Abstract
Pathogens impose a high selective pressure on populations, leading to
evolution of the host. Caenorhabditis elegans and its naturally infecting
pathogen, the Orsay virus, form an attractive model to investigate evolved
host defence mechanisms. We have found that the Hawaiian isolate CB4856
is less susceptible to the Orsay virus than the commonly used laboratory
strain N2. We are investigating candidate loci, genes and alleles accountable
for the susceptibility of the N2 strain.
We have measured the viral susceptibility of 52 recombinant inbred lines
(N2xCB4856). This trait was used for QTL mapping, resulting in two loci
on chromosome IV that are related to viral susceptibility: the first spans
from 2.6-4.0 Mb and the second from 12.5-14.9 Mb. Next, this data was
confirmed using a panel of 18 introgression lines containing a CB4856
fragment in an N2 background. The gene drh-1, that was related to viral
susceptibility previously, is not located on the detected loci. Furthermore,
transcriptome data of (un)infected N2 and CB4856 strains was obtained
using microarrays. Although a full analysis of this data has to be performed
yet, mainly small effects were observed between infected and uninfected
strains. Nevertheless, some genes were specifically involved in viral
infection, indicating these could be part of an anti-viral mechanism.
Our results show that undiscovered viral immunity genes and/or pathways
exist in C. elegans. In the end, this project will contribute to identify allelic
variants that evolved as a viral immunity elements. Future work will include
fine mapping of the QTL loci and pinpointing gene specific effects using
CRISPR-Cas9.
evolution of the host. Caenorhabditis elegans and its naturally infecting
pathogen, the Orsay virus, form an attractive model to investigate evolved
host defence mechanisms. We have found that the Hawaiian isolate CB4856
is less susceptible to the Orsay virus than the commonly used laboratory
strain N2. We are investigating candidate loci, genes and alleles accountable
for the susceptibility of the N2 strain.
We have measured the viral susceptibility of 52 recombinant inbred lines
(N2xCB4856). This trait was used for QTL mapping, resulting in two loci
on chromosome IV that are related to viral susceptibility: the first spans
from 2.6-4.0 Mb and the second from 12.5-14.9 Mb. Next, this data was
confirmed using a panel of 18 introgression lines containing a CB4856
fragment in an N2 background. The gene drh-1, that was related to viral
susceptibility previously, is not located on the detected loci. Furthermore,
transcriptome data of (un)infected N2 and CB4856 strains was obtained
using microarrays. Although a full analysis of this data has to be performed
yet, mainly small effects were observed between infected and uninfected
strains. Nevertheless, some genes were specifically involved in viral
infection, indicating these could be part of an anti-viral mechanism.
Our results show that undiscovered viral immunity genes and/or pathways
exist in C. elegans. In the end, this project will contribute to identify allelic
variants that evolved as a viral immunity elements. Future work will include
fine mapping of the QTL loci and pinpointing gene specific effects using
CRISPR-Cas9.
| Original language | English |
|---|---|
| Publication status | Published - 2 Apr 2016 |
| Event | Evolutionary Biology of Caenorhabditis and other nematodes - Cold Spring Harbor Laboratory, Cold Spring Harbor, United States Duration: 30 Mar 2016 → 2 Apr 2016 |
Conference/symposium
| Conference/symposium | Evolutionary Biology of Caenorhabditis and other nematodes |
|---|---|
| Country/Territory | United States |
| City | Cold Spring Harbor |
| Period | 30/03/16 → 2/04/16 |