The molecular architecture of Drosophila melanogaster defense against Beauveria bassiana explored through evolve and resequence and quantitative trait locus mapping. Issue 12 (17th September 2021)

• Record Type: Journal Article
• Authors: Shahrestani, Parvin; King, Elizabeth; Ramezan, Reza; Phillips, Mark; Riddle, Melissa; Thornburg, Marisa; Greenspan, Zachary; Estrella, Yonathan; Garcia, Kelly; Chowdhury, Pratik; Malarat, Glen; Zhu, Ming; Rottshaefer, Susan M; Wraight, Stephen; Griggs, Michael; Vandenberg, John; Long, Anthony D; Clark, Andrew G; Lazzaro, Brian P
• Editors: Anholt, R
• Is Part Of: G3. Volume 11:Issue 12(2021)
• Publication Date: 2021-09-17
• Subjects: Drosophila melanogaster -- Beauveria bassiana -- immunity -- DSPR -- QTL mapping -- E&R -- experimental evolution; Genetics -- Research -- Periodicals; Genomics -- Periodicals; Genetics; Genomics; Genes; Genetics -- Research; Genomics; Electronic journals; Periodical; Periodicals; Fulltext; Internet Resources; Periodicals; 572.8
• DOI: 10.1093/g3journal/jkab324
• Languages: English
• ISSNs: 2160-1836

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.