Host–parasite genotypic interactions in the honey bee: the dynamics of diversity

Abstract

Parasites are thought to be a major driving force shaping genetic variation in their host, and are suggested to be a significant reason for the maintenance of sexual reproduction. A leading hypothesis for the occurrence of multiple mating (polyandry) in social insects is that the genetic diversity generated within-colonies through this behavior promotes disease resistance. This benefit is likely to be particularly significant when colonies are exposed to multiple species and strains of parasites, but host–parasite genotypic interactions in social insects are little known. We investigated this using honey bees, which are naturally polyandrous and consequently produce genetically diverse colonies containing multiple genotypes (patrilines), and which are also known to host multiple strains of various parasite species. We found that host genotypes differed significantly in their resistance to different strains of the obligate fungal parasite that causes chalkbrood disease, while genotypic variation in resistance to the facultative fungal parasite that causes stonebrood disease was less pronounced. Our results show that genetic variation in disease resistance depends in part on the parasite genotype, as well as species, with the latter most likely relating to differences in parasite life history and host–parasite coevolution. Our results suggest that the selection pressure from genetically diverse parasites might be an important driving force in the evolution of polyandry, a mechanism that generates significant genetic diversity in social insects.

Innate expression of antimicrobial peptides does not explain genotypic diversity in resistance to fungal brood parasites in the honey bee

“…1), and host genotypes (patrilines) were assigned through microsatellite genotyping (Sect. 2; both detailed in Evison et al 2013). Following this, the same host colony was used to assess the general level of immunocompetence of each host genotype through measuring expression of abaecin and defensin 2 in unchallenged larvae (Sect.…”

“…Strain I was formed by isolates ARSEF 7405+7406, and the A. flavus strain was NRRL 1957, both of which were obtained from the Agricultural Research Service Entomopathogenic Fungus Collection, USA. Spore concentrations were prepared to a predetermined LD 50 as follows: A. apis strain I 5.0×10 5 , A. apis strain E 3.75×10 6 , A. apis strain F 1.95×10 6 and A. flavus 1.0×10 5 spores/ml to account for differences between parasites in virulence and spore viability (which were determined as detailed in Evison et al 2013;Vojvodic et al 2011). The four parasite treatments plus the control treatment were administered to equal numbers of larvae (288 larvae dosed per treatment).…”

“…Larvae that died due to other causes (which was 23 % of those under experimental conditions) showed rapid bacterial decomposition, which made them unsuitable for DNA extraction and were therefore excluded. A total of 698 larvae were successfully genotyped at eight microsatellite loci: A7, A29, B124, A35, A79, A107, A014 (Estoup et al 1994) and AP243 (Solignac et al 2003), with detailed protocols described in Evison et al (2013). Multi-locus offspring genotypes were used to deduce the genotype of the colony queen and her multiple mates, and the workers were assigned to patrilines within the colony with extremely low detection errors (0.0001 %; Boomsma and Ratnieks 1996).…”

“…Here, we follow on from a previous study showing the differential resistance of genotypes (patrilines) within colonies of honey bees to a set of fungal brood parasites (Evison et al 2013), by assessing whether the variation in resistance levels of genotypes from one colony can be explained by differences in constitutive expression levels of the AMP genes abaecin and defensin 2 . Considering honey bee AMPs are activated by the Toll pathway, which is stimulated by both bacteria and fungi (Evans et al 2006), and both abaecin and defensin 1 have previously been shown to be upregulated in response to infection by A. apis , we hypothesised that AMPs may be involved in larval resistance to the fungi tested in Evison et al (2013).…”

“…Considering honey bee AMPs are activated by the Toll pathway, which is stimulated by both bacteria and fungi (Evans et al 2006), and both abaecin and defensin 1 have previously been shown to be upregulated in response to infection by A. apis , we hypothesised that AMPs may be involved in larval resistance to the fungi tested in Evison et al (2013). First, we examine the level of variation in the constitutive expression of the two AMPs between different larval host genotypes in both 2nd and 5th instar larvae.…”