5 research outputs found
Estimation of C-derived introgression into A. m. mellifera colonies in the Russian Urals using microsatellite genotyping
Large-scale mitochondrial DNA analysis of native honey bee Apis mellifera populations reveals a new African subgroup private to the South West Indian Ocean islands
Innate expression of antimicrobial peptides does not explain genotypic diversity in resistance to fungal brood parasites in the honey bee
The genetic basis of host resistance to parasites is a fundamental aspect of host-parasite co-evolution, yet the precise mechanisms often remain unclear. Here, we follow on from a previous study on the genetically mediated variation in resistance to two common fungal brood parasites that cause chalkbrood and stonebrood in the honey bee. We assessed whether genetically mediated variation in resistance can be explained by the baseline immunocompetence of different larval genotypes by correlating the constitutive expression of two key immune genes with the observed level of resistance of each larval genotype to four different fungal brood parasites. We found significant variation between larval genotypes in the constitutive expression of abaecin but not defensin 2, but despite a suggestion of negative correlations between gene expression and resistance level in older larvae, there was no consistent evidence that baseline abaecin expression is a relevant predictor of resistance to these parasites. These results suggest that the constitutive expression of abaecin appears to have a genetic basis in honey bee larvae but that mechanisms other than innate expression of antimicrobial peptides might be more important in defence against the specific fungal brood parasites assessed here