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Individuals affected by the autosomal recessive disorder Werner's syndrome (WS) develop many of the symptoms characteristic of premature ageing. Primary fibroblasts cultured from WS patients exhibit karyotypic abnormalities and a reduced replicative life span. The WRN gene encodes a 3'-5' DNA helicase, and is a member of the RecQ family, which also includes the product of the Bloom's syndrome gene (BLM). In this work, we show that WRN promotes the ATP-dependent translocation of Holliday junctions, an activity that is also exhibited by BLM. In cells arrested in S-phase with hydroxyurea, WRN localizes to discrete nuclear foci that coincide with those formed by the single-stranded DNA binding protein replication protein A. These results are consistent with a model in which WRN prevents aberrant recombination events at sites of stalled replication forks by dissociating recombination intermediates.

Original publication




Journal article



Publication Date





80 - 84


Adenosine Triphosphatases, Adenosine Triphosphate, Bacterial Proteins, Cell Nucleus, DNA, DNA Helicases, DNA Replication, Exodeoxyribonucleases, HeLa Cells, Humans, Microscopy, Fluorescence, RecQ Helicases, Recombinant Proteins, Recombination, Genetic, Werner Syndrome, Werner Syndrome Helicase