Exposure to bacterial signals does not alter pea aphids' survival upon a second challenge or investment in production of winged offspring

PLoS One. 2013 Aug 29;8(8):e73600. doi: 10.1371/journal.pone.0073600. eCollection 2013.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aphids / microbiology*
  • Aphids / physiology*
  • Escherichia coli / immunology
  • Female
  • Host-Pathogen Interactions*
  • Micrococcus luteus / immunology
  • Reproduction, Asexual*
  • Symbiosis / genetics
  • Symbiosis / immunology*
  • Wings, Animal

Grants and funding

Research was funded by the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG) (AL902/4-1) (BA) and National Science Foundation grant IOS-1025853 (NMG & AML). BJP was funded through a National Science Foundation graduate research fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.