title: Lack of phenotypic and evolutionary cross-resistance against parasitoids and pathogens in Drosophila melanogaster.
abstract: BACKGROUND
  When organisms are attacked by multiple natural enemies, the evolution of a resistance mechanism to one natural enemy will be influenced by the degree of cross-resistance to another natural enemy. Cross-resistance can be positive, when a resistance mechanism against one natural enemy also offers resistance to another; or negative, in the form of a trade-off, when an increase in resistance against one natural enemy results in a decrease in resistance against another. Using Drosophila melanogaster, an important model system for the evolution of invertebrate immunity, we test for the existence of cross-resistance against parasites and pathogens, at both a phenotypic and evolutionary level.
  
  
  METHODS
  We used a field strain of D. melanogaster to test whether surviving parasitism by the parasitoid Asobara tabida has an effect on the resistance against Beauveria bassiana, an entomopathogenic fungus; and whether infection with the microsporidian Tubulinosema kingi has an effect on the resistance against A. tabida. We used lines selected for increased resistance to A. tabida to test whether increased parasitoid resistance has an effect on resistance against B. bassiana and T. kingi. We used lines selected for increased tolerance against B. bassiana to test whether increased fungal resistance has an effect on resistance against A. tabida.
  
  
  CONCLUSIONS
  We found no positive cross-resistance or trade-offs in the resistance to parasites and pathogens. This is an important finding, given the use of D. melanogaster as a model system for the evolution of invertebrate immunity. The lack of any cross-resistance to parasites and pathogens, at both the phenotypic and the evolutionary level, suggests that evolution of resistance against one class of natural enemies is largely independent of evolution of resistance against the other.
authors.affiliation: NERC Centre for Population Biology, Imperial College London, Silwood Park Campus, London, United Kingdom. arkraa@soton.ac.uk
authors.forename: Alex R
authors.initials: AR
authors.lastname: Kraaijeveld
authors.forename: Sophie J
authors.initials: SJ
authors.lastname: Layen
authors.forename: Peter H
authors.initials: PH
authors.lastname: Futerman
authors.forename: H Charles J
authors.initials: HC
authors.lastname: Godfray
mesh_terms: D000818:Animals; D016817:Apansporoblastina / Q000276:immunology; D052982:Beauveria / Q000276:immunology; D060467:Disease Resistance / Q000235:genetics* / Q000276:immunology; D004331:Drosophila melanogaster / Q000235:genetics / Q000276:immunology* / Q000382:microbiology*; D019143:Evolution, Molecular; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology; D006927:Hymenoptera / Q000276:immunology; D056265:Microbial Interactions / Q000276:immunology; D010641:Phenotype