Molecular evolutionary consequences of niche restriction in Francisella tularensis, a facultative intracellular pathogen.
Molecular evolutionary consequences of niche restriction in Francisella tularensis, a facultative intracellular pathogen.
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DOI：
10.1371/journal.ppat.1000472
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发表时间：
2009-06
期刊：
影响因子：
6.7
通讯作者：
Johansson A
中科院分区：
文献类型：
--
作者：
Larsson P;Elfsmark D;Svensson K;Wikström P;Forsman M;Brettin T;Keim P;Johansson A
土拉热弗朗西丝菌是一种适应细胞内环境的哺乳动物病原菌，而土拉热弗朗西丝菌是一种适应细胞内环境的哺乳动物病原菌。novicida和F. Philomiragia在哺乳动物中毒性较低，并且似乎具有较不专门的生命周期。我们探讨了属内的适应，可能与增加主机协会，如下。首先，我们测定了F.土拉热亚种mediasiatica是唯一一个之前没有被测序的亚种。该基因组和其他12个F. tularensis分离株，然后将其与F. novicida（三株）和F. philomiragia（一个分离物）。在19.2%的F. novicida和F. philomiragia基因，而F.土拉热菌基因组此外，插入序列元件的随机插入似乎为F.土拉热菌，例如用于弗朗西丝氏菌致病性岛的复制和推定的糖基转移酶基因的增殖。此外，F.土拉热似乎已经通过基因功能独立丧失而沿着沿着独立的路线向共同的基因集合会聚。我们的观察表明，尽管平均核苷酸同一性> 97%，F。tularensis和F.杀螨目具有两个明显的种群谱系，前者以克隆结构为特征，净化选择较弱，后者以重组频率较高，净化选择较强。F. tularensis和F.鉴于它们的高度相似性，novicida可以被认为是相同的细菌物种，但是基于这项工作中描述的进化分析，我们建议保留单独的物种名称。胞内细菌土拉热弗朗西丝氏菌（Francisella tularensis）在包括人类在内的各种哺乳动物中引起土拉菌病，并且具有高度传染性（传染性如此之强，以至于在冷战期间开发了高毒性形式的病原体作为生物气溶胶武器）。很少有人知道F。土拉菌存在于自然界中，以及它是如何进化的，但有趣的是，密切相关的弗朗西斯菌的危险性较小。因此，我们探索了形成F的进化事件。通过对17株弗朗西斯菌基因组序列的分析，它的进化似乎涉及许多代谢功能的丧失和随机突变，F.土拉菌菌株此外，增加主机协会似乎有不可逆的分离F。图拉热菌种群与其他弗朗西斯菌种群的区别。这项研究提供了有关相对无害的弗朗西斯菌进化为哺乳动物细胞侵袭性入侵者的过程的新信息。我们的研究结果支持了以前的建议，即识别不同的种群谱系提供了有意义的细菌之间的物种界限。
Francisella tularensis is a potent mammalian pathogen well adapted to intracellular habitats, whereas F. novicida and F. philomiragia are less virulent in mammals and appear to have less specialized lifecycles. We explored adaptations within the genus that may be linked to increased host association, as follows. First, we determined the genome sequence of F. tularensis subsp. mediasiatica, the only subspecies that had not been previously sequenced. This genome, and those of 12 other F. tularensis isolates, were then compared to the genomes of F. novicida (three isolates) and F. philomiragia (one isolate). Signs of homologous recombination were found in ∼19.2% of F. novicida and F. philomiragia genes, but none among F. tularensis genomes. In addition, random insertions of insertion sequence elements appear to have provided raw materials for secondary adaptive mutations in F. tularensis, e.g. for duplication of the Francisella Pathogenicity Island and multiplication of a putative glycosyl transferase gene. Further, the five major genetic branches of F. tularensis seem to have converged along independent routes towards a common gene set via independent losses of gene functions. Our observations suggest that despite an average nucleotide identity of >97%, F. tularensis and F. novicida have evolved as two distinct population lineages, the former characterized by clonal structure with weak purifying selection, the latter by more frequent recombination and strong purifying selection. F. tularensis and F. novicida could be considered the same bacterial species, given their high similarity, but based on the evolutionary analyses described in this work we propose retaining separate species names. The intracellular bacterium Francisella tularensis causes the disease tularemia in various mammals, including humans, and is highly infectious (so infectious that highly virulent forms of the pathogen were developed as biological aerosol weapons during the Cold War). Little is known about where F. tularensis resides in nature and how it evolved but, intriguingly, closely related Francisella bacteria are less dangerous. Therefore, we have explored the evolutionary events that shaped F. tularensis by analyzing 17 Francisella genome sequences. Its evolution appears to have involved many losses of metabolic functions and random mutations, with little exchange of genetic material among F. tularensis strains. Furthermore, increased host association appears to have irreversibly separated F. tularensis populations from other populations of Francisella bacteria. This study provides new information on the processes whereby relatively harmless Francisella bacteria evolved into aggressive invaders of mammalian cells. Our findings support previous proposals that identification of distinct population lineages provides meaningful species boundaries among bacteria.
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影响因子：
3.3
作者：
Didelot, Xavier;Falush, Daniel
通讯作者：
Falush, Daniel
DOI：
10.1073/pnas.0409727102
发表时间：
2005-02-15
影响因子：
11.1
作者：
Konstantinidis, KT;Tiedje, JM
通讯作者：
Tiedje, JM
影响因子：
3.2
作者：
Baek, Chang-Ho;Wang, Shifeng;Curtiss, Roy, III
通讯作者：
Curtiss, Roy, III
影响因子：
3.2
作者：
Dempsey, Michael P.;Nietfeldt, Joseph;Benson, Andrew K.
通讯作者：
Benson, Andrew K.
影响因子：
30.8
作者：
Larsson, P;Oyston, PCF;Titball, RW
通讯作者：
Titball, RW