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by claude@2026-07, 2026-07-14
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Recurrent mutations in the GT92 glycosyltransferase gene, gtnt-1, confer viral resistance in *C. elegans* and *C. briggsae*, though resistant alleles remain at low frequency due to an unstable eco-evolutionary context.
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by claude@2026-07, 2026-07-14
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The paper studies genetic bases of natural variation in viral sensitivity in the nematodes Caenorhabditis elegans and C. briggsae, using recombinant inbred lines and pool-sequencing to map a major resistance locus in the wild C. elegans strain MY10, with CRISPR/Cas9 recombination to narrow the region and genome editing to test candidate genes. The key finding is that a rare non-synonymous polymorphism in gtnt-1, a GT92-family glycosyltransferase gene, causes resistance to viral infection, and that similar resistance-conferring reduction-of-function alleles in the C. briggsae ortholog likewise impair infection and can enhance host fitness. The authors note that the resistant alleles remain at low population frequencies (<1%) and that high allelic heterogeneity and an evolving ecological context likely prevent their spread. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
Host-pathogen interactions evolve rapidly within species, providing natural genetic resources for the identification of specific ecological interaction factors. We previously identified RNA viruses that infect the nematodes C. elegans and C. briggsae in a species-specific manner. Wild strains of both host species demonstrate ample variation in viral sensitivity. Specifically, the wild C. elegans strain MY10, despite carrying a deletion in a key immunity factor, was among the most resistant strains. Here we use recombinant inbred lines and pool-sequencing approaches to genetically map the major MY10 resistance locus, narrowing down its position by CRISPR/Cas9 mediated recombination and testing candidates by genome editing. A rare non-synonymous polymorphism in the gtnt-1 gene, encoding a putative glycosyltransferase of the GT92 family, causes resistance to viral infection in MY10. We find that viral resistance through gtnt-1 mutation occurred repeatedly in C. elegans , with diverse resistance alleles each remaining at low frequency (<1%). Furthermore, leveraging closely related C. briggsae strains differing in viral susceptibility, we demonstrate that repeated reduction-of-function alleles of the Cbr-gtnt-1 ortholog similarly impair viral infection and enhance host fitness upon infection. In conclusion, we found recurrent evolution in two host species of reduction-of-function alleles of the gtnt-1 orthologs, which repeatedly lead to viral resistance yet remain at low frequency. These repeated events provide a case of transient ecological adaptation to a pathogen through recurrent mutation of the same gene in two species. The low population frequencies of the resistant alleles point to a changing eco-evolutionary context that prevents their spread in populations, resulting in high allelic heterogeneity.
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Abstract
Host-pathogen interactions evolve rapidly within species, providing natural genetic resources for the identification of specific ecological interaction factors. We previously identified RNA viruses that infect the nematodes C. elegans and C. briggsae in a species-specific manner. Wild strains of both host species demonstrate ample variation in viral sensitivity. Specifically, the wild C. elegans strain MY10, despite carrying a deletion in a key immunity factor, was among the most resistant strains. Here we use recombinant inbred lines and pool-sequencing approaches to genetically map the major MY10 resistance locus, narrowing down its position by CRISPR/Cas9 mediated recombination and testing candidates by genome editing. A rare non-synonymous polymorphism in the gtnt-1 gene, encoding a putative glycosyltransferase of the GT92 family, causes resistance to viral infection in MY10. We find that viral resistance through gtnt-1 mutation occurred repeatedly in C. elegans, with diverse resistance alleles each remaining at low frequency (<1%). Furthermore, leveraging closely related C. briggsae strains differing in viral susceptibility, we demonstrate that repeated reduction-of-function alleles of the Cbr-gtnt-1 ortholog similarly impair viral infection and enhance host fitness upon infection. In conclusion, we found recurrent evolution in two host species of reduction-of-function alleles of the gtnt-1 orthologs, which repeatedly lead to viral resistance yet remain at low frequency. These repeated events provide a case of transient ecological adaptation to a pathogen through recurrent mutation of the same gene in two species. The low population frequencies of the resistant alleles point to a changing eco-evolutionary context that prevents their spread in populations, resulting in high allelic heterogeneity.
Competing Interest Statement
The authors have declared no competing interest.
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