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The molecular architecture ofDrosophila melanogasterdefense againstBeauveria bassianaexplored through evolve and resequence and quantitative trait locus mapping
Author(s) -
Parvin Shahrestani,
Elizabeth G. King,
Reza Ramezan,
Mark Phillips,
Melissa Riddle,
Marisa Thornburg,
Zachary Greenspan,
Yonathan Estrella,
Kelly Garcia,
Pratik Chowdhury,
Glen Malarat,
Ming Zhu,
Susan M. Rottshaefer,
Stephen P. Wraight,
Michael H. Griggs,
John D. Vandenberg,
Anthony D. Long,
Andrew G. Clark,
Brian P. Lazzaro
Publication year - 2021
Publication title -
g3 genes genomes genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.468
H-Index - 66
ISSN - 2160-1836
DOI - 10.1093/g3journal/jkab324
Subject(s) - biology , beauveria bassiana , quantitative trait locus , bassiana , genetics , wolbachia , genetic architecture , drosophila melanogaster , locus (genetics) , population , candidate gene , sexual dimorphism , inbred strain , gene , zoology , botany , demography , biological pest control , sociology
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.

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