Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2012 Aug 3;31(18):3757–3767. doi: 10.1038/emboj.2012.219

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2012, European Molecular Biology Organization

This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial Share Alike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.

PMC Copyright notice

A model for the role of Endo III in the stimulation of CTXΦ-integration. CTXΦ-integration result from the reversible formation of a pseudo-HJ intermediate between dif and attP(+) by XerC-catalysis. The length and width of the arrows indicate which of the two opposite reactions is favoured in the absence or presence of Endo III. Endo III (hexagons) inhibits XerC-cleavage after pseudo-HJ formation because it specifically recognizes and binds to four-way DNA junctions. Endo III binding results in the final displacement of the XerC recombinases. This might be due to a competition between XerC and Endo III for binding to the pseudo-HJ (arrow 1). Our results are in favour of a second pathway in which Endo III binding to the pseudo-HJ induces structural changes that perturb interactions between XerC and the DNA or XerC and XerD, leading to its destabilization (arrow 2).