Genetic variation in Drosophila melanogaster resistance to infection: a comparison across bacteria.
Insects use a generalized immune response to combat bacterial infection. We have previously noted that natural populations of D. melanogaster harbor substantial genetic variation for antibacterial immunocompetence and that much of this variation can be mapped to genes that are known to play direct roles in immunity. It was not known, however, whether the phenotypic effects of variation in these genes are general across the range of potentially infectious bacteria. To address this question, we have reinfected the same set of D. melanogaster lines with Serratia marcescens, the bacterium used in the previous study, and with three additional bacteria that were isolated from the hemolymph of wild-caught D. melanogaster. Two of the new bacteria, Enterococcus faecalis and Lactococcus lactis, are gram positive. The third, Providencia burhodogranaria, is gram negative like S. marcescens. Drosophila genotypes vary highly significantly in bacterial load sustained after infection with each of the four bacteria, but mean loads are largely uncorrelated across bacteria. We have tested statistical associations between immunity phenotypes and nucleotide polymorphism in 21 candidate immunity genes. We find that molecular variation in some genes, such as Tehao, contributes to phenotypic variation in the suppression of only a subset of the pathogens. Variation in SR-CII and 18-wheeler, however, has effects that are more general. Although markers in SR-CII and 18-wheeler explain >20% of the phenotypic variation in resistance to L. lactis and E. faecalis, respectively, most of the molecular polymorphisms tested explain <10% of the total variance in bacterial load sustained after infection.
Lazzaro
Brian P
BP
Department of Entomology, Field of Ecology and Evolutionary Biology, Cornell University, Ithaca, New York 14853, USA. bl89@cornell.edu
Sackton
Timothy B
TB
Clark
Andrew G
AG
D000818:Animals; D001419:Bacteria / Q000254:growth & development / Q000276:immunology* / Q000472:pathogenicity; D001424:Bacterial Infections / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D004331:Drosophila melanogaster / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology; D013293:Enterococcus faecalis / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity; D004843:Epistasis, Genetic; D017344:Genes, Insect; D005819:Genetic Markers; D014644:Genetic Variation; D006239:Haplotypes; D006458:Hemolymph / Q000382:microbiology; D007113:Immunity, Innate / Q000235:genetics; D007121:Immunocompetence / Q000235:genetics; D013294:Lactococcus lactis / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011532:Providencia / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity; D012706:Serratia marcescens / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity
D005819:Genetic Markers