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J. Biol. Chem., Vol. 280, Issue 49, 40474-40480, December 9, 2005

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Functions of Early (AP-2) and Late (AIP1/ALIX) Endocytic Proteins in Equine Infectious Anemia Virus Budding^*

Chaoping Chen, Olivier Vincent1, Jing Jin, Ora A. Weisz¶||, and Ronald C. Montelaro2

From the Molecular Genetics and Biochemistry, ^¶Cell Biology and Physiology, and ^||Medicine, Renal-Electrolyte Division, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261 and the Departamento de Microbiologia Molecular, Centro de Investigaciones Biologicas del Consejo Superior de Investigaciones Cientificas, Madrid 28006, Spain

The proline-rich L domains of human immunodeficiency virus 1 (HIV-1) and other retroviruses interact with late endocytic proteins during virion assembly and budding. In contrast, the YPDL L domain of equine infectious anemia virus (EIAV) is apparently unique in its reported ability to interact both with the µ2 subunit of the AP-2 adaptor protein complex and with ALG-2-interacting protein 1 (AIP1/Alix) protein factors involved in early and late endosome formation, respectively. To define further the mechanisms by which EIAV adapts vesicle trafficking machinery to facilitate virion production, we have examined the specificity of EIAV p9 binding to endocytic factors and the effects on virion production of alterations in early and late endocytic protein expression. The results of these studies demonstrated that (i) an 300-residue region of AIP1/Alix-(409-715) was sufficient for binding to the EIAV YPDL motif; (ii) overexpression of AIP1/Alix or AP-2 µ2 subunit specifically inhibited YPDL-mediated EIAV budding; (iii) virion budding from a replication-competent EIAV variant with its L domain replaced by the HIV PTAP sequence was inhibited by wild type or mutant µ2 to a level similar to that observed when a dominant-negative mutant of Tsg101 was expressed; and (iv) overexpression or siRNA silencing of AIP1/Alix and AP-2 revealed additive suppression of YPDL-mediated EIAV budding. Taken together, these results indicated that both early and late endocytic proteins facilitate EIAV production mediated by either YPDL or PTAP L domains, suggesting a comprehensive involvement of endocytic factors in retroviral assembly and budding that can be accessed by distinct L domain specificities.

Received for publication, August 24, 2005 , and in revised form, October 6, 2005.

^* This work was supported in part by National Institutes of Health Grant 2RO1 CA49296 (to R. C. M.), National Institutes of Health postdoctoral training Grant T32 AI49820 (to C. C.), and Comision Interministerial de Ciencia y Tecnología Grant BIO2002-00803 (to O. V.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by the Ramón y Cajal Program (Ministerio de Ciencia y Tecnología, Spain).

² To whom correspondence should be addressed: Dept. of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, W1144 Biomedical Science Tower, Pittsburgh, PA 15261. Tel.: 412-648-8869; Fax: 412-383-8859; E-mail: rmont{at}pitt.edu.

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