International Journal of Hematology

DOI: 10.1007/s12185-011-0818-7 Pages: 440-445

Fanconi anaemia proteins are associated with sister chromatid bridging in mitosis

1. University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital

2. University of Copenhagen, Department of Cellular and Molecular Medicine, Center for Healthy Aging, Panum Institute

Correspondence to:
Ian D. Hickson
Tel: +45-35326738



The maintenance of genome stability is critical for the suppression of cancer and premature ageing. The maintenance of the human genome requires hundreds of proteins involved in DNA repair, DNA replication, chromosome segregation and cell cycle checkpoint responses. A number of genetic disorders exist in man where a breakdown in genome maintenance is associated with cancer predisposition. Amongst these are Bloom’s syndrome (BS) and Fanconi anaemia (FA). The BS and FA gene products co-operate in the repair of damaged DNA. In this review, we focus on interactions between BS and FA proteins that specifically occur during chromosome segregation in mitosis. The BS protein, BLM, was shown recently to define a novel class of anaphase DNA bridge structures that, in some cases, also contain FA proteins. We will discuss the possible source of these bridges and the role that FA proteins and BLM might play in their removal.

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