scholarly journals The genetic basis of Drosophila melanogaster defense against Beauveria bassiana explored through evolve and resequence and quantitative trait locus mapping

2021 ◽  
Author(s):  
Parvin Shahrestani ◽  
Elizabeth King ◽  
Reza Ramezan ◽  
Mark Phillips ◽  
Melissa Riddle ◽  
...  

Many of the molecular mechanisms for antifungal immunity in Drosophila melanogaster have been defined, but relatively little is known about the genetic basis for variation in antifungal immunity in natural populations. Using two population genetic approaches, Quantitative Trait Locus (QTL) Mapping and Evolve and Resequence (E&R), we explored the genetics underlying D. melanogaster immune defense against infection with the fungus Beauveria bassiana. Immune defense was highly variable both in the recombinant inbred lines from the Drosophila Synthetic Population Resource used for our QTL Mapping and in the synthetic outbred populations used in our E&R study. Survivorship of infection improved dramatically over just 10 generations in the E&R study, and continued to increase for an additional 9 generations, revealing a trade-off with uninfected longevity. Populations selected for increased defense against B. bassiana evolved cross resistance to a second, distinct B. bassiana strain but not to bacterial pathogens. The QTL mapping study revealed that sexual dimorphism in defense depends on host genotype, and the E&R study indicated that dimorphism also depends on the specific pathogen to which the host is exposed. Both the QTL Mapping and E&R experiments generated lists of potentially causal candidate genes, although these lists were non-overlapping.

Author(s):  
Parvin Shahrestani ◽  
Elizabeth King ◽  
Reza Ramezan ◽  
Mark Phillips ◽  
Melissa Riddle ◽  
...  

Abstract Little is known about the genetic architecture of antifungal immunity in natural populations. Using two population genetic approaches, Quantitative Trait Locus (QTL) Mapping and Evolve and Resequence (E&R), we explored D. melanogaster immune defense against infection with the fungus Beauveria bassiana. Immune defense was highly variable both in the recombinant inbred lines from the Drosophila Synthetic Population Resource used for our QTL mapping and in the synthetic outbred populations used in our E&R study. Survivorship of infection improved dramatically over just 10 generations in the E&R study, and continued to increase for an additional 9 generations, revealing a trade-off with uninfected longevity. Populations selected for increased defense against B. bassiana evolved cross resistance to a second, distinct B. bassiana strain but not to bacterial pathogens. The QTL mapping study revealed that sexual dimorphism in defense depends on host genotype, and the E&R study indicated that sexual dimorphism also depends on the specific pathogen to which the host is exposed. Both the QTL mapping and E&R experiments generated lists of potentially causal candidate genes, although these lists were non-overlapping.


Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 581-588
Author(s):  
Mohamed A F Noor ◽  
Aimee L Cunningham ◽  
John C Larkin

Abstract We examine the effect of variation in gene density per centimorgan on quantitative trait locus (QTL) mapping studies using data from the Drosophila melanogaster genome project and documented regional rates of recombination. There is tremendous variation in gene density per centimorgan across this genome, and we observe that this variation can cause systematic biases in QTL mapping studies. Specifically, in our simulated mapping experiments of 50 equal-effect QTL distributed randomly across the physical genome, very strong QTL are consistently detected near the centromeres of the two major autosomes, and few or no QTL are often detected on the X chromosome. This pattern persisted with varying heritability, marker density, QTL effect sizes, and transgressive segregation. Our results are consistent with empirical data collected from QTL mapping studies of this species and its close relatives, and they explain the “small X-effect” that has been documented in genetic studies of sexual isolation in the D. melanogaster group. Because of the biases resulting from recombination rate variation, results of QTL mapping studies should be taken as hypotheses to be tested by additional genetic methods, particularly in species for which detailed genetic and physical genome maps are not available.


2021 ◽  
Author(s):  
Alex N. Nguyen Ba ◽  
Katherine R. Lawrence ◽  
Artur Rego-Costa ◽  
Shreyas Gopalakrishnan ◽  
Daniel Temko ◽  
...  

Mapping the genetic basis of complex traits is critical to uncovering the biological mechanisms that underlie disease and other phenotypes. Genome-wide association studies (GWAS) in humans and quantitative trait locus (QTL) mapping in model organisms can now explain much of the observed heritability in many traits, allowing us to predict phenotype from genotype. However, constraints on power due to statistical confounders in large GWAS and smaller sample sizes in QTL studies still limit our ability to resolve numerous small-effect variants, map them to causal genes, identify pleiotropic effects across multiple traits, and infer non-additive interactions between loci (epistasis). Here, we introduce barcoded bulk quantitative trait locus (BB-QTL) mapping, which allows us to construct, genotype, and phenotype 100,000 offspring of a budding yeast cross, two orders of magnitude larger than the previous state of the art. We use this panel to map the genetic basis of eighteen complex traits, finding that the genetic architecture of these traits involves hundreds of small-effect loci densely spaced throughout the genome, many with widespread pleiotropic effects across multiple traits. Epistasis plays a central role, with thousands of interactions that provide insight into genetic networks. By dramatically increasing sample size, BB-QTL mapping demonstrates the potential of natural variants in high-powered QTL studies to reveal the highly polygenic, pleiotropic, and epistatic architecture of complex traits.Significance statementUnderstanding the genetic basis of important phenotypes is a central goal of genetics. However, the highly polygenic architectures of complex traits inferred by large-scale genome-wide association studies (GWAS) in humans stand in contrast to the results of quantitative trait locus (QTL) mapping studies in model organisms. Here, we use a barcoding approach to conduct QTL mapping in budding yeast at a scale two orders of magnitude larger than the previous state of the art. The resulting increase in power reveals the polygenic nature of complex traits in yeast, and offers insight into widespread patterns of pleiotropy and epistasis. Our data and analysis methods offer opportunities for future work in systems biology, and have implications for large-scale GWAS in human populations.


Author(s):  
Hannah E. Bainbridge ◽  
Melanie N. Brien ◽  
Carlos Morochz ◽  
Patricio A. Salazar ◽  
Pasi Rastas ◽  
...  

AbstractMimetic systems allow us to address the question of whether the same genes control similar phenotypes in different species. Although widespread parallels have been found for major effect loci, much less is known about genes that control quantitative trait variation. In this study, we identify and compare the loci that control subtle changes in the size and shape of forewing pattern elements in two Heliconius butterfly co-mimics. We use quantitative trait locus (QTL) analysis with a multivariate phenotyping approach to map the variation in red pattern elements across the whole forewing surface of Heliconius erato and Heliconius melpomene. These results are compared to a QTL analysis of univariate trait changes, and show that our resolution for identifying small effect loci is improved with the multivariate approach. QTL likely corresponding to the known patterning gene optix were found in both species but otherwise, a remarkably low level of genetic parallelism was found. This lack of similarity indicates that the genetic basis of convergent traits may not be as predictable as assumed from studies that focus solely on Mendelian traits.


Author(s):  
Hui-Chen Hsu ◽  
Lu Lu ◽  
Nengjun Yi ◽  
Gary Zant ◽  
Robert W. Williams ◽  
...  

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