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The Influence of FEN-1 Gene on Cell Cycle and Genetic Stability

Bin-Shan Shi1, Ying-Nian Yu, Zhu-Nan Cai

  • 1Department of Pathophysiology, School of Medicine, Zhejiang University, Hangzhou 310031, China. ynyu@mail.hz.zj.cn

Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao Acta Biochimica Et Biophysica Sinica
|June 7, 2002
PubMed

Insights

Blocking the flap endonuclease 1 (FEN-1) gene impacts DNA replication and repair. FEN-1 gene suppression in cells causes cell cycle arrest and increased mutation frequency, affecting genetic stability.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Flap endonuclease 1 (FEN-1) is crucial for DNA replication, repair, and maintaining genetic stability.
  • FEN-1 plays a vital role in various DNA metabolic processes.

Purpose of the Study:

  • To investigate the functional consequences of FEN-1 gene suppression in a cellular model.
  • To determine the impact of reduced FEN-1 expression on cell cycle progression and mutation frequency.

Main Methods:

  • Construction of a cell line (FL-FEN-1(-)) with suppressed FEN-1 gene expression using antisense mRNA.
  • Flow cytometry analysis to assess cell cycle distribution.
  • Mutation assay using the shuttle-plasmid pZ189 to measure mutation frequency.
  • Treatment with MNNG (an alkylating agent) to evaluate cellular sensitivity.

Main Results:

  • FEN-1 gene suppression led to cell cycle delay in S-phase and arrest in G1 phase.
  • Spontaneous mutation frequency in FL-FEN-1(-) cells was significantly higher (19.1x10^4) compared to control cells (2.9-3.0x10^4).
  • FL-FEN-1(-) cells showed increased sensitivity to the alkylating agent MNNG.

Conclusions:

  • FEN-1 is essential for normal cell cycle progression and preventing spontaneous mutations.
  • FEN-1 deficiency disrupts DNA replication and repair pathways, leading to genetic instability.
  • The study suggests distinct pathways for FEN-1-dependent mutations and MNNG-induced mutations.

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