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SNIP1 Recruits TET2 to Regulate c-MYC Target Genes and Cellular DNA Damage Response.

Lei-Lei Chen1, Huai-Peng Lin2, Wen-Jie Zhou1

  • 1Huashan Hospital and Key Laboratory of Medical Epigenetics and Metabolism and Molecular and Cell Biology Lab, Institute of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.

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Summary

The TET2 enzyme

Keywords:
DNA damageDNA demethylationSNIP1TET2c-MYCcell deathtranscription

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Area of Science:

  • Epigenetics
  • Molecular Biology
  • Genomics

Background:

  • The TET2 enzyme (ten-eleven translocation 2) is crucial for epigenetic regulation via DNA demethylation.
  • TET2 lacks a DNA-binding domain, making its targeted genomic recruitment unclear.
  • Understanding TET2 recruitment is key to its role in gene expression and cellular processes.

Purpose of the Study:

  • To identify proteins interacting with TET2.
  • To elucidate the mechanism of TET2 recruitment to specific genomic loci.
  • To investigate the functional significance of TET2-interacting proteins in DNA damage response.

Main Methods:

  • Mammalian two-hybrid screening to identify TET2-interacting proteins.
  • Co-immunoprecipitation and Western blotting to confirm physical interactions.
  • Chromatin immunoprecipitation (ChIP) assays to assess promoter recruitment.
  • Apoptosis assays to evaluate cellular response to DNA damage.

Main Results:

  • SMAD nuclear interacting protein 1 (SNIP1) was identified as a TET2-interacting protein.
  • SNIP1 acts as a bridge, facilitating TET2 binding to transcription factors like c-MYC.
  • SNIP1 recruits TET2 to promoters of c-MYC target genes involved in DNA damage response and cell viability.
  • TET2, via SNIP1, protects cells from DNA damage-induced apoptosis.

Conclusions:

  • A novel mechanism for targeting TET2 to specific promoters involves a ternary complex with SNIP1 and sequence-specific DNA-binding factors.
  • A TET2-SNIP1-c-MYC pathway is identified, linking epigenetic regulation to DNA damage response and genome stability.
  • This pathway highlights the interplay between epigenetic modifiers and transcription factors in maintaining genomic integrity.