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Nucleic Acids Research, 2000, Vol. 28, No. 23 4805-4813
© 2000 Oxford University Press

Enhanced flexibility and aphidicolin-induced DNA breaks near mammalian replication origins: implications for replicon mapping and chromosome fragility

Franck Toledo*, Arnaud Coquelle, Ekaterina Svetlova and Michelle Debatisse

Unité de Génétique Somatique (URA CNRS 1960), Institut Pasteur, 25 rue du Dr Roux, 75724 Paris Cedex 15, France

Common fragile sites are chromosomal loci prone to breakage and rearrangement that can be induced by aphidicolin, an inhibitor of DNA polymerases. Within these loci, sites of preferential DNA breaks were proposed to correlate with peaks of enhanced DNA flexibility, the function of which remains elusive. Here we show that mammalian DNA replication origins are enriched in peaks of enhanced flexibility. This finding suggests that the search for these features may help in the mapping of replication origins, and we present evidence supporting this hypothesis. The association of peaks of flexibility with replication origins also suggests that some origins may associate with minor levels of fragility. As shown here, an increased sensitivity to aphidicolin was found near two mammalian DNA replication origins.

* To whom correspondence should be addressed at present address: Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. Tel: +1 858 453 4100 ext. 1551; Fax: +1 858 535 1871; Email: toledo{at}pop.salk.edu Present address: Arnaud Coquelle, Unité de Cytogénétique Moléculaire et Oncologie (UMR CNRS 147), Institut Curie, 26 rue d’Ulm, 75248 Paris Cedex 05, France


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