title: Exposure to bacterial signals does not alter pea aphids' survival upon a second challenge or investment in production of winged offspring.
abstract: Pea aphids have an obligate nutritional symbiosis with the bacteria Buchneraaphidicola and frequently also harbor one or more facultative symbionts. Aphids are also susceptible to bacterial pathogen infections, and it has been suggested that aphids have a limited immune response towards such pathogen infections compared to other, more well-studied insects. However, aphids do possess at least some of the genes known to be involved in bacterial immune responses in other insects, and immune-competent hemocytes. One possibility is that immune priming with microbial elicitors could stimulate immune protection against subsequent bacterial infections, as has been observed in several other insect systems. To address this hypothesis we challenged aphids with bacterial immune elicitors twenty-four hours prior to live bacterial pathogen infections and then compared their survival rates to aphids that were not pre-exposed to bacterial signals. Using two aphid genotypes, we found no evidence for immune protection conferred by immune priming during infections with either Serratia marcescens or with Escherichia coli. Immune priming was not altered by the presence of facultative, beneficial symbionts in the aphids. In the absence of inducible immune protection, aphids may allocate energy towards other defense traits, including production of offspring with wings that could escape deteriorating conditions. To test this, we monitored the ratio of winged to unwinged offspring produced by adult mothers of a single clone that had been exposed to bacterial immune elicitors, to live E. coli infections or to no challenge. We found no correlation between immune challenge and winged offspring production, suggesting that this mechanism of defense, which functions upon exposure to fungal pathogens, is not central to aphid responses to bacterial infections.
authors.affiliation: Department of Biology, Emory University, Atlanta, Georgia, USA.
authors.forename: Bas
authors.initials: B
authors.lastname: ter Braak
authors.forename: Alice M
authors.initials: AM
authors.lastname: Laughton
authors.forename: Boran
authors.initials: B
authors.lastname: Altincicek
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Parker
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Gerardo
mesh_terms: D000818:Animals; D001042:Aphids / Q000382:microbiology* / Q000502:physiology*; D004926:Escherichia coli / Q000276:immunology; D005260:Female; D054884:Host-Pathogen Interactions; D016982:Micrococcus luteus / Q000276:immunology; D012100:Reproduction, Asexual; D013559:Symbiosis / Q000235:genetics / Q000276:immunology*; D014921:Wings, Animal