Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The formation of RAD51 foci in response to ionizing radiation (IR) represents an important step in the repair of DNA double-strand breaks. RAD51 foci also appear during S phase and are thought to be required for the restart of stalled or broken replication forks. The RAD51 recombinase interacts directly with the breast cancer-associated tumour suppressor BRCA2, an interaction that is required for normal recombination proficiency, radiation resistance and genome stability. In CAPAN-1 cells, which express a truncated form of BRCA2 that is cytoplasmic because of loss of the nuclear localization signal, the formation of IR-induced RAD51 foci is impaired. In this work, we show that S-phase RAD51 foci form normally in CAPAN-1 cells expressing truncated BRCA2. Moreover, we find that RAD51 specifically associates with chromatin at S phase in a reaction that is BRCA2-independent. The observed BRCA2-dependent and independent formation of RAD51 foci shows that intact BRCA2 is not required for RAD51 focus formation per se, leading us to suggest that S phase and IR-induced RAD51 foci assemble by distinct pathways with defined protein requirements.

Original publication

DOI

10.1038/sj.onc.1206263

Type

Journal article

Journal

Oncogene

Publication Date

27/02/2003

Volume

22

Pages

1115 - 1123

Keywords

Active Transport, Cell Nucleus, BRCA2 Protein, Breast Neoplasms, Carcinoma, Cell Nucleus, Chromatin, Cytoplasm, DNA Damage, DNA Repair, DNA Replication, DNA, Neoplasm, DNA-Binding Proteins, Genes, BRCA2, HeLa Cells, Humans, Multienzyme Complexes, Neoplasm Proteins, Pancreatic Neoplasms, Protein Sorting Signals, Rad51 Recombinase, S Phase, Tumor Cells, Cultured