Evans D, Pringle C R, Szilágyi J F
J Virol. 1979 Aug;31(2):325-33. doi: 10.1128/JVI.31.2.325-333.1979.
In vesicular stomatitis virus New Jersey serotype polyacrylamide gel electrophoresis was unable to distinguish the polypeptides of the temperature-sensitive (ts) mutants of complementation groups A, B, C, and F from those of the wild-type virus. However, the NS polypeptide of the representative mutant of group E, ts E1, had a significantly greater electrophoretic mobility than that of the wild-type virus NS polypeptide. The electrophoretic mobilities of the NS polypeptides of the three mutants of complementation group E varied, being greatest in the case of ts E1, slightly less for ts E2, and only a little greater than that of wild-type virus NS polypeptide in the case of ts E3. Since the NS polypeptides of the revertant clones ts E1/R1 and ts E3/R1 have mobilities identical to that of wild-type NS polypeptide, the observed altered mobilities of the group E mutants are almost certainly the direct result of the ts mutations in the E locus. The electrophoretic mobilities of the intracellular NS polypeptides of the group E mutants were indistinguishable from those of their virion NS polypeptides. The electrophoretic mobilities of the NS polypeptides of the group E mutants synthesized in vitro using mRNA synthesized in vitro by TNP were identical to those of the NS polypeptides of their purified virions. The NS polypeptides of all three mutants were labeled with (32)P(i) to approximately the same extent as wild-type virus NS polypeptide, indicating that gross differences in phosphorylation of this polypeptide are unlikely to account for the altered mobilities. We propose a model in which the NS polypeptide consists of at least three loops held in this configuration by hydrophobic or ionic forces or both and stabilized by phosphodiester bridges. If a mutation affects one of the amino acids to which the phosphate is covalently linked, the phosphodiester bridge cannot be formed, and, as a result, in the presence of sodium dodecyl sulfate the affected loop opens and thus the NS polypeptide migrates further into the gel. Such a configuration may also explain the multifunctional nature of the NS polypeptide.
在水疱性口炎病毒新泽西血清型中,聚丙烯酰胺凝胶电泳无法区分互补组A、B、C和F的温度敏感(ts)突变体的多肽与野生型病毒的多肽。然而,E组代表性突变体ts E1的NS多肽的电泳迁移率明显高于野生型病毒NS多肽。互补组E的三个突变体的NS多肽的电泳迁移率各不相同,ts E1的迁移率最大,ts E2稍小,而ts E3仅比野生型病毒NS多肽略大。由于回复克隆ts E1/R1和ts E3/R1的NS多肽的迁移率与野生型NS多肽相同,因此观察到的E组突变体迁移率的改变几乎肯定是E基因座中ts突变的直接结果。E组突变体的细胞内NS多肽的电泳迁移率与其病毒粒子NS多肽的电泳迁移率无法区分。使用TNP体外合成的mRNA体外合成的E组突变体的NS多肽的电泳迁移率与纯化病毒粒子的NS多肽的电泳迁移率相同。所有三个突变体的NS多肽用(32)P(i)标记的程度与野生型病毒NS多肽大致相同,这表明该多肽磷酸化的总体差异不太可能解释迁移率的改变。我们提出了一个模型,其中NS多肽由至少三个环组成,这些环通过疏水或离子力或两者保持这种构型,并由磷酸二酯桥稳定。如果突变影响与磷酸共价连接的氨基酸之一,则无法形成磷酸二酯桥,结果,在十二烷基硫酸钠存在下,受影响的环打开,因此NS多肽进一步迁移到凝胶中。这样的构型也可以解释NS多肽的多功能性质。