High-throughput phenotyping of infection by diverse microsporidia species reveals a wild C. elegans strain with opposing resistance and susceptibility traits.
High-throughput phenotyping of infection by diverse microsporidia species reveals a wild C. elegans strain with opposing resistance and susceptibility traits.
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对不同微孢子虫物种感染的高通量表型分析揭示了一种具有相反耐药性和易感性特征的野生线虫菌株。
DOI：
10.1371/journal.ppat.1011225
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发表时间：
2023-03
期刊：
影响因子：
6.7
通讯作者：
中科院分区：
文献类型：
--
作者：
动物不断受到来自无数不同病原体的选择压力。微孢子虫是无处不在的动物寄生虫，但它们对塑造动物基因组的影响大多是未知的。采用多重竞争法测定了4种不同微孢子虫对22株秀丽隐杆线虫野生分离株的影响。这导致了13个菌株的鉴定和确认，这些菌株在感染条件下的种群适应度谱发生了显著变化。其中鉴定的菌株JU1400对一种表皮感染物种敏感，对感染缺乏耐受性。JU1400对一种肠道感染菌也有抗性，并能特异性识别和摧毁这种病原体。JU1400的遗传图谱表明，这两种相反的表型是由不同的基因座引起的。转录分析显示，JU1400对表皮微孢子虫感染的敏感性导致了与毒素诱导反应相似的反应模式。相反，我们没有观察到在转录水平上调控JU1400肠道耐药。对这四种微孢子虫的转录反应是保守的，秀丽隐杆线虫在潜在免疫基因上存在菌株特异性差异。总之，我们的研究结果表明，秀丽隐杆线虫对微孢子虫感染的表型差异是常见的，动物可以进化出物种特异性的遗传相互作用。动物在一个种群中表现出多种不同的特征。不同人群的一个特征是对传染病的易感性。微孢子虫是一种普遍存在的动物寄生虫，可感染大多数动物，但这些寄生虫对动物进化和多样性的影响尚不清楚。利用模式生物秀丽隐杆线虫（Caenorhabditis elegans）的野生分离株，我们测试了四种自然发生的微孢子虫对感染的反应多样性。这些实验是用一种混合分析方法完成的，这种方法可以确定不同感染条件下人群中菌株的相对丰度。这些实验确定了一种秀丽隐杆线虫菌株，它对一种微孢子虫感染敏感，但对另一种微孢子虫感染有抗性。遗传作图实验表明，不同的遗传区域负责这些不同的感染反应。总之，我们的研究表明秀丽隐杆线虫对微孢子虫感染的易感性存在差异，并表明这些寄生虫可能对动物进化有很大影响。
Animals are under constant selective pressure from a myriad of diverse pathogens. Microsporidia are ubiquitous animal parasites, but the influence they exert on shaping animal genomes is mostly unknown. Using multiplexed competition assays, we measured the impact of four different species of microsporidia on 22 wild isolates of Caenorhabditis elegans. This resulted in the identification and confirmation of 13 strains with significantly altered population fitness profiles under infection conditions. One of these identified strains, JU1400, is sensitive to an epidermal-infecting species by lacking tolerance to infection. JU1400 is also resistant to an intestinal-infecting species and can specifically recognize and destroy this pathogen. Genetic mapping of JU1400 demonstrates that these two opposing phenotypes are caused by separate loci. Transcriptional analysis reveals the JU1400 sensitivity to epidermal microsporidia infection results in a response pattern that shares similarity to toxin-induced responses. In contrast, we do not observe JU1400 intestinal resistance being regulated at the transcriptional level. The transcriptional response to these four microsporidia species is conserved, with C. elegans strain-specific differences in potential immune genes. Together, our results show that phenotypic differences to microsporidia infection amongst C. elegans are common and that animals can evolve species-specific genetic interactions. Animals display a large diversity of different characteristics within a population. One characteristic that varies within populations is susceptibility to infectious disease. Microsporidia are ubiquitous animal parasites that infect most types of animals, but the influence that these parasites have had on animal evolution and diversity is not well understood. Using wild isolates of the model organism Caenorhabditis elegans, we tested the diversity of responses to infection by four naturally occurring microsporidia species. These experiments were done with a pooled assay that allowed for the determination of the relative abundance of strains within a population under different infection conditions. These experiments identified a C. elegans strain that is sensitive to infection by one species of microsporidia but resistant to another. Genetic mapping experiments show that different genetic regions are responsible for these different infection responses. Together our study demonstrates that there is variability in the susceptibility of C. elegans to microsporidia infection and suggests that these parasites have likely had a large influence on animal evolution.
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DOI：
10.1038/ismej.2015.259
发表时间：
2016-08
期刊：
The ISME journal
影响因子：
--
作者：
通讯作者：
--
影响因子：
14.9
作者：
Cook, Daniel E.;Zdraljevic, Stefan;Andersen, Erik C.
通讯作者：
Andersen, Erik C.
DOI：
10.1073/pnas.1909369117
发表时间：
2020-02-18
影响因子：
11.1
作者：
Edgerton, Elizabeth B.;McCrea, Abigail R.;Povelones, Michael
通讯作者：
Povelones, Michael
影响因子：
2.6
作者：
Dirksen, Philipp;Assie, Adrien;Samuel, Buck S.
通讯作者：
Samuel, Buck S.
影响因子：
3.3
作者：
Capaul, M;Ebert, D
通讯作者：
Ebert, D