Home LiteratureArticle Details
PMID: 7653094 Published · ppublish English Journal Article

Human parainfluenza virus type 3: analysis of the cytoplasmic tail and transmembrane anchor of the hemagglutinin-neuraminidase protein in promoting cell fusion.

Virus research ·Vol. 36 ·No. 2-3 ·1995-05-00 ·Pages 131-49

Tanaka Y, Galinski MS

Abstract

The role of the cytoplasmic tail and transmembrane anchor of the human parainfluenza virus type 3 (HPIV3) hemagglutinin-neuraminidase (HN) glycoprotein in promoting cell fusion was investigated. A series of amino terminal deletion mutants (d10, d20, d27, d31, d40, d44, and d73) were compared for processing, cell surface expression, and maintenance of their biological attributes by recombinant expression of mutant genes using a plasmid vector (pcDL-SR alpha-296) in CV-1 and HeLa cells. To determine the fusion promoting activity (FPA) of the various mutant proteins, a simple assay was developed which quantified the fusion of two different HeLa cell types. One of the cell types, HeLa-tat, constitutively expressed the human immunodeficiency virus type I (HIV-1) tat protein from a Moloney murine leukemia virus long terminal repeat (LTR), while the second cell type, HeLa beta-gal, contained a reporter gene, beta-galactosidase, under the control of an HIV1-LTR. Fusion of mixed HeLa cell monolayers (50:50, HeLa-tat: HeLa beta-gal), following transfection with appropriate plasmids, resulted in transactivation of the reporter gene which was then measured by direct staining of cells or using cell lysates with appropriate substrates. Cell fusion was observed only when both the HPIV3 F and functional HN proteins were both co-transfected into cells. Of the seven deletion mutants examined, only d10, d20, d27 and d31 were expressed to significant levels on the cell surface and only these four mutant proteins maintained FPA. Compared with the wt HN at 48 h post transfection, d10 and d20 had enhanced FPA (119% and 158%, respectively), while d27 and d31 were diminished (74% and > 4%, respectively). Analysis of protein expression suggested that the reason for the increase in FPA of the mutant proteins was that the levels of protein expressed at the cell surface was twofold or threefold higher for d10 and d20, respectively, compared to the wt HN.

MeSH Terms
Amino Acid Sequence Base Sequence Cell Fusion Cells, Cultured Gene Expression Regulation, Viral Gene Products, tat/metabolism HN Protein/genetics,metabolism HeLa Cells Hemadsorption Humans Molecular Sequence Data Mutation Parainfluenza Virus 3, Human/enzymology,genetics,metabolism Transfection Viral Fusion Proteins/genetics,metabolism Viral Matrix Proteins/genetics,metabolism Viral Tail Proteins/genetics,metabolism beta-Galactosidase/metabolism
Chemicals
Gene Products, tat HN Protein Viral Fusion Proteins Viral Matrix Proteins Viral Tail Proteins F protein, parainfluenza virus 3 beta-Galactosidase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Tanaka Y
Department of Molecular Biology, Cleveland Clinic Foundation, Ohio 44195, USA.
Galinski M S
Article Info
Journal
Virus research
Abbr.
Virus Res
ISSN
0168-1702
Published
1995-05-00
Pages
131-49
Language
English
Region
Netherlands
NLM ID
8410979
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]