Role of Matrix and Fusion Proteins in Budding of Sendai Virus

doi:10.1128/JVI.75.23.11384-11391.2001

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Journal of Virology, December 2001, p. 11384-11391, Vol. 75, No. 23
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.23.11384-11391.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of Matrix and Fusion Proteins in Budding of Sendai Virus

Toru Takimoto,¹^,^* K. Gopal Murti,¹ Tatiana Bousse,¹ Ruth Ann Scroggs,¹ and Allen Portner¹^,²

Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105,¹ and Department of Pathology, The Health Science Center, University of Tennessee $---$ Memphis, Memphis, Tennessee 38163²

Received 31 May 2001/Accepted 5 September 2001

Paramyxoviruses are assembled at the surface of infected cells, where virions are formed by the process of budding. We investigatedthe roles of three Sendai virus (SV) membrane proteins in theproduction of virus-like particles. Expression of matrix (M) proteinsfrom cDNA induced the budding and release of virus-like particlesthat contained M, as was previously observed with human parainfluenzavirus type 1 (hPIV1). Expression of SV fusion (F) glycoproteinfrom cDNA caused the release of virus-like particles bearing surfaceF, although their release was less efficient than that of particlesbearing M protein. Cells that expressed only hemagglutinin-neuraminidase(HN) released no HN-containing vesicles. Coexpression of M andF proteins enhanced the release of F protein by a factor greaterthan 4. The virus-like particles containing F and M were foundin different density gradient fractions of the media of cellsthat coexpressed M and F, a finding that suggests that the twoproteins formed separate vesicles and did not interact directly.Vesicles released by M or F proteins also contained cellular actin;therefore, actin may be involved in the budding process inducedby viral M or F proteins. Deletion of C-terminal residues of Mprotein, which has a sequence similar to that of an actin-bindingdomain, significantly reduced release of the particles into medium.Site-directed mutagenesis of the cytoplasmic tail of F revealedtwo regions that affect the efficiency of budding: one domaincomprising five consecutive amino acids conserved in SV and hPIV1and one domain that is similar to the actin-binding domain requiredfor budding induced by M protein. Our results indicate that bothM and F proteins are able to drive the budding of SV and proposethe possible role of actin in the buddingprocess.

^* Corresponding author. Mailing address: Department of Virology and Molecular Biology, St. Jude Children's Research Hospital,332 N. Lauderdale, Memphis, TN 38105-2794. Phone: (901) 495-3438.Fax: (901) 523-2622. E-mail: toru.takimoto{at}stjude.org

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