Skip Navigation


Nucleic Acids Research Advance Access originally published online on October 31, 2008
Nucleic Acids Research 2008 36(21):6907-6917; doi:10.1093/nar/gkn793
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (497K) Freely available
Right arrow Screen PDF (282K) Freely available
Right arrow Supplementary Data
Right arrowOA All Versions of this Article:
36/21/6907    most recent
gkn793v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Kappeler, M.
Right arrow Articles by Schaffner, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kappeler, M.
Right arrow Articles by Schaffner, W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2008, Vol. 36, No. 21 6907-6917
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome integrity, repair and replication

Drosophila bloom helicase maintains genome integrity by inhibiting recombination between divergent DNA sequences

Michael Kappeler, Elisabeth Kranz, Katrina Woolcock, Oleg Georgiev and Walter Schaffner*

Insitut für Molekularbiologie der Universität Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland

*To whom correspondence should be addressed. Tel: +41 44 635 31 50; Fax: +41 44 635 68 11; Email: Walter.Schaffner{at}molbio.uzh.ch

Received July 21, 2008. Revised October 8, 2008. Accepted October 12, 2008.

DNA double strand breaks (DSB) can be repaired either via a sequence independent joining of DNA ends or via homologous recombination. We established a detection system in Drosophila melanogaster to investigate the impact of sequence constraints on the usage of the homology based DSB repair via single strand annealing (SSA), which leads to recombination between direct repeats with concomitant loss of one repeat copy. First of all, we find the SSA frequency to be inversely proportional to the spacer length between the repeats, for spacers up to 2.4 kb in length. We further show that SSA between divergent repeats (homeologous SSA) is suppressed in cell cultures and in vivo in a sensitive manner, recognizing sequence divergences smaller than 0.5%. Finally, we demonstrate that the suppression of homeologous SSA depends on the Bloom helicase (Blm), encoded by the Drosophila gene mus309. Suppression of homeologous recombination is a novel function of Blm in ensuring genomic integrity, not described to date in mammalian systems. Unexpectedly, distinct from its function in Saccharomyces cerevisiae, the mismatch repair factor Msh2 encoded by spel1 does not suppress homeologous SSA in Drosophila.


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




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.