首页> 美国卫生研究院文献>other >Environmental T4-Family Bacteriophages Evolve to Escape Abortive Infection via Multiple Routes in a Bacterial Host Employing Altruistic Suicide through Type III Toxin-Antitoxin Systems
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Environmental T4-Family Bacteriophages Evolve to Escape Abortive Infection via Multiple Routes in a Bacterial Host Employing Altruistic Suicide through Type III Toxin-Antitoxin Systems

机译:通过使用III型毒素-抗毒素系统利他性自杀的细菌宿主中的环境T4家族噬菌体进化为通过多种途径逃逸堕胎感染。

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摘要

Abortive infection is an anti-phage mechanism employed by a bacterium to initiate its own death upon phage infection. This reduces, or eliminates, production of viral progeny and protects clonal siblings in the bacterial population by an act akin to an “altruistic suicide.” Abortive infection can be mediated by a Type III toxin-antitoxin system called ToxINPa consisting of an endoribonuclease toxin and RNA antitoxin. ToxINPa is a heterohexameric quaternary complex in which pseudoknotted RNA inhibits the toxicity of the toxin until infection by certain phages causes destabilization of ToxINPa, leading to bacteriostasis and, eventually, lethality. However, it is still unknown why only certain phages are able to activate ToxINPa. To try to address this issue we first introduced ToxINPa into the Gram-negative enterobacterium, Serratia sp. ATCC 39006 (S 39006) and then isolated new environmental S 39006 phages that were scored for activation of ToxINPa and abortive infection capacity. We isolated three T4-like phages from a sewage treatment outflow point into the River Cam, each phage being isolated at least a year apart. These phages were susceptible to ToxINPa-mediated abortive infection but produced spontaneous “escape” mutants that were insensitive to ToxINPa. Analysis of these resistant mutants revealed three different routes of escaping ToxINPa, namely by mutating asiA (the product of which is a phage transcriptional co-activator); by mutating a conserved, yet functionally unknown, orf84; or by deleting a 6.5–10 kb region of the phage genome. Analysis of these evolved escape mutants may help uncover the nature of the corresponding phage product(s) involved in activation of ToxINPa.
机译:流产感染是细菌在噬菌体感染后引发自身死亡的一种抗噬菌体机制。这减少或消除了病毒后代的产生,并通过类似于“利他性自杀”的行为保护了细菌种群中的克隆同胞。流产感染可以通过称为ToxINPa的III型毒素-抗毒素系统介导,该系统由核糖核酸内切酶毒素和RNA抗毒素组成。 ToxINPa是一种异六聚体四元复合物,其中假结RNA抑制毒素的毒性,直到被某些噬菌体感染导致ToxINPa不稳定,导致细菌稳定,并最终导致致死性。但是,仍然未知为什么只有某些噬菌体才能激活ToxINPa。为了解决这个问题,我们首先将ToxINPa引入革兰氏阴性肠杆菌Serratia sp.。 ATCC 39006(S 39006),然后分离出新的环境S 39006噬菌体,并对其进行ToxINPa激活和流产感染能力评分。我们从一个污水处理流出点分离了三个T4样噬菌体,它们进入了坎河(River Cam),每个噬菌体至少间隔一年。这些噬菌体易受ToxINPa介导的流产感染,但产生了对ToxINPa不敏感的自发“逃逸”突变体。对这些抗性突变体的分析揭示了逃脱ToxINPa的三种不同途径,即通过突变asiA(其产物是噬菌体转录共激活因子)来实现。通过变异保守但功能未知的orf84;或者删除噬菌体基因组的6.5–10 kb区域。对这些进化的逃逸突变体的分析可能有助于揭示与ToxINPa激活有关的相应噬菌体产物的性质。

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