Bandyopadhyay P N, Das Gupta B, Joshi A, Chakravorty M
J Virol. 1979 Oct;32(1):98-101. doi: 10.1128/JVI.32.1.98-101.1979.
It was demonstrated earlier in this laboratory that phage P22 induces a transient depression in the cellular transport processes of the host Salmonella typhimurium immediately after infection and that an effective injection process is enough to cause the depression. By using defective phage particles that contain host DNA instead of phage DNA for infection, it has been demonstrated that the injection of phage-specific DNA is essential for this. The defective particles adsorbed to the host and injected their DNA, but the cellular transport processes of the host were not altered. Thus, the injection of host DNA by the phage fails to affect the transport process. Insensitivity of the phage DNA-induced depression in transport to chloramphenicol rules out the involvement of newly synthesized protein in this change and indirectly suggests the possible role of phage DNA-associated internal proteins of P22.
本实验室先前已证明,噬菌体P22在感染宿主鼠伤寒沙门氏菌后,会立即引起宿主细胞转运过程的短暂抑制,且有效的注射过程足以导致这种抑制。通过使用含有宿主DNA而非噬菌体DNA的缺陷噬菌体颗粒进行感染,已证明注射噬菌体特异性DNA对此至关重要。缺陷颗粒吸附到宿主上并注射其DNA,但宿主的细胞转运过程未发生改变。因此,噬菌体注射宿主DNA未能影响转运过程。噬菌体DNA诱导的转运抑制对氯霉素不敏感,排除了新合成蛋白质参与此变化的可能性,并间接表明了P22噬菌体DNA相关内部蛋白质可能发挥的作用。