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Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway

James Hejna1, Megan Holtorf, Jennie Hines

  • 1Department of Molecular and Medical Genetics, Oregon Health & Science University, 3181 Sam Jackson Parkway, Portland, OR 97239, USA.

The Journal of Biological Chemistry
|February 12, 2008
PubMed

Insights

The chromatin remodeler Tip60 interacts with FANCD2, aiding genome stability in Fanconi anemia. Tip60 is crucial for DNA cross-link repair, working alongside Fanconi anemia proteins.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Fanconi anemia is a genome instability disorder.
  • Cells with Fanconi anemia are sensitive to DNA cross-linking agents.
  • FANCD2 is a key protein in maintaining genome stability.

Purpose of the Study:

  • To investigate the interaction between Tip60 and FANCD2.
  • To determine Tip60's role in DNA interstrand cross-link repair.

Main Methods:

  • Yeast two-hybrid system to test protein interactions.
  • Co-immunoprecipitation and co-localization in human cells.
  • Depletion of Tip60 in normal and Fanconi anemia cells.

Main Results:

  • Tip60 directly interacts with FANCD2.
  • Tip60 depletion reduces cellular survival after DNA cross-linking.
  • Tip60 functions independently of FANCD2 monoubiquitination and foci formation.
  • Tip60's role in DNA repair is distinct from its interaction with FANCD2.

Conclusions:

  • Tip60 is a chromatin remodeler involved in DNA interstrand cross-link repair.
  • Tip60 functions in concert with Fanconi anemia proteins to maintain genome stability.
  • The interaction between Tip60 and FANCD2 is important for genome maintenance.

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