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A major switch for the Fanconi anemia DNA damage–response pathway

Nature Structural & Molecular Biology volume 15, pages 1128–1130 (2008)Cite this article

The Fanconi anemia pathway is part of the DNA-damage network including breast cancer–susceptibility proteins BRCA1 and BRCA2. This pathway is activated by the ataxia telangiectasia and Rad3–related (ATR) kinase, but the underlying mechanism remains unclear. A new study demonstrates that a major switch activating the pathway is the ATR-dependent phosphorylation of FANCI.

Fanconi anemia is a rare genetic disease characterized by genomic instability, cancer predisposition, bone marrow failure and various developmental abnormalities. Increasing excitement has been generated from studies of this disease, as three Fanconi anemia genes, FANCD1, FANCN and FANCJ, have been found to be identical to breast cancer susceptibility (BRCA) genes BRCA2, PALB2 and BACH1, respectively. The disease has since become an attractive model to dissect the mechanism of actions by BRCA proteins1.

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Figure 1: Activation of the Fanconi anemia pathway.

Katie Ris-Vicari

Figure 2: Models for the switch function of FANCI phosphorylation.

Katie Ris-Vicari

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Acknowledgements

I thank D. Schlessinger for critical reading of the manuscript. The work in the Wang group is supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, and by the Fanconi Anemia Research Foundation.

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  1. Weidong Wang is at the Laboratory of Genetics, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Room 10B113, 251 Bayview Boulevard, Baltimore, Maryland 21224, USA. wangw@grc.nia.nih.gov,

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Wang, W. A major switch for the Fanconi anemia DNA damage–response pathway. Nat Struct Mol Biol 15, 1128–1130 (2008). https://doi.org/10.1038/nsmb1108-1128

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