The Bloom syndrome protein limits the lethality associated with RAD51 deficiency

Little is known about the functional interaction between the Bloom's syndrome protein (BLM) and the recombinase RAD51 within cells. Using RNA interference technology, we provide the first demonstration that RAD51 acts upstream from BLM to prevent anaphase bridge formation. RAD51 downregulation...

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Bibliographic Details
Published in:Molecular cancer research 2010-03, Vol.8 (3), p.385-394
Main Authors: Lahkim Bennani-Belhaj, Kenza, Rouzeau, Sébastien, Buhagiar-Labarchède, Géraldine, Chabosseau, Pauline, Onclercq-Delic, Rosine, Bayart, Emilie, Cordelières, Fabrice, Couturier, Jérôme, Amor-Guéret, Mounira
Format: Article
Language:English
Subjects:
Anaphase - genetics
Biochemistry, Molecular Biology
Cell Death - genetics
Cell Survival - genetics
Cellular Biology
Down-Regulation - genetics
Gene Expression Regulation, Neoplastic - genetics
HeLa Cells
Humans
Life Sciences
Neoplasms - genetics
Neoplasms - metabolism
Rad51 Recombinase - genetics
RecQ Helicases - genetics
RecQ Helicases - metabolism
RNA Interference - physiology
Sister Chromatid Exchange - genetics
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Summary:Little is known about the functional interaction between the Bloom's syndrome protein (BLM) and the recombinase RAD51 within cells. Using RNA interference technology, we provide the first demonstration that RAD51 acts upstream from BLM to prevent anaphase bridge formation. RAD51 downregulation was associated with an increase in the frequency of BLM-positive anaphase bridges, but not of BLM-associated ultrafine bridges. Time-lapse live microscopy analysis of anaphase bridge cells revealed that BLM promoted cell survival in the absence of Rad51. Our results directly implicate BLM in limiting the lethality associated with RAD51 deficiency through the processing of anaphase bridges resulting from the RAD51 defect. These findings provide insight into the molecular basis of some cancers possibly associated with variants of the RAD51 gene family.
ISSN:1541-7786
1557-3125
DOI:10.1158/1541-7786.MCR-09-0534