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肠染色体岛:DNA 包装特异性和 λ 样辅助噬菌体终止酶的作用。

Enteric Chromosomal Islands: DNA Packaging Specificity and Role of λ-like Helper Phage Terminase.

机构信息

Fundación Ciencia & Vida, Av. Zañartu, Santiago 1482, Chile.

Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.

出版信息

Viruses. 2022 Apr 15;14(4):818. doi: 10.3390/v14040818.

Abstract

The phage-inducible chromosomal islands (PICIs) of Gram-negative bacteria are analogous to defective prophages that have lost the ability to propagate without the aid of a helper phage. PICIs have acquired genes that alter the genetic repertoire of the bacterial host, including supplying virulence factors. Recent work by the Penadés laboratory elucidates how a helper phage infection or prophage induction induces the island to excise from the bacterial chromosome, replicate, and become packaged into functional virions. PICIs lack a complete set of morphogenetic genes needed to construct mature virus particles. Rather, PICIs hijack virion assembly functions from an induced prophage acting as a helper phage. The hijacking strategy includes preventing the helper phage from packaging its own DNA while enabling PICI DNA packaging. In the case of recently described Gram-negative PICIs, the PICI changes the specificity of DNA packaging. This is achieved by an island-encoded protein (Rpp) that binds to the phage protein (TerS), which normally selects phage DNA for packaging from a DNA pool that includes the helper phage and host DNAs. The Rpp-TerS interaction prevents phage DNA packaging while sponsoring PICI DNA packaging. Our communication reviews published data about the hijacking mechanism and its implications for phage DNA packaging. We propose that the Rpp-TerS complex binds to a site in the island DNA that is positioned analogous to that of the phage DNA but has a completely different sequence. The critical role of TerS in the Rpp-TerS complex is to escort TerL to the PICI , ensuring appropriate DNA cutting and packaging.

摘要

革兰氏阴性菌的噬菌体诱导染色体岛 (PICI) 类似于失去在辅助噬菌体帮助下繁殖能力的缺陷性前噬菌体。PICI 获得了改变细菌宿主遗传成分的基因,包括提供毒力因子。Penadés 实验室的最近研究阐明了辅助噬菌体感染或前噬菌体诱导如何导致该岛从细菌染色体上切除、复制并被包装成功能性病毒粒子。PICI 缺乏构建成熟病毒颗粒所需的整套形态发生基因。相反,PICI 劫持了作为辅助噬菌体的诱导前噬菌体的病毒装配功能。劫持策略包括阻止辅助噬菌体包装其自身的 DNA,同时允许 PICI DNA 包装。在最近描述的革兰氏阴性 PICIs 的情况下,PICI 改变了 DNA 包装的特异性。这是通过岛编码的蛋白 (Rpp) 实现的,该蛋白与噬菌体蛋白 (TerS) 结合,TerS 通常从包括辅助噬菌体和宿主 DNA 的 DNA 池中选择噬菌体 DNA 进行包装。Rpp-TerS 相互作用阻止噬菌体 DNA 包装,同时赞助 PICI DNA 包装。我们的通讯回顾了关于劫持机制及其对噬菌体 DNA 包装影响的已发表数据。我们提出,Rpp-TerS 复合物结合到岛 DNA 中的一个位置,该位置类似于噬菌体 DNA 的位置,但具有完全不同的序列。TerS 在 Rpp-TerS 复合物中的关键作用是护送 TerL 到 PICI,确保适当的 DNA 切割和包装。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb93/9026076/5c5c42d24341/viruses-14-00818-g001.jpg

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