrests the cell cycle and activates mating pathways, highlighting its dual role in cell division and differentiation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The cell cycle is a fundamental process controlling cell division.
  • Fission yeast is a model organism for studying cell cycle regulation.
  • The START transition is a critical checkpoint in the cell cycle.

Purpose of the Study:

  • To identify and characterize a novel gene involved in regulating the cell cycle START.
  • To elucidate the function of the identified gene in both cell cycle progression and differentiation.
  • To investigate the relationship between the new gene and known cell cycle regulators.

Main Methods:

  • Gene identification and functional analysis through gene deletion and mutation.
  • Analysis of cell cycle progression using microscopy and flow cytometry.
  • Investigation of gene expression patterns related to cell cycle and mating pathways.

Main Results:

  • A novel fission yeast gene, sct1, was identified as essential for cell cycle progression at START.
  • Loss of sct1 function leads to cell cycle arrest at START and derepression of the mating pathway.
  • The protein p72sct1 interacts with p85cdc10 in a transcription complex, regulating cell cycle genes.
  • A dominant mutation in sct1's DNA-binding domain confers cdc10-independent START execution.

Conclusions:

  • Sct1 is a key regulator acting as both an activator of the mitotic cell cycle and a repressor of differentiation.
  • Sct1 functions in partnership with Cdc10 within a transcription complex to control cell cycle progression.
  • Targeted mutations in Sct1 can bypass the requirement for Cdc10, offering insights into cell cycle control mechanisms.

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