The Bloom syndrome protein limits the lethality associated with RAD51 deficiency.

K. Lahkim Bennani-Belhaj, S. Rouzeau, G. Buhagiar-Labarchede, P. Chabosseau, R. Onclercq-Delic, E. Bayart, F. Cordelieres, J. Couturier, M. Amor-Gueret
Molecular Cancer Research. 2010-03-01; 8(3): 385-394
DOI: 10.1158/1541-7786.mcr-09-0534

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1. Mol Cancer Res. 2010 Mar;8(3):385-94. doi: 10.1158/1541-7786.MCR-09-0534. Epub
2010 Mar 9.

The Bloom syndrome protein limits the lethality associated with RAD51 deficiency.

Lahkim Bennani-Belhaj K(1), Rouzeau S, Buhagiar-Labarchède G, Chabosseau P,
Onclercq-Delic R, Bayart E, Cordelières F, Couturier J, Amor-Guéret M.

Author information:
(1)Institut Curie, Centre de Recherche, Centre Universitaire, Orsay, France.

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.

DOI: 10.1158/1541-7786.MCR-09-0534
PMID: 20215422 [Indexed for MEDLINE]

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