Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in two Caenorhabditis species
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 Caenorhabditis elegans and Caenorhabditis briggsae in a species-specific manner. Wild strains of both host species demonstrate ample variation in viral sensitivity. Here we use recombinant inbred lines and pool-sequencing approaches to genetically map a major resistance locus in the C. elegans MY10 strain, 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. Loss-of-function gtnt-1 alleles conferred host protection only at late developmental stages, highlighting the importance of multigenerational assays capturing the full course of viral infection and transmission. Viral resistance through gtnt-1 mutation occurred repeatedly in C. elegans, with diverse alleles each remaining at low frequency (<1%). Furthermore, leveraging closely related C. briggsae strains differing in viral susceptibility, we find that repeated loss-of-function alleles of the Cbr-gtnt-1 ortholog similarly enhanced resistance and host fitness upon infection. In conclusion, recurrent evolution in two host species of loss-of-function alleles of gtnt-1 orthologs leads to viral resistance. The gtnt-1 gene being conserved between Caenorhabditis species, these repeated inactivation 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 resistant alleles point to a changing eco-evolutionary context that prevents their spread in populations.
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BibTeX
@article{richaud2026repeated,
title = {{Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in two Caenorhabditis species}},
author = {Aurélien Richaud and Gaotian Zhang and Cigdem Alkan and Daria Martynow and Tony Bélicard and Nanako Takeda and Eillen Tecle and Marie-Anne Félix},
journal = {Molecular Biology and Evolution},
year = {2026},
month = oct,
doi = {10.1093/molbev/msag208},
url = {https://hal.science/hal-05795640v1},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in two Caenorhabditis species
AU - Aurélien Richaud
AU - Gaotian Zhang
AU - Cigdem Alkan
AU - Daria Martynow
AU - Tony Bélicard
AU - Nanako Takeda
AU - Eillen Tecle
AU - Marie-Anne Félix
PY - 2026
DA - 2026/10/12
JO - Molecular Biology and Evolution
DO - 10.1093/molbev/msag208
UR - https://hal.science/hal-05795640v1
AB - 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 Caenorhabditis elegans and Caenorhabditis briggsae in a species-specific manner. Wild strains of both host species demonstrate ample variation in viral sensitivity. Here we use recombinant inbred lines and pool-sequencing approaches to genetically map a major resistance locus in the C. elegans MY10 strain, 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. Loss-of-function gtnt-1 alleles conferred host protection only at late developmental stages, highlighting the importance of multigenerational assays capturing the full course of viral infection and transmission. Viral resistance through gtnt-1 mutation occurred repeatedly in C. elegans, with diverse alleles each remaining at low frequency (<1%). Furthermore, leveraging closely related C. briggsae strains differing in viral susceptibility, we find that repeated loss-of-function alleles of the Cbr-gtnt-1 ortholog similarly enhanced resistance and host fitness upon infection. In conclusion, recurrent evolution in two host species of loss-of-function alleles of gtnt-1 orthologs leads to viral resistance. The gtnt-1 gene being conserved between Caenorhabditis species, these repeated inactivation 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 resistant alleles point to a changing eco-evolutionary context that prevents their spread in populations.
SN - 0737-4038
SN - 1537-1719
ER -