Cell-type-specific replication initiation programs set fragility of the FRA3B fragile site

Anne Letessier, Gaël A. Millot, Stéphane Koundrioukoff, Anne-Marie Lachagès, Nicolas Vogt, R. Scott Hansen, Bernard Malfoy, Olivier Brison and Michelle Debatisse ()
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Anne Letessier: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Gaël A. Millot: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Stéphane Koundrioukoff: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Anne-Marie Lachagès: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Nicolas Vogt: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
R. Scott Hansen: University of Washington School of Medicine
Bernard Malfoy: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Olivier Brison: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France
Michelle Debatisse: Institut Curie, Centre de Recherche, 26 rue d’Ulm, 75248 Paris, France

Nature, 2011, vol. 470, issue 7332, 120-123

Abstract: The origins of fragility Some chromosomal locations, known as common fragile sites, are predisposed to breakage. These sites have pathological relevance because they are often associated with chromosomal translocations. An analysis of the replication dynamics along a 1.6-Mb region of FRA3B, a common fragile site in human lymphocytes that hosts the FHIT tumour suppressor gene, shows that, rather than breakage being due to replication stalling, FRA3B site fragility results from an unusually low density of replication origins. Surprisingly, fragility is cell-type-specific, which may have implications for current models of translocations and tumorigenesis.

Date: 2011
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DOI: 10.1038/nature09745

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