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Vol. 18, Issue 8, 3193-3203, August 2007

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The Clathrin Adaptor Complex AP-1 Binds HIV-1 and MLV Gag and Facilitates Their Budding

Grégory Camus^*,,, Carolina Segura-Morales^,, Dorothee Molle, Sandra Lopez-Vergès^*,, Christina Begon-Pescia, Chantal Cazevieille^||, Peter Schu^¶, Edouard Bertrand, Clarisse Berlioz-Torrent^*,,#, and Eugenia Basyuk^,#

*Institut Cochin, Université Paris Descartes, Centre National de la Recherche Scientifique (UMR 8104), Paris, France; and Institut National de la Santé et de la recherche Médicale, U567, Paris, France; Institut de Génétique Moléculaire de Montpellier-Centre National de la Recherché Scientifique Unité Mixte de Recherché 5535, 34293 Montpellier, France; ^||Centre Régional d'Imagerie Cellulaire/Institut Universitaire de Recherché Clinique, 34093 Montpellier, France; and ^¶University of Göttingen, Center for Biochemistry and Molecular Cell Biology, Biochemistry II, 37073 Göttingen, Germany

Submitted December 26, 2006; Revised May 14, 2007; Accepted May 23, 2007
Monitoring Editor: Jennifer Lippincott-Schwartz

Retroviral assembly is driven by Gag, and nascent viral particles escape cells by recruiting the machinery that forms intralumenal vesicles of multivesicular bodies. In this study, we show that the clathrin adaptor complex AP-1 is involved in retroviral release. The absence of AP-1µ obtained by genetic knock-out or by RNA interference reduces budding of murine leukemia virus (MLV) and HIV-1, leading to a delay of viral propagation in cell culture. In contrast, overexpression of AP-1µ enhances release of HIV-1 Gag. We show that the AP-1 complex facilitates retroviral budding through a direct interaction between the matrix and AP-1µ. Less MLV Gag is found associated with late endosomes in cells lacking AP-1, and our results suggest that AP-1 and AP-3 could function on the same pathway that leads to Gag release. In addition, we find that AP-1 interacts with Tsg101 and Nedd4.1, two cellular proteins known to be involved in HIV-1 and MLV budding. We propose that AP-1 promotes Gag release by transporting it to intracellular sites of active budding, and/or by facilitating its interactions with other cellular partners.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

These authors contributed equally to this work.

^# These authors contributed equally to this work.

Address correspondence to: Clarisse Berlioz-Torrent (Berlioz{at}cochin.inserm.fr) or Eugenia Basyuk (Eugenia.Basyuk{at}igmm.cnrs.fr).

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