The genetic basis of variation immune defense against Lysinibacillus fusiformis infection in Drosophila melanogaster

The genetic causes of phenotypic variation often differ depending on the population examined, particularly if the populations were founded by relatively small numbers of genotypes. Similarly, the genetic causes of phenotypic variation among similar traits (resistance to different xenobiotic compounds or pathogens) may also be completely different or only partially overlapping. Differences in genetic causes for variation in the same trait among populations suggests considerable context dependence for how selection might act on those traits. Similarities in the genetic causes of variation for different traits, on the other hand, suggests pleiotropy which also would influence how natural selection would shape variation in a trait. We characterized immune defense against a natural Drosophila pathogen, the Gram-positive Lysinibacillus fusiformis, in three different populations and found almost no overlap in the genetic architecture of variation in survival post infection. However, when comparing our results to a similar experiment with the fungal pathogen, B. bassiana, we found a convincing shared QTL peak for both pathogens. This peak contains the Bomanin cluster of Drosophila immune effectors. RNAi knockdown experiments confirms a role of some of these genes in immune defense against both pathogens. This suggests that natural selection may act on the entire cluster of Bomanin genes (and the linked region under the QTL) or specific peptides for specific pathogens. Author SummaryLike most traits, the way individuals respond to infection vary among individuals within a population. Some of this variation is caused by genetic differences in the host organism. Over the past decade, two prominent resources were developed to assess genetic variation for complex traits of the fruit fly, Drosophila melanogaster and map the genetic variants responsible. We recently described a strain of Lysinibacillus fusiformis bacteria, which was isolated from fruit flies and is moderately virulent when flies are infected. We mapped genetic variation in resistance L. fusiformis using these mapping resources. We find that among the resources, different changes were associated with immune defense. However, we also found that within a resource, the same region of the genome was associated with resistance to both L. fusiformis and a fungal pathogen. These results suggest that different populations adapt differently to the same pathogens, but two distinct pathogens share similar causes of genetic variation within a single population.