FANCI Regulates Recruitment of the FA Core Complex at Sites of DNA Damage Independently of FANCD2

• DOI: 10.1371/journal.pgen.1005563
• Publication Date: 2015-10-02T18:02:41Z
• Authors: Maria Castella; Celine Jacquemont; Elizabeth L. Thom...; Jung Eun Yeo; Ronald S. Cheung; Jen-Wei Huang; Alexandra Sobeck; Eric A. Hendrickson; Toshiyasu Taniguchi
• Keywords: FANCD2

The Fanconi anemia (FA)-BRCA pathway mediates repair of DNA interstrand crosslinks. FA core complex, a multi-subunit ubiquitin ligase, participates in the detection lesions and monoubiquitinates two downstream proteins, FANCD2 FANCI (or ID complex). However, regulation complex itself is poorly understood. Here we show that proteins are recruited to sites damage form nuclear foci S G2 phases cell cycle. ATR kinase activity, an intact FANCM-FAAP24 were crucial for this recruitment. Surprisingly, FANCI, but not its partner FANCD2, was needed efficient formation. Monoubiquitination or ATR-dependent phosphorylation required recruitment, deubiquitination by USP1 was. Additionally, BRCA1 These findings indicate functions upstream recruitment independently alter current view FA-BRCA pathway.