Department of Biosciences, Durham University, Stockton Road, Durham DH1 3LE, UK.
Department of Biosciences, Durham University, Stockton Road, Durham DH1 3LE, UK.
Curr Opin Microbiol. 2023 Jun;73:102293. doi: 10.1016/j.mib.2023.102293. Epub 2023 Mar 21.
Bacteria have evolved a broad range of defence mechanisms to protect against infection by their viral parasites, bacteriophages (phages). Toxin-antitoxin (TA) systems are small loci found throughout bacteria and archaea that in some cases provide phage defence. The recent explosion in phage defence system discovery has identified multiple novel TA systems with antiphage activity. Due to inherent toxicity, TA systems are thought to mediate abortive infection (Abi), wherein the host cell dies in response to phage infection, removing the phage, and protecting clonal siblings. Recent studies, however, have uncovered molecular mechanisms by which TA systems are activated by phages, how they mediate toxicity, and how phages escape the defences. These new models reveal dazzling complexity in phage-host interactions and provide further evidence that TA systems do not in all cases inherently perform classic Abi, suggesting an evolved conceptual definition is required.
细菌已经进化出广泛的防御机制来抵御病毒寄生虫(噬菌体)的感染。毒素-抗毒素(TA)系统是在细菌和古细菌中发现的小基因座,在某些情况下可以提供噬菌体防御。最近对噬菌体防御系统的发现呈爆炸式增长,确定了多种具有抗噬菌体活性的新型 TA 系统。由于固有的毒性,TA 系统被认为介导了流产感染(Abi),其中宿主细胞因噬菌体感染而死亡,从而去除噬菌体并保护克隆兄弟姐妹。然而,最近的研究揭示了 TA 系统被噬菌体激活的分子机制,它们如何介导毒性,以及噬菌体如何逃避防御。这些新模型揭示了噬菌体-宿主相互作用令人眼花缭乱的复杂性,并进一步证明 TA 系统并非在所有情况下都固有地执行经典的 Abi,这表明需要一个经过进化的概念定义。