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ZNF212 promotes genomic integrity through direct interaction with TRAIP.

Hee Jin Chung1, Joo Rak Lee1, Tae Moon Kim1,2

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Zinc finger protein 212 (ZNF212) is identified as a novel TRAIP binding partner crucial for DNA damage response (DDR) and repair pathways, including homologous recombination and interstrand crosslink repair.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • TRAIP is essential for DNA damage response (DDR), homologous recombination (HR), and interstrand crosslink (ICL) repair.
  • The precise roles of TRAIP in mammalian DNA repair pathways remain incompletely elucidated.

Purpose of the Study:

  • To identify novel binding partners of TRAIP involved in DNA repair.
  • To elucidate the function of ZNF212 in the DDR, HR, and ICL repair pathways.

Main Methods:

  • Co-immunoprecipitation to identify TRAIP binding partners.
  • Immunofluorescence microscopy to assess colocalization at DNA damage sites.
  • siRNA-mediated depletion and epistatic analysis in mammalian cells and mouse embryonic stem cells (mESCs).

Main Results:

  • ZNF212 was identified as a novel TRAIP binding partner that colocalizes with TRAIP at DNA damage sites.
  • Recruitment of TRAIP and ZNF212 to DNA damage sites is mutually dependent.
  • ZNF212 functions epistatically to TRAIP in DDR and HR-mediated repair.
  • ZNF212 acts upstream of Neil3 and Fanconi anemia (FA) pathways in ICL repair.
  • ZNF212 directly interacts with NEIL3, promoting its recruitment to ICL lesions.

Conclusions:

  • ZNF212 is a novel component of the DDR, HR, and ICL repair pathways.
  • ZNF212 functions in concert with TRAIP and NEIL3 to facilitate DNA repair.
  • These findings expand our understanding of the molecular mechanisms governing genome stability.