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[Role of hREV3 in cell cycle and proliferation]

Fang Xu1, Yuan-Jie Li

  • 1Department of Medical Genetics and Cell Biology, Ningxia Medical College, Yinchuan 750004, China. xufang@nxmc.edu.cn

Yi Chuan = Hereditas
|September 10, 2008
PubMed

Insights

Suppression of the REV3 gene delays cell cycle progression and increases cell arrest following DNA damage. This suggests REV3

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Context:

  • The REV3 gene encodes a subunit of DNA polymerase zeta, crucial for translesion synthesis.
  • Understanding REV3's role is vital for comprehending mutagenesis and tumorigenesis pathways.
  • Previous studies indicated REV3's involvement in limiting both spontaneous and DNA damage-induced mutagenesis.

Purpose:

  • To investigate the specific roles of REV3 in cell cycle progression and proliferation.
  • To evaluate the impact of REV3 suppression on cellular responses to DNA damaging agents.

Summary:

  • HEK-293-M-REV3- cells with suppressed REV3 expression exhibited delayed spontaneous S phase progression.
  • Treatment with methyl methanesulfonate (MMS) or UVB irradiation led to cell cycle arrest at S or G2-M phases.
  • Suppression of REV3 resulted in an increased proliferation index (PI) under DNA damaging conditions.

Impact:

  • Failure in translesion synthesis due to REV3 ablation may cause replication fork arrest, prolonging the cell cycle.
  • Persistent replication fork arrest could potentially lead to cell death or apoptosis.
  • These findings highlight REV3's critical function in maintaining genomic stability and cell cycle regulation.

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