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Zinc finger protein 668 interacts with Tip60 to promote H2AX acetylation after DNA damage

Ruozhen Hu1, Edward Wang, Guang Peng

  • 1Department of Systems Biology; The University of Texas MD Anderson Cancer Center; Houston, TX, USA.

Cell Cycle (Georgetown, Tex.)
|June 20, 2013
PubMed

Insights

Zinc finger protein 668 (ZNF668) regulates DNA repair by promoting chromatin relaxation. Its absence impairs DNA damage response, affecting cell survival and homologous recombination repair.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Tumor suppressors are crucial in DNA damage pathways.
  • Zinc finger protein 668 (ZNF668) is a potential breast cancer tumor suppressor.
  • The role of ZNF668 in DNA damage response remains unclear.

Purpose of the Study:

  • To investigate the function of ZNF668 in DNA damage response.
  • To determine ZNF668's role in DNA repair mechanisms.
  • To elucidate the link between ZNF668, chromatin relaxation, and DNA repair.

Main Methods:

  • ZNF668 knockdown experiments in cancer cells.
  • Analysis of DNA damage signaling pathways (ATM/ATR).
  • Assessment of repair protein recruitment to DNA lesions (e.g., RPA, Tip60).
  • Evaluation of histone modifications (H2AX hyperacetylation) and chromatin relaxation.
  • Investigation of homologous recombination (HR) repair efficiency.
  • Assessment of cell survival after DNA damage (IR and UV).

Main Results:

  • ZNF668 knockdown impairs cell survival post-DNA damage without affecting ATM/ATR signaling.
  • ZNF668 deficiency reduces repair protein recruitment to DNA lesions.
  • Knockdown of ZNF668 impairs Tip60-H2AX interaction and histone H2AX hyperacetylation, hindering chromatin relaxation.
  • Impaired chromatin relaxation leads to defective homologous recombination (HR) repair and reduced cell survival after IR.
  • ZNF668 knockdown decreases RPA phosphorylation and recruitment after UV damage.
  • Restored chromatin relaxation counteracts DNA repair defects in ZNF668-deficient cells.

Conclusions:

  • ZNF668 is a critical regulator of DNA repair.
  • ZNF668 facilitates DNA damage response by promoting chromatin relaxation.
  • Impeded chromatin accessibility due to ZNF668 deficiency causes DNA repair defects.
  • ZNF668 acts as a molecular link between chromatin relaxation and DNA damage control.
Keywords:
DNA damage repairH2AX acetylationTip60ZNF668

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