Suppr超能文献

噬菌体T4对裂解抑制崩溃的抗性。

Bacteriophage T4 resistance to lysis-inhibition collapse.

作者信息

Abedon S T

机构信息

Department of Microbiology, Ohio State University, Mansfield 44906, USA.

出版信息

Genet Res. 1999 Aug;74(1):1-11. doi: 10.1017/s0016672399003833.

Abstract

Lysis inhibition is a mechanism of latent-period extension and burst-size increase that is induced by the T4 bacteriophage adsorption of T4-infected cells. Mutants of T4 genes imm, sp and 5 (specifically the ts1 mutant of 5) display some lysis inhibition. However, these mutants experience lysis-inhibition collapse, the lysis of lysis-inhibited cells, earlier than wild-type-infected cells (i.e. their collapse occurs prematurely). Lysis from without is a lysis induced by excessive T4 adsorption. Gp5 is an inducer of lysis from without while gpimm and gpsp effect resistance to lysis from without. This paper shows that interfering with the adsorption of phages to imm-, sp- or 5ts1-mutant-infected cells, in a variety of contexts, inhibits premature lysis-inhibition collapse. From these data it is inferred that wild-type T4-infected cells display resistance to lysis-inhibition collapse by a mechanism resembling resistance to lysis from without.

摘要

裂解抑制是一种潜伏期延长和爆发量增加的机制,由T4噬菌体吸附于T4感染细胞所诱导。T4基因imm、sp和5的突变体(特别是5的ts1突变体)表现出一定程度的裂解抑制。然而,这些突变体比野生型感染细胞更早经历裂解抑制崩溃,即裂解抑制细胞的裂解(也就是说它们的崩溃过早发生)。体外裂解是由过量的T4吸附所诱导的裂解。gp5是体外裂解的诱导剂,而gpimm和gpsp影响对体外裂解的抗性。本文表明,在多种情况下,干扰噬菌体对imm-、sp-或5ts1突变体感染细胞的吸附可抑制过早的裂解抑制崩溃。从这些数据可以推断,野生型T4感染细胞通过一种类似于对体外裂解抗性的机制表现出对裂解抑制崩溃的抗性。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验