Bacteriophage T4 resistance to lysis-inhibition collapse
Bacteriophage T4 resistance to lysis-inhibition collapse
复制标题
DOI：
10.1017/s0016672399003833
复制
发表时间：
1999-08-01
影响因子：
1.5
通讯作者：
Abedon, ST
中科院分区：
文献类型：
--
作者：
Abedon, ST
裂解抑制是 T4 感染细胞的 T4 噬菌体吸附诱导的潜伏期延长和爆发大小增加的机制。 T4 基因 imm、sp 和 5 的突变体（特别是 5 的 ts1 突变体）表现出一定的裂解抑制作用。然而，这些突变体比野生型感染的细胞更早经历裂解抑制崩溃，即裂解抑制细胞的裂解（即它们的崩溃过早发生）。外部裂解是由过量的 T4 吸附引起的裂解。 Gp5 是外部裂解的诱导剂，而 gpimm 和 gpsp 则对外部裂解产生抵抗作用。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，可以抑制过早裂解抑制崩溃。从这些数据推断，野生型T4感染的细胞通过类似于对来自外部的裂解的抵抗的机制表现出对裂解抑制崩溃的抵抗。
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.