Genome replication dynamics of a bacteriophage and its satellite reveal strategies for parasitism and viral restriction
Genome replication dynamics of a bacteriophage and its satellite reveal strategies for parasitism and viral restriction
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DOI：
10.1093/nar/gkz1005
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发表时间：
2020-01-10
影响因子：
14.9
通讯作者：
Seed, Kimberley D.
中科院分区：
文献类型：
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作者：
Barth, Zachary K.;Silvas, Tania V.;Seed, Kimberley D.
噬菌体诱导染色体岛状元件(PLE)是在霍乱弧菌中发现的噬菌体卫星。PLE寄生于裂解噬菌体ICP1，从细菌染色体上切除，复制，并在细胞裂解后动员到新的宿主细胞。PLE通过完全限制ICP1后代的产生来保护它们的宿主细胞群体。此前发现，在PLE(+)感染过程中ICP1复制减少。尽管PLE基因组复制强劲，但产生的转导单位相对较少。我们研究了PLE DNA复制本身是否对ICP1复制具有拮抗作用。在这里，我们确定了PLE复制的关键成分，并评估了它们在ICP1干扰中的作用。PLE编码一种REPA N启动因子，足以在ICP1感染期间驱动从PLE复制起点的复制。与以前鉴定的噬菌体卫星不同，在没有噬菌体的情况下，PLE起始因子的表达不足以支持PLE的复制。复制PLE对于干扰ICP1DNA复制是必要的，但复制最小化的PLE复制子不足以干扰ICP1DNA复制。尽管ICP1DNA复制得到了恢复，但非复制型PLE对ICP1DNA仍有广泛的抑制作用。这些结果表明，PLE DNA复制是导致ICP1限制的多种机制之一。
Phage-inducible chromosomal island-like elements (PLEs) are bacteriophage satellites found in Vibrio cholerae. PLEs parasitize the lytic phage ICP1, excising from the bacterial chromosome, replicating, and mobilizing to new host cells following cell lysis. PLEs protect their host cell populations by completely restricting the production of ICP1 progeny. Previously, it was found that ICP1 replication was reduced during PLE(+) infection. Despite robust replication of the PLE genome, relatively few transducing units are produced. We investigated if PLE DNA replication itself is antagonistic to ICP1 replication. Here we identify key constituents of PLE replication and assess their role in interference of ICP1. PLE encodes a RepA N initiation factor that is sufficient to drive replication from the PLE origin of replication during ICP1 infection. In contrast to previously characterized bacteriophage satellites, expression of the PLE initiation factor was not sufficient for PLE replication in the absence of phage. Replication of PLE was necessary for interference of ICP1 DNA replication, but replication of a minimalized PLE replicon was not sufficient for ICP1 DNA replication interference. Despite restoration of ICP1 DNA replication, non-replicating PLE remained broadly inhibitory against ICP1. These results suggest that PLE DNA replication is one of multiple mechanisms contributing to ICP1 restriction.