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Published online
doi:10.1083/jcb.200610051
The Journal of Cell Biology, Vol. 178, No. 1, 9-14
The Rockefeller University Press, 0021-9525 $30.00
© Tripathi et al.
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BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination



Vivek Tripathi, Tirunelvely Nagarjuna, and Sagar Sengupta

National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India

Correspondence to Sagar Sengupta: sagar{at}nii.res.in

Mutations in BLM helicase cause Bloom syndrome, characterized by predisposition to all forms of cancer. We demonstrate that BLM, signal transducer 53BP1, and RAD51 interact during stalled replication. Interactions between the three proteins have functional consequences. Lack of 53BP1 decreases the cell survival and enhanced chromosomal aberration after replication arrest. 53BP1 exhibits both BLM-dependent and -independent anti-recombinogenic functions in human and mouse cells. Both BLM and 53BP1 abrogate endogenous RAD51 foci formation and disrupt RAD51 polymerization. Consequently, loss of BLM and 53BP1 synergistically enhances stress-dependent homologous recombination. These results provide evidence regarding the cooperation between BLM and 53BP1 during maintenance of genomic integrity.

Abbreviations used in this paper: BS, Bloom syndrome; HR, homologous recombination; hTERT, human telomerase reverse transcriptase; HU, hydroxyurea; IP, immunoprecipitation; IR, ionizing radiation; NHF, normal human fibroblast; SCE, sister chromatid exchange.


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