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新型古菌质粒pAH1及其与脂毛病毒AFV1的相互作用。

Novel archaeal plasmid pAH1 and its interactions with the lipothrixvirus AFV1.

作者信息

Basta Tamara, Smyth John, Forterre Patrick, Prangishvili David, Peng Xu

机构信息

Institut Pasteur, 25 Rue du Dr. Roux, 75015 Paris, France.

出版信息

Mol Microbiol. 2009 Jan;71(1):23-34. doi: 10.1111/j.1365-2958.2008.06488.x. Epub 2008 Nov 10.

Abstract

At present very little is known about interactions between extrachromosomal genetic elements in Archaea. Here we describe an Acidianus strain which carries naturally a novel 28 kb conjugative plasmid-like element, pAH1, and also serves as a laboratory host for lipothrixvirus AFV1. In an attempt to establish a system for studying plasmid-virus interactions we characterized the genome of pAH1 which closely resembles those of the Sulfolobus conjugative plasmids pARN3 and pARN4. pAH1 integrates site specifically into, and excises from, the host chromosome indicating a dynamic interaction with the latter. Although nucleotide sequence comparisons revealed extensive intergenomic exchange during the evolution of archaeal conjugative plasmids, pAH1 was shown to be stably maintained suggesting that the host system is suitable for studying plasmid-virus interactions. AFV1 infection and propagation leads to a loss of the circular form of pAH1 and this effect correlates positively with the increase in the intracellular quantity of AFV1 DNA. We infer that the virus inhibits plasmid replication since no pAH1 degradation was observed. This mechanism of archaeal viral inhibition of plasmid propagation is not observed in bacteria where relevant bacteriophages either are dependent on a conjugative plasmid for successful infection or are excluded by a resident plasmid.

摘要

目前,关于古菌中染色体外遗传元件之间的相互作用,人们了解甚少。在此,我们描述了一株嗜酸菌,它天然携带一种新型的28 kb接合性质粒样元件pAH1,并且还作为脂毛病毒AFV1的实验室宿主。为了建立一个研究质粒 - 病毒相互作用的系统,我们对pAH1的基因组进行了表征,它与硫化叶菌接合质粒pARN3和pARN4的基因组非常相似。pAH1特异性地整合到宿主染色体中,并从宿主染色体上切除,这表明它与宿主染色体存在动态相互作用。尽管核苷酸序列比较显示在古菌接合质粒的进化过程中发生了广泛的基因组间交换,但pAH1被证明能稳定维持,这表明宿主系统适合用于研究质粒 - 病毒相互作用。AFV1感染和繁殖会导致pAH1的环状形式丢失,并且这种效应与AFV1 DNA细胞内数量的增加呈正相关。我们推断病毒抑制了质粒复制,因为未观察到pAH1的降解。在细菌中未观察到古菌病毒抑制质粒传播的这种机制,在细菌中,相关噬菌体要么依赖接合质粒进行成功感染,要么被常驻质粒排除。

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