Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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Record number 538733
Title Predicting individual differences in viral susceptibility caused by natural genetic variation within species
Author(s) Sluijs, L. van; Sterken, M.G.; Wang, Yiru; Ritmahan, Wannisa; Gultom, Mitra; Pankok, Frederik; Blokhina, T.; Riksen, J.A.G.; Volkers, J.M.; Snoek, L.B.; Pijlman, G.P.; Kammenga, J.E.
Event EMBO Workshop: C. elegans Development, Cell Biology, and Gene Expression, Barcelona, 2018-06-13/2018-06-17
Department(s) Laboratory of Nematology
Systems and Synthetic Biology
PE&RC
Laboratory of Virology
EPS
Publication type Poster (scientific)
Publication year 2018
Abstract Natural genetic variation within species can underlie different individual susceptibilities upon viral infection. The molecular mechanisms by which genetic variation affects the viral susceptibility are currently poorly understood. Here we use Caenorhabditis elegans as a model organism to identify which polymorphisms alter the viral susceptibility. Moreover, we predict how the molecular mechanisms behind altered susceptibilities may work. The viral susceptibility towards Orsay virus of the commonly used lab strain, N2, is higher than that of the Hawaiian isolate CB4856. The phenotype of N2xCB4856 recombinant inbred strains was obtained by measuring the viral load upon infection and these viral loads were correlated to the genotypes by quantitative trait locus (QTL) mapping. A region on chromosome IV was found to correlate with changes in the viral susceptibility. This QTL region, containing hundreds of candidate polymorphisms, was fine mapped using two introgression line panels. The first introgression line panel contained an introgression of N2 into the genome of CB4856, whereas the second panel contained an introgression of CB4856 into the genome of N2. Using these two panels the QTL region was fine mapped to a region containing about 30 polymorphisms. Using known protein structures we predicted possible effects of candidate polymorphisms. An example is a single nucleotide polymorphism in a conserved region of the known antiviral defence gene cul-6. This polymorphism may be responsible for an altered stability of the SCF complex that targets viral particles for degradation. A causal relationship could be experimentally verified by exchanging the polymorphism of the resistant and susceptible strain, an approach we are currently taking.
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