Academic journal article Genetics

Genetic Variation in Drosophila Melanogaster Resistance to Infection: A Comparison across Bacteria

Academic journal article Genetics

Genetic Variation in Drosophila Melanogaster Resistance to Infection: A Comparison across Bacteria

Article excerpt

ABSTRACT

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.

THE stereotypical insect defense against microbial pathogens (reviewed in Leclerc and Reichhart 2004) includes defensive phagocytosis (cellular immunity) and the production of extracellular antibiotic peptides (humoral immunity). Insect immune responses are distinct from those of vertebrates in that insect immune systems lack the adaptive memory of previous infections and high degree of specificity that characterize vertebrate immune systems. Instead, insect antibacterial defenses are generalized and mechanistically simple, with only a small set of genes used to fight against an extremely broad range of bacteria. Despite substantial and increasing understanding of gene function underlying Drosophila antibacterial defense, little is known about the extent and consequences of genetic polymorphism for immune function in natural insect populations. There is evidence that increased immunocompetence in insects can be detrimental to other components of fitness (e.g., KRAAIJEVELD and GODFRAY 1997; MCKEAN and NUNNEY 2001; KUMAR et al. 2003), potentially allowing selective maintenance of genetic variation in immune function. Additionally, because a comparatively small set of genes is used to combat a broad range of pathogens, it is in principle possible that mutation could increase the quality of response to some bacteria at the expense of the response to others, providing another potential mechanism for the adaptive maintenance of polymorphism. In this study, we evaluate resistance to four different bacteria across a panel of Drosophila melanogaster genetic lines to test the degree of concordance in resistance to distinct bacteria and to identify genes harboring natural polymorphism that contributes to phenotypic variation in resistance to infection.

In Drosophila, the humoral immune response to bacteria is initiated when pathogen recognition proteins, such as peptidoglycan recognition proteins (PGRPs) and gram-negative binding proteins (GNBPs), react with conserved components of prokaryotic cell walls. Different PGRP isoforms of the same gene can have different recognition spectra and PGRPs and GNBPs have been shown to interact epistatically (GOBERT et al. 2003; WERNER et al. 2003; PILI-FLOURY et al. 2004; TAKEHANA et al. 2004; CHOE et al. …

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