Genes and Development Attend a BioResearch Product Faire

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

Published online before print November 14, 2007, 10.1101/gad.1609007
GENES & DEVELOPMENT 21:3085-3094, 2007
©2007 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Research Data
Right arrow All Versions of this Article:
gad.1609007v1
21/23/3085    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bugreev, D. V.
Right arrow Articles by Mazin, A. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bugreev, D. V.
Right arrow Articles by Mazin, A. V.
Related Content
Right arrowRelated Articles
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Novel pro- and anti-recombination activities of the Bloom’s syndrome helicase

Dmitry V. Bugreev1,2, Xiong Yu3, Edward H. Egelman3, and Alexander V. Mazin1,4

1 Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA; 2 Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Science, Novosibirsk 630090, Russia; 3 Department of Biochemistry and Molecular Genetics, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA

Bloom’s syndrome (BS) is an autosomal recessive disorder characterized by a strong cancer predisposition. The defining feature of BS is extreme genome instability. The gene mutated in Bloom’s syndrome, BLM, encodes a DNA helicase (BLM) of the RecQ family. BLM plays a role in homologous recombination; however, its exact function remains controversial. Mutations in the BLM cause hyperrecombination between sister chromatids and homologous chromosomes, indicating an anti-recombination role. Conversely, other data show that BLM is required for recombination. It was previously shown that in vitro BLM helicase promotes disruption of recombination intermediates, regression of stalled replication forks, and dissolution of double Holliday junctions. Here, we demonstrate two novel activities of BLM: disruption of the Rad51-ssDNA (single-stranded DNA) filament, an active species that promotes homologous recombination, and stimulation of DNA repair synthesis. Using in vitro reconstitution reactions, we analyzed how different biochemical activities of BLM contribute to its functions in homologous recombination.

[Keywords: Bloom’s syndrome; BLM helicase; homologous recombination; Rad51; RecQ; Rad54]]

Received August 24, 2007; revised version accepted October 2, 2007.

4 Corresponding author.

E-MAIL amazin{at}drexelmed.edu; FAX (215) 762-4452.

Supplemental material is available at http://www.genesdev.org.

Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.1609007


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Articles

RecQ helicases queuing with Srs2 to disrupt Rad51 filaments and suppress recombination
Dana Branzei and Marco Foiani
Genes & Dev. 2007 21: 3019-3026. [Extract] [Full Text] [PDF]

RECQL5/Recql5 helicase regulates homologous recombination and suppresses tumor formation via disruption of Rad51 presynaptic filaments
Yiduo Hu, Steven Raynard, Michael G. Sehorn, Xincheng Lu, Wendy Bussen, Lu Zheng, Jeremy M. Stark, Ellen L. Barnes, Peter Chi, Pavel Janscak, Maria Jasin, Hannes Vogel, Patrick Sung, and Guangbin Luo
Genes & Dev. 2007 21: 3073-3084. [Abstract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
S. Raynard, W. Zhao, W. Bussen, L. Lu, Y.-Y. Ding, V. Busygina, A. R. Meetei, and P. Sung
Functional Role of BLAP75 in BLM-Topoisomerase III{alpha}-dependent Holliday Junction Processing
J. Biol. Chem., June 6, 2008; 283(23): 15701 - 15708.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
V. Busygina, M. G. Sehorn, I. Y. Shi, H. Tsubouchi, G. S. Roeder, and P. Sung
Hed1 regulates Rad51-mediated recombination via a novel mechanism
Genes & Dev., March 15, 2008; 22(6): 786 - 795.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
D. Branzei and M. Foiani
RecQ helicases queuing with Srs2 to disrupt Rad51 filaments and suppress recombination
Genes & Dev., December 1, 2007; 21(23): 3019 - 3026.
[Full Text] [PDF]

Home page
 Genes Dev.Home page
Y. Hu, S. Raynard, M. G. Sehorn, X. Lu, W. Bussen, L. Zheng, J. M. Stark, E. L. Barnes, P. Chi, P. Janscak, et al.
RECQL5/Recql5 helicase regulates homologous recombination and suppresses tumor formation via disruption of Rad51 presynaptic filaments
Genes & Dev., December 1, 2007; 21(23): 3073 - 3084.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Genome Res. Learn. Mem.
Protein Science RNA Genes Dev.
Copyright © 2007 by Cold Spring Harbor Laboratory Press.