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 Blood, 1 October 2007, Vol. 110, No. 7, pp. 2390-2398.
Prepublished online as a Blood First Edition Paper on June 27, 2007; DOI 10.1182/blood-2006-11-057273.

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HEMATOPOIESIS

FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein

Rigu Gupta1, Sudha Sharma1, Joshua A. Sommers1, Mark K. Kenny2, Sharon B. Cantor3, and Robert M. Brosh, Jr1

1 Laboratory of Molecular Gerontology, National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, MD; 2 Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY; 3 Department of Cancer Biology, University of Massachusetts Medical School, Worcester

The BRCA1 associated C-terminal helicase (BACH1, designated FANCJ) is implicated in the chromosomal instability genetic disorder Fanconi anemia (FA) and hereditary breast cancer. A critical role of FANCJ helicase may be to restart replication as a component of downstream events that occur during the repair of DNA cross-links or double-strand breaks. We investigated the potential interaction of FANCJ with replication protein A (RPA), a single-stranded DNA-binding protein implicated in both DNA replication and repair. FANCJ and RPA were shown to coimmunoprecipitate most likely through a direct interaction of FANCJ and the RPA70 subunit. Moreover, dependent on the presence of BRCA1, FANCJ colocalizes with RPA in nuclear foci after DNA damage. Our data are consistent with a model in which FANCJ associates with RPA in a DNA damage-inducible manner and through the protein interaction RPA stimulates FANCJ helicase to better unwind duplex DNA substrates. These findings identify RPA as the first regulatory partner of FANCJ. The FANCJ-RPA interaction is likely to be important for the role of the helicase to more efficiently unwind DNA repair intermediates to maintain genomic stability.


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Y. Wu, K. Shin-ya, and R. M. Brosh Jr.
FANCJ Helicase Defective in Fanconia Anemia and Breast Cancer Unwinds G-Quadruplex DNA To Defend Genomic Stability
Mol. Cell. Biol., June 15, 2008; 28(12): 4116 - 4128.
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