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噬菌体T4感染后大肠杆菌中硫代甲基-β-半乳糖苷积累能力的恢复

Recovery of the accumulation ability of thiomethyl-beta-galactoside in Escherichia coli after bacteriophage T4 infection.

作者信息

Saijo N, Okamoto K

出版信息

J Virol. 1976 Feb;17(2):299-306. doi: 10.1128/JVI.17.2.299-306.1976.

Abstract

Effects of UV-irridiated and unirradiated T4 phage infection on the beta-galactoside accumulation ability in Eschericia coli have been examined by the use of 14C-labeled thiomethyl-beta-galactoside (TMG). Under conditions where a synchronous adsorption of phage takes place, the cellular ability for TMG accumulation is found to be largely inhibited immediately after phage adsorption, but it recovers with time to a new level, which is dependent on the multiplicity of infection. When cells are infected with UV-irradiated T4 at the same multiplicity as that of unirradiated phage, the cellular accumulation ability is more severely inhibited and there is no recovery from the inhibition. The recovery process in T4-infected cells is mostly sensitive to puromycin. These results suggest that the initial inhibition of the TMG accumulation ability is probably caused by the adsorption of phage coats, and the subsequent restoration occurs through the action of a phage-directed protein(s). In the recovery process, no new transport system appears to be involved. The restored ability of TMG accumulation is resistant to the action of superinfecting UV phage. However, different mechanisms appear to be operating in T4-infected cells for the establishment of resistance to ghosts and for the recovery from the phage coat-induced inhibition.

摘要

通过使用¹⁴C标记的硫代甲基-β-半乳糖苷(TMG),研究了紫外线照射的和未照射的T4噬菌体感染对大肠杆菌中β-半乳糖苷积累能力的影响。在噬菌体同步吸附的条件下,发现噬菌体吸附后,细胞积累TMG的能力立即受到很大抑制,但随着时间的推移会恢复到一个新水平,这个新水平取决于感染复数。当用与未照射噬菌体相同感染复数的紫外线照射的T4噬菌体感染细胞时,细胞积累能力受到更严重的抑制,且抑制没有恢复。T4感染细胞中的恢复过程对嘌呤霉素最为敏感。这些结果表明,TMG积累能力的初始抑制可能是由噬菌体外壳的吸附引起的,随后的恢复是通过噬菌体指导的一种或多种蛋白质的作用发生的。在恢复过程中,似乎没有新的转运系统参与。恢复后的TMG积累能力对超感染的紫外线噬菌体的作用具有抗性。然而,在T4感染的细胞中,建立对噬菌体空壳的抗性和从噬菌体外壳诱导的抑制中恢复似乎涉及不同的机制。

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