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

. 2014 Dec 11;11:117. doi: 10.1186/s12977-014-0117-5

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

© Blondot et al.; licensee BioMed Central. 2014

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

PMC Copyright notice

Model for Vpr-mediated G2 arrest through remodeling of the SLX4 complex. In a physiological contex activation of the SLX4 complex (SLX4com) intervenes to allow the resolution of DNA replication intermediates, such as Holliday Junctions (HJ), found in collapsed replication forks after DNA replication (phases of SLX4 activation are symbolized by green arrows). This leads to a proper G2/M phase transition (left panel). HIV-1 Vpr protein interacts with SLX4 on its SLX1 binding domain, the CUL4A–DDB1^DCAF1 ubiquitin ligase and PLK1/p-PLK1. These interactions lead to MUS81 ubiquitination, and phosphorylation of EME1 by p-PLK1, resulting in aberrant activation of SLX4com. This inappropriate activation perturbs progression of ongoing replication forks (RF) in S phase and the resolution of abnormal DNA replication intermediates. As a consequence, cells arrest at the G2 phase of the cell cycle (right panel).