Skip Navigation



Nucleic Acids Research Advance Access published online on October 23, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp843
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (1161K) Freely available
Right arrow Screen PDF (384K) Freely available
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 Graham, J. E.
Right arrow Articles by Arciszewska, L. K.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Graham, J. E.
Right arrow Articles by Arciszewska, L. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/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

FtsK translocation on DNA stops at XerCD-dif

James E. Graham, Viknesh Sivanathan, David J. Sherratt and Lidia K. Arciszewska*

Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK

*To whom correspondence should be addressed. Tel: +44 (0)1865 613236; Fax: +44 (0)1865 613238; Email: lidia.arciszewska{at}bioch.ox.ac.uk

Received August 27, 2009. Revised September 22, 2009. Accepted September 22, 2009.

Escherichia coli FtsK is a powerful, fast, double-stranded DNA translocase, which can strip proteins from DNA. FtsK acts in the late stages of chromosome segregation by facilitating sister chromosome unlinking at the division septum. KOPS-guided DNA translocation directs FtsK towards dif, located within the replication terminus region, ter, where FtsK activates XerCD site-specific recombination. Here we show that FtsK translocation stops specifically at XerCD-dif, thereby preventing removal of XerCD from dif and allowing activation of chromosome unlinking by recombination. Stoppage of translocation at XerCD-dif is accompanied by a reduction in FtsK ATPase and is not associated with FtsK dissociation from DNA. Specific stoppage at recombinase-DNA complexes does not require the FtsK{gamma} regulatory subdomain, which interacts with XerD, and is not dependent on either recombinase-mediated DNA cleavage activity, or the formation of synaptic complexes.

Present address: Viknesh Sivanathan, Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115, USA.


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.