Abstract :
[en] In this study, we determined the minimal N-terminal fusion peptide of the gp30 of
the bovine leukemia virus on the basis of the tilted peptide theory. We first
used molecular modelling to predict that the gp30 minimal fusion peptide
corresponds to the 15 first residues. Liposome lipid-mixing and leakage assays
confirmed that the 15-residue long peptide induces fusion in vitro and that it is
the shortest peptide inducing optimal fusion since longer peptides destabilize
liposomes to the same extent but not shorter ones. The 15-residue long peptide
can thus be considered as the minimal fusion peptide. The effect of mutations
reported in the literature was also investigated. Interestingly, mutations
related to glycoproteins unable to induce syncytia in cell-cell fusion assays
correspond to peptides predicted as non-tilted. The relationship between
obliquity and fusogenicity was also confirmed in vitro for one tilted and one
non-tilted mutant peptide.
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