Abstract
Mutations were introduced in the transmembrane region of the spike protein of the murine coronavirus A59. The maturation of these mutant S proteins was not affected, they were all expressed at the cell surface, and became acylated, however some mutant S proteins did not induce cell-to-cell fusion. An I-->K change in the middle of the predicted transmembrane (TM) anchor and mutation of the first three cysteine residues of the TM domain resulted in a fusion-negative phenotype. We propose a model by which these data can be explained.
MeSH terms
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Amino Acid Sequence
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Animals
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Cell Fusion*
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Membrane Glycoproteins / biosynthesis
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Membrane Glycoproteins / chemistry
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Membrane Glycoproteins / physiology*
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Mice
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Models, Biological
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Molecular Sequence Data
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Murine hepatitis virus / genetics
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Murine hepatitis virus / metabolism*
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Mutagenesis, Site-Directed
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Point Mutation
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Protein Conformation
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Recombinant Proteins / biosynthesis
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Recombinant Proteins / chemistry
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Recombinant Proteins / metabolism
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Spike Glycoprotein, Coronavirus
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Viral Envelope Proteins / biosynthesis
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Viral Envelope Proteins / chemistry
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Viral Envelope Proteins / physiology*
Substances
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Membrane Glycoproteins
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Recombinant Proteins
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Spike Glycoprotein, Coronavirus
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Viral Envelope Proteins