The molecular architecture of Drosophila melanogaster defense against Beauveria bassiana explored through evolve and resequence and quantitative trait locus mapping

Author:

Shahrestani Parvin1ORCID,King Elizabeth2,Ramezan Reza3,Phillips Mark4,Riddle Melissa1,Thornburg Marisa1,Greenspan Zachary5,Estrella Yonathan6,Garcia Kelly6,Chowdhury Pratik6,Malarat Glen6,Zhu Ming6,Rottshaefer Susan M6,Wraight Stephen7,Griggs Michael7,Vandenberg John7,Long Anthony D5,Clark Andrew G8,Lazzaro Brian P6

Affiliation:

1. Department of Biological Science, California State University Fullerton, Fullerton, CA 92831, USA

2. Division of Biological Sciences, University of Missouri, Columbia, MO 65211, USA

3. Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, ON N2L 3G1, Canada

4. Department of Integrative Biology, Oregon State University, Corvallis, OR 97331, USA

5. Department of Ecology and Evolutionary Biology, University of California Irvine, Irvine, CA 92692, USA

6. Department of Entomology, Cornell University, Ithaca, NY 14853, USA

7. USDA ARS Emerging Pets and Pathogens Research Unit, Robert W. Holley Center for Agriculture & Health, Ithaca, NY 14853, USA

8. Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA

Abstract

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. The 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 nine 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 nonoverlapping.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology

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