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MBC in Press, published online ahead of print October 3, 2007
Mol. Biol. Cell 10.1091/mbc.E07-04-0392

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Submitted on May 3, 2007
Revised on September 7, 2007
Accepted on September 26, 2007

AP-1 and ARF1 Control Endosomal Dynamics at Sites of FcR-mediated Phagocytosis

Virginie Braun,*{dagger}{ddagger}{sect} Chantal Deschamps,{sect}||para; Graça Raposo,*{dagger} Philippe Benaroch,*# Alexandre Benmerah,||¶ Philippe Chavrier,*{dagger} and Florence Niedergang||¶

*Institut Curie, Centre de Recherche, Paris, F-75248 France; {dagger}Centre National de la Recherche Scientifique, Unité Mixte de Recherche 144, Paris, F-75248 France; ||Institut Cochin, Université Paris Descartes, Centre National de la Recherche Scientifique (Unité Mixte de Recherche 8104), F-75014 Paris, France; Institut National de la Santé et de la Recherche Médicale, U567, Paris, France; #Institut National de la Santé et de la Recherche Médicale U653, Paris, France

Monitoring Editor: Jean Gruenberg

Phagocytosis, the mechanism of ingestion of large material and microorganisms, relies on actin polymerization and on the focal delivery of intracellular endocytic compartments. The molecular mechanisms involved in the formation and delivery of the endocytic vesicles that are recruited at sites of phagocytosis are not well characterized. Here we show that AP-1 but not AP-2 clathrin adaptor complexes are recruited early below the sites of particle attachment and are required for efficient receptor-mediated phagocytosis in murine macrophages. Clathrin, however, is not recruited with the AP complexes. We further show that the recruitement of AP-1 positive structures at sites of phagocytosis is regulated by the GTP-binding protein ARF1 but is not sensitive to brefeldin A. Furthermore, AP-1 depletion leads to increased surface levels of TNF-{alpha}, a cargo known to traffic through the endosomes to the plasma membrane upon stimulation of the macrophages. Together, our results support a clathrin-independent role for AP complexes in endosomal dynamics in macrophages by retaining some cargo proteins, a process important for membrane remodeling during phagocytosis.

{sect}These authors contributed equally to this work.

{ddagger}Present address: Hospital for Sick Children, Cell Biology Program, Laboratory of Dr. J. H. Brumell, Toronto, ON, M5G1X8, Canada.

Address correspondence to: Florence Niedergang (niedergang{at}cochin.inserm.fr)






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