Figure 6
The fusion capacity of the VSV G protein was sequence dependent. (a) Amino acid sequence alignment of TMs from VSV G and influenza HA. Black: identical, blue: homologous, red: non-conserved. (b and c) WT and mutated VSV G had similar expression levels. (d) Point mutations in TM did not affect the surface localization of VSV G. The localization of WT and mutated VSV G-EGFP fusion proteins was analyzed by confocal microscopy. Scale bar, 10 μm. (e) Point mutations in the TM region impaired the cell-cell fusion activity of VSV G. (f) WT and mutated VSV G proteins were packaged into lentiviruses at similar levels. (g) Point mutations in the TM region decreased the lentivirus infection efficiency mediated by VSV G. HeLa cells were infected by lentivirus containing WT or mutated VSV G and analyzed by flow cytometry. Asterisks indicate statistically significant differences (*P < 0.05; **P < 0.01; ***P < 0.001).
