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Related Experiment Videos

Mutations in RAD27 define a potential link between G1 cyclins and DNA replication

E A Vallen1, F R Cross

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

Molecular and Cellular Biology
|August 1, 1995
PubMed
Summary

Yeast CLN1 and CLN2 cyclins regulate DNA replication and repair. Mutations in RAD27/ERC11, a DNA repair gene, cause cell cycle arrest, which CLN1/CLN2 can suppress, unlike CLN3.

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Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • DNA Repair

Background:

  • The yeast Saccharomyces cerevisiae possesses three G1 cyclin (CLN) genes (CLN1, CLN2, CLN3) with overlapping functions.
  • Understanding the specific roles of these CLN genes requires analyzing their interactions with other essential cellular processes.

Purpose of the Study:

  • To investigate the functions of CLN genes in DNA replication and repair by examining synthetic lethal interactions.
  • To elucidate the role of RAD27/ERC11 (yeast FEN-1 homolog) in cell cycle progression and DNA integrity.

Main Methods:

  • Analysis of yeast mutants, specifically cln1 cln2 rad27/erc11 triple mutants.
  • Phenotypic characterization including cell cycle arrest, DNA damage sensitivity, mitotic recombination, and mutation rates.

Related Experiment Videos

  • Suppression analysis using different CLN gene expressions (CLN1, CLN2, CLN3).

    • Main Results:

    • cln1 cln2 rad27/erc11 cells exhibit S-phase arrest, suppressible by CLN1/CLN2 but not CLN3.
    • rad27/erc11 mutants show defects in DNA damage repair, increased mutation rates, and recombination, which are not suppressed by CLN1/CLN2.
    • Overexpression of CLN1 in mec1-1 mutants leads to cell death and chromosome loss.

    Conclusions:

    • CLN1 and CLN2 play critical roles in regulating DNA replication, potentially through an RAD27/ERC11-independent pathway.
    • These cyclins may also override checkpoint responses, contributing to cell cycle progression.
    • CLN1/CLN2 function in DNA replication and repair is distinct from CLN3's role.