Overexpression of Escherichia coli udk mimics the absence of T7 Gp2 function and thereby abrogates successful infection by T7 phage.
Overexpression of Escherichia coli udk mimics the absence of T7 Gp2 function and thereby abrogates successful infection by T7 phage.
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大肠杆菌 udk 的过度表达模拟 T7 Gp2 功能的缺失，从而消除 T7 噬菌体的成功感染。
DOI：
10.1099/mic.0.064527-0
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Shadrin A
中科院分区：
文献类型：
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作者：
Shadrin A
T7噬菌体成功感染大肠杆菌依赖于T7基因组被两种不同的RNA聚合酶（RNAps）转录。细菌RNAp转录早期T7启动子，而中期和晚期T7基因由T7 RNAp转录。Gp 2是一种T7编码的转录因子，是一种必需的中间T7基因2的7 kDa产物，是宿主RNA β的有效抑制剂。Gp 2的基本生物学作用是抑制未能有效终止的早期T7基因的转录，以促进宿主和噬菌体RNPs对T7基因组的协调使用。过量表达E.大肠杆菌udk基因编码尿苷/胞苷激酶，干扰T7感染。我们证明过表达fudk拮抗E.大肠杆菌在T7感染的情况下，因此独立于T7编码的因子。似乎fudk的过表达降低了T7感染期间Gp 2的稳定性和功能性，从而导致宿主RNAp的抑制不足和早期T7转录物的积累。换句话说，在T7感染过程中，过表达fudk模拟Gp 2的缺失。我们的研究表明，T7基因组的转录调节非常复杂，并且可能在多个水平上受到噬菌体和宿主编码因子的影响。
Successful infection ofEscherichia coliby bacteriophage T7 relies upon the transcription of the T7 genome by two different RNA polymerases (RNAps). The bacterial RNAp transcribes early T7 promoters, whereas middle and late T7 genes are transcribed by the T7 RNAp. Gp2, a T7-encoded transcription factor, is a 7 kDa product of an essential middle T7 gene2, and is a potent inhibitor of the host RNAp. The essential biological role of Gp2 is to inhibit transcription of early T7 genes that fail to terminate efficiently in order to facilitate the coordinated usage of the T7 genome by both host and phage RNAps. Overexpression of theE. coli udkgene, which encodes a uridine/cytidine kinase, interferes with T7 infection. We demonstrate that overexpression ofudkantagonizes Gp2 function inE. coliin the absence of T7 infection and thus independently of T7-encoded factors. It seems that overexpression ofudkreduces Gp2 stability and functionality during T7 infection, which consequently results in inadequate inhibition of host RNAp and in the accumulation of early T7 transcripts. In other words, overexpression ofudkmimics the absence of Gp2 during T7 infection. Our study suggests that the transcriptional regulation of the T7 genome is surprisingly complex and might potentially be affected at many levels by phage- and host-encoded factors.