Reguera Juan, Grueso Esther, Carreira Aura, Sánchez-Martínez Cristina, Almendral José M, Mateu Mauricio G
Centro de Biología Molecular "Severo Ochoa" (Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid), Universidad Autónoma de Madrid, Cantoblanco 28049 Madrid, Spain.
J Biol Chem. 2005 May 6;280(18):17969-77. doi: 10.1074/jbc.M500867200. Epub 2005 Feb 23.
In the spherical virion of the parvovirus minute virus of mice, several amino acid side chains of the capsid were previously found to be involved in interactions with the viral single-stranded DNA molecule. We have individually truncated by mutation to alanine many (ten) of these side chains and analyzed the effects on capsid assembly, stability and conformation, viral DNA encapsidation, and virion infectivity. Mutation of residues Tyr-270, Asp-273, or Asp-474 led to a drastic reduction in infectivity. Mutant Y270A was defective in capsid assembly; mutant D273A formed stable capsids, but it was essentially unable to encapsidate the viral DNA or to externalize the N terminus of the capsid protein VP2, a connected conformational event. Mutation of residues Asp-58, Trp-60, Asn-183, Thr-267, or Lys-471 led to a moderate reduction in infectivity. None of these mutations had an effect on capsid assembly or stability, or on the DNA encapsidation process. However, those five mutant virions were substantially less stable than the parental virion in thermal inactivation assays. The results with this model spherical virus indicate that several capsid residues that are found to be involved in polar interactions or multiple hydrophobic contacts with the viral DNA molecule contribute to preserving the active conformation of the infectious viral particle. Their effect appears to be mediated by the non-covalent interactions they establish with the viral DNA. In addition, at least one acidic residue at each DNA-binding region is needed for DNA packaging.
在小鼠细小病毒的球形病毒粒子中,先前发现衣壳的几个氨基酸侧链参与了与病毒单链DNA分子的相互作用。我们通过突变将其中许多(十个)侧链逐个截短为丙氨酸,并分析了对衣壳组装、稳定性和构象、病毒DNA包装以及病毒粒子感染性的影响。酪氨酸-270(Tyr-270)、天冬氨酸-273(Asp-273)或天冬氨酸-474(Asp-474)残基的突变导致感染性急剧降低。突变体Y270A在衣壳组装方面存在缺陷;突变体D273A形成了稳定的衣壳,但基本上无法包装病毒DNA或使衣壳蛋白VP2的N末端外化,这是一个相关的构象事件。天冬氨酸-58(Asp-58)、色氨酸-60(Trp-60)、天冬酰胺-183(Asn-183)、苏氨酸-267(Thr-267)或赖氨酸-471(Lys-471)残基的突变导致感染性适度降低。这些突变均未对衣壳组装或稳定性或DNA包装过程产生影响。然而,在热灭活试验中,这五个突变病毒粒子比亲本病毒粒子的稳定性要低得多。用这种模型球形病毒得到的结果表明,发现与病毒DNA分子参与极性相互作用或多个疏水接触的几个衣壳残基有助于保持感染性病毒粒子的活性构象。它们的作用似乎是通过与病毒DNA建立的非共价相互作用介导的。此外,DNA包装需要每个DNA结合区域至少有一个酸性残基。