A FANCD2 domain activates Tip60-dependent apoptosis

James Hejna, Donald Bruun, Daniel Pauw, Robb E. Moses

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

The FA (Fanconi anaemia) FANCD2 protein is pivotal in the cellular response to DNA interstrand cross-links. Establishing cells expressing exogenous FANCD2 has proven to be difficult compared with other DNA repair genes. We find that in transformed normal human fibroblasts, exogenous nuclear expression of FANCD2 induces apoptosis, dependent specifically on exons 10-13. This is the same region required for interaction with the histone acetyltransferase, Tip60. Deletion of exons 10-13 from FANCD2 N-terminal constructs (nucleotides 1-1100) eliminates the binary interaction with Tip60 and the cellular apoptotic response; moreover, cells can stably express FANCD2 at high levels if Tip60 is depleted. The results indicate that FANCD2-sponsored apoptosis requires an interaction with Tip60 and depends on Tip60.

Original languageEnglish (US)
Pages (from-to)893-899
Number of pages7
JournalCell Biology International
Volume34
Issue number9
DOIs
StatePublished - Sep 1 2010

Keywords

  • Apoptosis
  • Fanconi anaemia
  • Histone acetyltransferase
  • Interstrand cross-link repair
  • Tip60

ASJC Scopus subject areas

  • Cell Biology

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