[A case of typical mycobacteriosis due to Mycobacterium ulcerans-like organism (author's transl)].

[A case of typical mycobacteriosis due to Mycobacterium ulcerans-like organism (author's transl)].
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[一例由类溃疡分枝杆菌引起的典型分枝杆菌病(作者译)]。

DOI:
10.1128/jb.187.5.1668-1676.2005
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发表时间:
1982
期刊:
Nihon Hifuka Gakkai zasshi. The Japanese journal of dermatology
影响因子:
--
通讯作者:
M. Tsukamura
M. Tsukamura
中科院分区:
--
文献类型:
--
作者:
H. Mikoshiba;Y. Shindo;H. Matsumoto;M. Mochizuki;M. Tsukamura

文献摘要

被引文献

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溃烂分枝杆菌Agy99菌株的174 kb毒力质粒pMUM001含有三个编码巨型聚酮合成酶(PKS)的同源基因,它们负责合成脂类毒素霉内酯。对FM进行更深入的调查。UlceransAgy99导致在也包含完整质粒的细胞群体中鉴定出两种类型的pMUM001自发缺失变体。这些变异产生于同一质粒序列的两个8kb片段之间的重组,导致带有三个霉菌内酯PKS基因中的两个的65kb区域的丢失。调查了九个不同的M。通过对8个pMUM001基因序列进行聚合酶链式反应和Southern杂交,证实在ALM中存在类似pMUM001的元件(统称为pMUM)。溃烂变种。对这些质粒的物理图谱显示,像M。UlceransAgy99,3个菌株的支原体内酯PKS基因发生了较大的缺失。脂类提取物的在线液相色谱-串联质谱仪分析证实,PKS缺失的菌株不能产生霉菌内酯或任何相关的共代谢产物。菌株间的核苷酸序列同源性超过98%,从这些序列推断的系统发育与以前的多位点序列分型研究中使用的染色体编码基因座的系统发育关系非常相似,这一结果与假设一致。溃疡杆菌通过获得pMUM而与密切相关的组织海洋分枝杆菌发生了分歧。我们的结果表明,pMUM是FM的一个决定性特征。但在缺乏纯化选择的情况下,很容易发生质粒序列的缺失和相应的菌内酯生产的损失。
The 174-kb virulence plasmid pMUM001 inMycobacterium ulceransepidemic strain Agy99 harbors three very large and homologous genes that encode giant polyketide synthases (PKS) responsible for the synthesis of the lipid toxin mycolactone. Deeper investigation ofM. ulceransAgy99 resulted in identification of two types of spontaneous deletion variants of pMUM001 within a population of cells that also contained the intact plasmid. These variants arose from recombination between two 8-kb sections of the same plasmid sequence, resulting in the loss of a 65-kb region bearing two of the three mycolactone PKS genes. Investigation of nine diverseM. ulceransstrains by using PCR and Southern hybridization for eight pMUM001 gene sequences confirmed the presence of pMUM001-like elements (collectively called pMUM) in allM. ulceransstrains. Physical mapping of these plasmids revealed that likeM. ulceransAgy99, three strains had undergone major deletions in their mycolactone PKS loci. Online liquid chromatography-sequential mass spectrometry analysis of lipid extracts confirmed that strains with PKS deletions were unable to produce mycolactone or any related cometabolites. Interstrain comparisons of the plasmid gene sequences revealed greater than 98% nucleotide identity, and the phylogeny inferred from these sequences closely mimicked the phylogeny from a previous multilocus sequence typing study in which chromosomally encoded loci were used, a result that is consistent with the hypothesis thatM. ulceransdiverged from the closely related organismMycobacterium marinumby acquiring pMUM. Our results suggest that pMUM is a defining characteristic ofM. ulceransbut that in the absence of purifying selection, deletion of plasmid sequences and a corresponding loss of mycolactone production readily arise.