ArticleBMC biology2016
A quantitative genome-wide RNAi screen in C. elegans for antifungal innate immunity genes.
Article in BMC biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 62 citations in OpenAlex.
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- Development and optimization of large-scale approaches to identify iron-related genes inFrontiers in microbiology · 2025Article
- A defining member of the new cysteine-cradle family is an aECM protein signalling skin damage inbioRxiv : the preprint server for biology · 2024Article
- The Caenorhabditis elegans cuticle and precuticle: a model for studying dynamic apical extracellular matrices in vivo.Genetics · 2024Review
- Alternative Non-Mammalian Animal and Cellular Methods for the Study of Host-Fungal Interactions.Journal of fungi (Basel, Switzerland) · 2023Review
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- Meisosomes, folded membrane microdomains between the apical extracellular matrix and epidermis.eLife · 2023Article
- A pals-25 gain-of-function allele triggers systemic resistance against natural pathogens of C. elegans.PLoS genetics · 2022Article
- Forward genetic screening identifies novel roles for N-terminal acetyltransferase C and histone deacetylase in C. elegans development.Scientific reports · 2022Article
- Identification of healthspan-promoting genes in Caenorhabditis elegans based on a human GWAS study.Biogerontology · 2022Article
- Quantification of tissue-specific protein translation in wholeCell reports methods · 2022Article
- Wild-type Caenorhabditis elegans isolates exhibit distinct gene expression profiles in response to microbial infection.BMC genomics · 2022Article
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- C. elegans: out on an evolutionary limb.Immunogenetics · 2022Review
- ATFS-1 plays no repressive role in the regulation of epidermal immune response.microPublication biology · 2022Article
- The small-secreted cysteine-rich protein CyrA is a virulence factor participating in the attack of Caenorhabditis elegans by Duddingtonia flagrans.PLoS pathogens · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundCaenorhabditis elegans has emerged over the last decade as a useful model for the study of innate immunity. Its infection with the pathogenic fungus Drechmeria coniospora leads to the rapid up-regulation in the epidermis of genes encoding antimicrobial peptides. The molecular basis of antimicrobial peptide gene regulation has been previously characterized through forward genetic screens. Reverse genetics, based on RNAi, provide a complementary approach to dissect the worm's immune defenses.
resultsWe report here the full results of a quantitative whole-genome RNAi screen in C. elegans for genes involved in regulating antimicrobial peptide gene expression. The results will be a valuable resource for those contemplating similar RNAi-based screens and also reveal the limitations of such an approach. We present several strategies, including a comprehensive class clustering method, to overcome these limitations and which allowed us to characterize the different steps of the interaction between C. elegans and the fungus D. coniospora, leading to a complete description of the MAPK pathway central to innate immunity in C. elegans. The results further revealed a cross-tissue signaling, triggered by mitochondrial dysfunction in the intestine, that suppresses antimicrobial peptide gene expression in the nematode epidermis.
conclusionsOverall, our results provide an unprecedented system's level insight into the regulation of C. elegans innate immunity. They represent a significant contribution to our understanding of host defenses and will lead to a better comprehension of the function and evolution of animal innate immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.