Discovery of a Natural Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis elegans.
Discovery of a Natural Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis elegans.
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DOI：
10.1371/journal.ppat.1005724
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发表时间：
2016-06
期刊：
影响因子：
6.7
通讯作者：
Troemel ER
中科院分区：
文献类型：
--
作者：
Luallen RJ;Reinke AW;Tong L;Botts MR;Félix MA;Troemel ER
微生物病原体通常在其宿主的特定小生境内建立感染以进行复制。确定感染如何优先发生在特定的宿主组织是理解宿主-微生物相互作用的一个关键方面。在这里，我们描述了一种天然的微孢子虫寄生虫的线虫秀丽隐杆线虫，显示出独特的组织向性相比，以前描述的寄生虫的这个主机的发现。我们描述了这个新物种的生命周期，杀线虫线虫，包括病原体进入，细胞内复制和退出。N.该菌可侵入多种宿主组织，包括表皮、肌肉、神经元和肠。优雅的。尽管肠的强大入侵很少发生复制，与大多数复制发生在肌肉和表皮。这一特征区别于N。两种密切相关的微孢子虫病原体N. parisii和N. sp.1，它只在肠道内侵入和复制。N.与N. parisii和N. sp. 1的结果表明，N.杀线虫是杀线虫属中最早分化的种。N.拟南芥基因组属于一个单一的物种特异性的RING结构域家族，包含功能未知的蛋白质，可能介导与宿主的相互作用。总而言之，该系统提供了一个强大的整体动物模型，以调查病原体在不同组织生态位中生长的因素。病原体在来自宿主生物体的选择压力下进化，以成功地在宿主的不同细胞和组织中侵入和增殖，以获得自身利益。微孢子虫是最成功的病原体之一，其基因组严重减少，核心细胞和代谢途径丧失，使其依赖于宿主细胞进行自身增殖。我们在法国巴黎周围进行了野生线虫感染自然病原体的采样，并发现了一种感染了新微孢子虫物种的野生秀丽隐杆线虫。我们描述了这个新物种的生命周期，显示病原体通过宿主进食进入，在多个宿主组织中复制，并通过一种新的外阴爆裂机制作为新的孢子退出，这使我们将这个物种命名为杀线虫线虫。尽管N.尽管寄生虫在感染过程中侵入多个宿主组织，但我们发现寄生虫在肠道中几乎没有复制。N.与此形成鲜明对比的是它的两个最接近的物种，杀线虫Parisii和杀线虫sp.1，这两个物种只在C.优美的我们比较了这些相关物种的基因组，发现N。Escherodere将其基因组的10%以上用于一个在任何其他物种中都没有发现的单一大基因家族，并提出它们编码的蛋白质可能在感染期间与宿主因子相互作用。
Microbial pathogens often establish infection within particular niches of their host for replication. Determining how infection occurs preferentially in specific host tissues is a key aspect of understanding host-microbe interactions. Here, we describe the discovery of a natural microsporidian parasite of the nematode Caenorhabditis elegans that displays a unique tissue tropism compared to previously described parasites of this host. We characterize the life cycle of this new species, Nematocida displodere, including pathogen entry, intracellular replication, and exit. N. displodere can invade multiple host tissues, including the epidermis, muscle, neurons, and intestine of C. elegans. Despite robust invasion of the intestine very little replication occurs there, with the majority of replication occurring in the muscle and epidermis. This feature distinguishes N. displodere from two closely related microsporidian pathogens, N. parisii and N. sp. 1, which exclusively invade and replicate in the intestine. Comparison of the N. displodere genome with N. parisii and N. sp. 1 reveals that N. displodere is the earliest diverging species of the Nematocida genus. Over 10% of the proteins encoded by the N. displodere genome belong to a single species-specific family of RING-domain containing proteins of unknown function that may be mediating interactions with the host. Altogether, this system provides a powerful whole-animal model to investigate factors responsible for pathogen growth in different tissue niches. Pathogens evolve under selective pressure from host organisms to successfully invade and proliferate in different cells and tissues of the host for their own benefit. Microsporidia represent one of the most successful phyla of pathogens, with severely reduced genomes and loss of core cellular and metabolic pathways making them dependent on host cells for their own proliferation. We sampled around Paris, France, for wild nematodes infected with natural pathogens, and discovered a wild Caenorhabditis elegans that was infected with a new species of microsporidia. We characterize the life cycle of this new species, showing the pathogen enters via host feeding, replicates in multiple host tissues, and exits as new spores via a novel vulva bursting mechanism, leading us to name this species Nematocida displodere. Despite the capacity of N. displodere to invade multiple host tissues during infection, we found that the parasite showed very little replication in the intestine. This unique tissue specificity of N. displodere stands in stark contrast to its two closest-related species, Nematocida parisii and Nematocida sp. 1, which exclusively infect and proliferate in the intestine of C. elegans. We compared the genomes of these related species and found that N. displodere devotes over 10% of its genome to a single large gene family not found in any other species, and propose that their encoded proteins may be interacting with host factors during infection.