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在表达小 RNA OOP 的 cII-oop 构建体中,噬菌体 λ CII 的互补、细胞毒性和复制抑制表型受到抑制。

The Bacteriophage Lambda CII Phenotypes for Complementation, Cellular Toxicity and Replication Inhibition Are Suppressed in cII-oop Constructs Expressing the Small RNA OOP.

机构信息

Department of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada.

出版信息

Viruses. 2018 Mar 7;10(3):115. doi: 10.3390/v10030115.

DOI:10.3390/v10030115
PMID:29518935
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5869508/
Abstract

The temperate bacteriophage lambda (λ) CII protein is a positive regulator of transcription from promoter , a component of the lysogenic response. The expression of was examined in vectors devoid of phage transcription-modulating elements. Their removal enabled evaluating if the expression of the small RNA OOP, on its own, could suppress CII activities, including complementing for a lysogenic response, cell toxicity and causing rapid cellular loss of ColE1 plasmids. The results confirm that OOP RNA expression from the genetic element can prevent the ability of plasmid-encoded CII to complement for a lysogenic response, suggesting that it serves as a powerful regulatory pivot in λ development. Plasmids with a promoter sequence of 45 nucleotides (45), containing the -10 and -35 regions for , were non-functional; whereas, plasmids with 94 prevented CII complementation, CII-dependent plasmid loss and suppressed CII toxicity, suggesting the promoter has an extended DNA sequence. All three CII activities were eliminated by the deletion of the COOH-terminal 20 amino acids of CII. Host mutations in the locus, in and in influenced CII activities. These studies suggest that the COOH-terminal end of CII likely interacts with the β-subunit of RNA polymerase.

摘要

温和噬菌体 λ(λ)CII 蛋白是启动子转录的正调控因子,是溶原反应的组成部分。在没有噬菌体转录调节元件的载体中检查了 的表达。它们的去除使得评估小 RNA OOP 的表达是否可以单独抑制 CII 活性,包括补充溶原反应、细胞毒性和导致 ColE1 质粒的快速细胞丢失成为可能。结果证实,来自遗传元件 的 OOP RNA 表达可以阻止质粒编码的 CII 补充溶原反应的能力,表明它在 λ 的发育中起着强大的调节枢轴作用。含有 45 个核苷酸(45)的 -10 和 -35 区域的 45 个核苷酸启动子序列的质粒无功能;而含有 94 个的质粒则阻止了 CII 的互补、CII 依赖性质粒丢失和抑制 CII 毒性,这表明 启动子具有扩展的 DNA 序列。CII 的三个活性均被 CII 的羧基末端 20 个氨基酸的缺失所消除。宿主在 基因座、 和 中的突变影响了 CII 的活性。这些研究表明,CII 的羧基末端可能与 RNA 聚合酶的 β 亚基相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/d61515a84470/viruses-10-00115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/195586f8fc14/viruses-10-00115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/11f2631fab6e/viruses-10-00115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/d61515a84470/viruses-10-00115-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/195586f8fc14/viruses-10-00115-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/11f2631fab6e/viruses-10-00115-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/418b/5869508/d61515a84470/viruses-10-00115-g003.jpg

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