Genetic Variation in Caenorhabditis elegans Responses to Pathogenic Microbiota

Huang, Yuqing; Kammenga, J.E.

doi:10.3390/microorganisms8040618

Cited by 8 publications

(9 citation statements)

References 61 publications

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“…To facilitate the study of natural diversity, hundreds of isolates of C. elegans have been collected from around the world [33]. These wild isolates have different levels of susceptibility to pathogens and natural variants have been discovered that impact traits such as bacterial avoidance and viral susceptibility [7,19,[34][35][36][37]. Although studying phenotypic variation in wild isolates is a powerful approach, measuring each strain individually is time-consuming and laborious.…”

Section: Introductionmentioning

confidence: 99%

High-throughput phenotyping of infection by diverse microsporidia species reveals a wildC. elegansstrain with opposing resistance and susceptibility traits

Mok

Xiao

Wan

et al. 2022

Preprint

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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 of 13 strains with altered resistance or sensitivity to infection. 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 alleles. Transcriptional analysis reveals that this lack of tolerance in JU1400 results in a response that shares similarity to that induced by toxins. In contrast, we do not observe JU1400 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.

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Section: Introductionmentioning

confidence: 99%

High-throughput phenotyping of infection by diverse microsporidia species reveals a wildC. elegansstrain with opposing resistance and susceptibility traits

Mok

Xiao

Wan

et al. 2022

Preprint

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“… 32 , 33 The worm has also been extensively used in the field of host-pathogen interaction, triggering the regulation of innate immunity 34 as well as a cascade of a wide variety of genes. 35 Similarly, Drosophila has been extensively used as a model to study the phenomenology and the underlying molecular and cellular mechanisms of microbiota-diet interactions and their influence on host biology including postnatal development (ie juvenile growth and maturation), adult physiology (ie immune and metabolic functions and behavior) and aging. 36 , 37 …”

Section: Part a Methods For Studying The Causal Role Of Gut Microbiotamentioning

confidence: 99%

Approaches to discern if microbiome associations reflect causation in metabolic and immune disorders

et al. 2022

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Our understanding of microorganisms residing within our gut and their roles in the host metabolism and immunity advanced greatly over the past 20 years. Currently, microbiome studies are shifting from association and correlation studies to studies demonstrating causality of identified microbiome signatures and identification of molecular mechanisms underlying these interactions. This transformation is crucial for the efficient translation into clinical application and development of targeted strategies to beneficially modulate the intestinal microbiota. As mechanistic studies are still quite challenging to perform in humans, the causal role of microbiota is frequently evaluated in animal models that need to be appropriately selected. Here, we provide a comprehensive overview on approaches that can be applied in addressing causality of host-microbe interactions in five major animal model organisms ( Caenorhabditis elegans, Drosophila melanogaster , zebrafish, rodents, and pigs). We particularly focused on discussing methods available for studying the causality ranging from the usage of gut microbiota transfer, diverse models of metabolic and immune perturbations involving nutritional and chemical factors, gene modifications and surgically induced models, metabolite profiling up to culture-based approached. Furthermore, we addressed the impact of the gut morphology, physiology as well as diet on the microbiota composition in various models and resulting species specificities. Finally, we conclude this review with the discussion on models that can be applied to study the causal role of the gut microbiota in the context of metabolic syndrome and host immunity. We hope this review will facilitate important considerations for appropriate animal model selection.

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“…By comparing viral susceptibility in three different backgrounds, Bristol N2, JU1580, and JU1511, we found that the genetic background may influence the interaction effect of HS and viral infection. It is well known that a different genetic background can have strong differential effects on complex phenotypes [34,35] and that even the phenotypic effects of strong single gene mutations can be modulated. Our results suggest that the genetic background may also have genetic modifiers that can modulate the effect of viral infection in combination with HS.…”

Section: Hs Effects On Orv Viral Load May Depend On the Genetic Backgroundmentioning

confidence: 99%

Heat Stress Reduces the Susceptibility of Caenorhabditis elegans to Orsay Virus Infection

Huang

Sterken

Zwet

et al. 2021

Genes

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The nematode Caenorhabditis elegans has been a versatile model for understanding the molecular responses to abiotic stress and pathogens. In particular, the response to heat stress and virus infection has been studied in detail. The Orsay virus (OrV) is a natural virus of C. elegans and infection leads to intracellular infection and proteostatic stress, which activates the intracellular pathogen response (IPR). IPR related gene expression is regulated by the genes pals-22 and pals-25, which also control thermotolerance and immunity against other natural pathogens. So far, we have a limited understanding of the molecular responses upon the combined exposure to heat stress and virus infection. We test the hypothesis that the response of C. elegans to OrV infection and heat stress are co-regulated and may affect each other. We conducted a combined heat-stress-virus infection assay and found that after applying heat stress, the susceptibility of C. elegans to OrV was decreased. This difference was found across different wild types of C. elegans. Transcriptome analysis revealed a list of potential candidate genes associated with heat stress and OrV infection. Subsequent mutant screens suggest that pals-22 provides a link between viral response and heat stress, leading to enhanced OrV tolerance of C. elegans after heat stress.

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Genetic Variation in Caenorhabditis elegans Responses to Pathogenic Microbiota

Cited by 8 publications

References 61 publications

High-throughput phenotyping of infection by diverse microsporidia species reveals a wildC. elegansstrain with opposing resistance and susceptibility traits

High-throughput phenotyping of infection by diverse microsporidia species reveals a wildC. elegansstrain with opposing resistance and susceptibility traits

Approaches to discern if microbiome associations reflect causation in metabolic and immune disorders

Heat Stress Reduces the Susceptibility of Caenorhabditis elegans to Orsay Virus Infection

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