Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans

M.G. Sterken, Y. Wang, L.B. Snoek, R.J.M. Volkers, J.A.G. Riksen, K.J. Bosman, G.P. Pijlman, J.E. Kammenga

Research output: Chapter in Book/Report/Conference proceedingAbstract

Abstract

Host-pathogen interactions play a major role in evolutionary selection and in shaping natural genetic variation. Recent identification of viral infection in C. elegans has prompted research into understanding the underlying pathways of Orsay virus (OrV) infection in natural populations. Here we report the dissection of the genetic architecture of OrV infection. We found that wild type Hawaii CB4856 strain was more resistant to OrV than the canonical Bristol N2 strain. To gain insight into the genetic architecture of resistance, 52 fully sequenced recombinant inbred lines (CB4856 x N2 RILs) were exposed to OrV using our recently developed quantitative assay. This led to the identification of two distinct loci on chromosome IV associated with OrV resistance. These loci were both associated with a lower viral load in the CB4856 genotype. Strikingly, these loci do not harbour the recently found drh-1 locus, which encodes a RIG-I like helicase that plays an important role in antiviral RNAi. To verify our results and gain additional insight into the genetic architecture, a panel of 18 introgression lines (ILs) (together covering chromosome IV entirely) was exposed to OrV. Both loci could be verified by ILs, also showing more resistance against OrV infection with the CB4856 locus. Our results provide insight in the loci underlying the higher viral resistance in CB4856. They also form an important step toward identifying polymorphic genes underlying resistance to viral infection in C. elegans.
Original languageEnglish
Title of host publicationProceedings of Evolutionary Biology of Caenorhabditis and other Nematodes
Pages111-111
Publication statusPublished - 2014
EventThe 2014 Evolutionary Biology of Caenorhabditis and other Nematodes Conference, Cambridge, UK -
Duration: 14 Jun 201417 Jun 2014

Conference

ConferenceThe 2014 Evolutionary Biology of Caenorhabditis and other Nematodes Conference, Cambridge, UK
Period14/06/1417/06/14

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Virus Diseases
Viruses
Chromosomes
Host-Pathogen Interactions
RNA Interference
Viral Load
Antiviral Agents
Dissection
Genotype
Research
Population
Genes

Cite this

Sterken, M. G., Wang, Y., Snoek, L. B., Volkers, R. J. M., Riksen, J. A. G., Bosman, K. J., ... Kammenga, J. E. (2014). Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans. In Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes (pp. 111-111)
Sterken, M.G. ; Wang, Y. ; Snoek, L.B. ; Volkers, R.J.M. ; Riksen, J.A.G. ; Bosman, K.J. ; Pijlman, G.P. ; Kammenga, J.E. / Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans. Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes. 2014. pp. 111-111
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abstract = "Host-pathogen interactions play a major role in evolutionary selection and in shaping natural genetic variation. Recent identification of viral infection in C. elegans has prompted research into understanding the underlying pathways of Orsay virus (OrV) infection in natural populations. Here we report the dissection of the genetic architecture of OrV infection. We found that wild type Hawaii CB4856 strain was more resistant to OrV than the canonical Bristol N2 strain. To gain insight into the genetic architecture of resistance, 52 fully sequenced recombinant inbred lines (CB4856 x N2 RILs) were exposed to OrV using our recently developed quantitative assay. This led to the identification of two distinct loci on chromosome IV associated with OrV resistance. These loci were both associated with a lower viral load in the CB4856 genotype. Strikingly, these loci do not harbour the recently found drh-1 locus, which encodes a RIG-I like helicase that plays an important role in antiviral RNAi. To verify our results and gain additional insight into the genetic architecture, a panel of 18 introgression lines (ILs) (together covering chromosome IV entirely) was exposed to OrV. Both loci could be verified by ILs, also showing more resistance against OrV infection with the CB4856 locus. Our results provide insight in the loci underlying the higher viral resistance in CB4856. They also form an important step toward identifying polymorphic genes underlying resistance to viral infection in C. elegans.",
author = "M.G. Sterken and Y. Wang and L.B. Snoek and R.J.M. Volkers and J.A.G. Riksen and K.J. Bosman and G.P. Pijlman and J.E. Kammenga",
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Sterken, MG, Wang, Y, Snoek, LB, Volkers, RJM, Riksen, JAG, Bosman, KJ, Pijlman, GP & Kammenga, JE 2014, Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans. in Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes. pp. 111-111, The 2014 Evolutionary Biology of Caenorhabditis and other Nematodes Conference, Cambridge, UK, 14/06/14.

Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans. / Sterken, M.G.; Wang, Y.; Snoek, L.B.; Volkers, R.J.M.; Riksen, J.A.G.; Bosman, K.J.; Pijlman, G.P.; Kammenga, J.E.

Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes. 2014. p. 111-111.

Research output: Chapter in Book/Report/Conference proceedingAbstract

TY - CHAP

T1 - Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans

AU - Sterken, M.G.

AU - Wang, Y.

AU - Snoek, L.B.

AU - Volkers, R.J.M.

AU - Riksen, J.A.G.

AU - Bosman, K.J.

AU - Pijlman, G.P.

AU - Kammenga, J.E.

PY - 2014

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N2 - Host-pathogen interactions play a major role in evolutionary selection and in shaping natural genetic variation. Recent identification of viral infection in C. elegans has prompted research into understanding the underlying pathways of Orsay virus (OrV) infection in natural populations. Here we report the dissection of the genetic architecture of OrV infection. We found that wild type Hawaii CB4856 strain was more resistant to OrV than the canonical Bristol N2 strain. To gain insight into the genetic architecture of resistance, 52 fully sequenced recombinant inbred lines (CB4856 x N2 RILs) were exposed to OrV using our recently developed quantitative assay. This led to the identification of two distinct loci on chromosome IV associated with OrV resistance. These loci were both associated with a lower viral load in the CB4856 genotype. Strikingly, these loci do not harbour the recently found drh-1 locus, which encodes a RIG-I like helicase that plays an important role in antiviral RNAi. To verify our results and gain additional insight into the genetic architecture, a panel of 18 introgression lines (ILs) (together covering chromosome IV entirely) was exposed to OrV. Both loci could be verified by ILs, also showing more resistance against OrV infection with the CB4856 locus. Our results provide insight in the loci underlying the higher viral resistance in CB4856. They also form an important step toward identifying polymorphic genes underlying resistance to viral infection in C. elegans.

AB - Host-pathogen interactions play a major role in evolutionary selection and in shaping natural genetic variation. Recent identification of viral infection in C. elegans has prompted research into understanding the underlying pathways of Orsay virus (OrV) infection in natural populations. Here we report the dissection of the genetic architecture of OrV infection. We found that wild type Hawaii CB4856 strain was more resistant to OrV than the canonical Bristol N2 strain. To gain insight into the genetic architecture of resistance, 52 fully sequenced recombinant inbred lines (CB4856 x N2 RILs) were exposed to OrV using our recently developed quantitative assay. This led to the identification of two distinct loci on chromosome IV associated with OrV resistance. These loci were both associated with a lower viral load in the CB4856 genotype. Strikingly, these loci do not harbour the recently found drh-1 locus, which encodes a RIG-I like helicase that plays an important role in antiviral RNAi. To verify our results and gain additional insight into the genetic architecture, a panel of 18 introgression lines (ILs) (together covering chromosome IV entirely) was exposed to OrV. Both loci could be verified by ILs, also showing more resistance against OrV infection with the CB4856 locus. Our results provide insight in the loci underlying the higher viral resistance in CB4856. They also form an important step toward identifying polymorphic genes underlying resistance to viral infection in C. elegans.

M3 - Abstract

SP - 111

EP - 111

BT - Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes

ER -

Sterken MG, Wang Y, Snoek LB, Volkers RJM, Riksen JAG, Bosman KJ et al. Dissecting the genetic architecture of resistance to orsay virus infection in C. elegans. In Proceedings of Evolutionary Biology of Caenorhabditis and other Nematodes. 2014. p. 111-111