BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination

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 c...

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Detalles Bibliográficos
Autores principales: Tripathi, Vivek, Nagarjuna, Tirunelvely, Sengupta, Sagar
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2007
Materias:
Research Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064412/
https://www.ncbi.nlm.nih.gov/pubmed/17591918
http://dx.doi.org/10.1083/jcb.200610051
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author Tripathi, Vivek
Nagarjuna, Tirunelvely
Sengupta, Sagar
author_facet Tripathi, Vivek
Nagarjuna, Tirunelvely
Sengupta, Sagar
author_sort Tripathi, Vivek
collection PubMed
description 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.
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spelling pubmed-20644122008-01-02 BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination Tripathi, Vivek Nagarjuna, Tirunelvely Sengupta, Sagar J Cell Biol Research Articles 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. The Rockefeller University Press 2007-07-02 /pmc/articles/PMC2064412/ /pubmed/17591918 http://dx.doi.org/10.1083/jcb.200610051 Text en Copyright © 2007, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Research Articles
Tripathi, Vivek
Nagarjuna, Tirunelvely
Sengupta, Sagar
BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title_full BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title_fullStr BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title_full_unstemmed BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title_short BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination
title_sort blm helicase–dependent and –independent roles of 53bp1 during replication stress–mediated homologous recombination
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064412/
https://www.ncbi.nlm.nih.gov/pubmed/17591918
http://dx.doi.org/10.1083/jcb.200610051
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AT nagarjunatirunelvely blmhelicasedependentandindependentrolesof53bp1duringreplicationstressmediatedhomologousrecombination
AT senguptasagar blmhelicasedependentandindependentrolesof53bp1duringreplicationstressmediatedhomologousrecombination

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