Abstract
The mechanistic basis for how genetic variants cause differences in phenotypic traits is often elusive. We identified a quantitative trait locus in Caenorhabditis elegans that affects three seemingly unrelated phenotypic traits: lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus. We found a QTL for all three traits arises from variation in the neuropeptide receptor gene npr-1. Moreover, we found that variation in npr-1 is also responsible for differences in 247 gene expression traits. Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn. We found that the allele that leads to aggregation is associated with reduced growth and reproductive output. The altered gene expression pattern caused by this allele suggests that the aggregation behavior might cause a weak starvation state, which is known to reduce growth rate and fecundity. Importantly, we show that variation in npr-1 causes each of these phenotypic differences through behavioral avoidance of ambient oxygen concentrations. These results suggest that variation in npr-1 has broad pleiotropic effects mediated by altered exposure to bacterial food.
Highlights
In recent years, quantitative genetic approaches in the nematode Caenorhabditis elegans have identified quantitative trait genes (QTGs) for a diverse set of phenotypes [1,2,3,4,5,6,7,8,9,10,11,12,13]
Variation in npr-1 is known to determine whether animals disperse throughout a bacterial lawn or aggregate at the edges of the lawn
Using the nematode roundworm Caenorhabditis elegans, we identified differences in lifetime fecundity, adult body size, and susceptibility to the human pathogen Staphyloccus aureus between the laboratory strain (N2) from Bristol, England and a wild strain (CB4856) from Hawaii, USA
Summary
Quantitative genetic approaches in the nematode Caenorhabditis elegans have identified quantitative trait genes (QTGs) for a diverse set of phenotypes [1,2,3,4,5,6,7,8,9,10,11,12,13]. For the 18 years, this strain was propagated in the laboratory for hundreds of generations, which likely led to adaptation to the laboratory environment [7]. The use of the Bristol strain as a parent in recombinant inbred line panels may be expected to result in the identification of variants selected during laboratory adaptation. The use of a laboratoryadapted strain in mapping panels has led to the identification of pleiotropic laboratory-derived variants in the classic model organisms S. cerevisiae [17,18] and A. thaliana [19]. Variants specific to laboratory strains may be expected to show large and widespread phenotypic effects when traits related to fitness are measured in the same laboratory environment in which they were selected
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