Section of Molecular Genetics and Microbiology, and Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Virology. 2010 Mar 15;398(2):176-86. doi: 10.1016/j.virol.2009.12.002. Epub 2009 Dec 29.
Loss of up to four amino acids from the C terminus of the 1318 residue bacteriophage T7 gp16 allows plaque formation at normal efficiencies. Loss of five residues results in non-infective virions, and loss of twelve prevents assembly of stable particles. However, replacing the C-terminal seven with nineteen non-native residues allows assembly of non-infective virions. The latter adsorb and eject internal core proteins into the cell envelope but no phage DNA enters the cytoplasm. Extragenic suppressors of the defective gene 16 lie in gene 15; the mutant gp15 proteins not only re-establish infectivity, they fully restore the kinetics of genome internalization to those exhibited by wild-type phage. After ejection from the infecting particle, gp15 and gp16 thus function together in ratcheting the leading end of the T7 genome into the cytoplasm of the infected cell.
从 1318 个残基的噬菌体 T7 gp16 的 C 末端丢失多达四个氨基酸残基允许以正常效率形成噬菌斑。丢失五个残基导致无感染性病毒粒子，丢失十二个残基阻止稳定颗粒的组装。然而，用 19 个非天然残基替换 C 末端七个残基允许组装无感染性病毒粒子。后者吸附并将内部核心蛋白喷射到细胞包膜中，但噬菌体 DNA 不会进入细胞质。缺陷基因 16 的外显子抑制子位于基因 15 中；突变的 gp15 蛋白不仅恢复了感染性，它们还完全恢复了基因组内化的动力学，使其与野生型噬菌体表现出的动力学相同。从感染颗粒中排出后，gp15 和 gp16 一起协同作用，将 T7 基因组的前端棘轮式地拉入感染细胞的细胞质中。
