Association of single nucleotide polymorphisms to resistance to chalkbrood in<i>Apis mellifera</i>

Holloway, Beth; Sylvester, H. Allen; Bourgeois, Lelania; Rinderer, Thomas E.

doi:10.3896/ibra.1.51.2.02

Cited by 20 publications

(26 citation statements)

References 16 publications

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“…In addition, variation in honey bee resistance to A. apis appears to be based around single nucleotide polymorphisms, which are in close proximity to genes involved in the host's chitin biosynthesis and development (Holloway et al 2012), so the gut lining (its composition and/or its products) may be a key point of defence against infection. This may give further explanation as to why our measures of host baseline immunocompetence did not fully explain how different larval genotypes resist the brood parasites tested here.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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-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.Apis mellifera / abaecin / defensin / antimicrobial peptide / Ascosphaera apis / Aspergillus flavus

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Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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“…Additional QTL studies have targeted mite grooming behavior (Arechavaleta-Velasco, Alcala-Escamilla et al, 2012) and mite reproductive success (Behrens, Huang et al, 2011). A QTL search was also performed for resistance to chalkbrood ( Ascosphaera apis ) (Holloway, Sylvester et al, 2012). However, over 70 different honey bee diseases are known (Schmid-Hempel, 1998) and studies of the genetic architecture of honey bee resistance to most of them are still lacking, even though a genetic basis for resistance against most diseases probably exists (Kulincevic and Rothenbuhler, 1975; Bailey and Ball, 1991; Palmer and Oldroyd, 2003; Huang, Kryger et al, 2012).…”

Section: Implications For Selective Breeding For Honey Bee Healthmentioning

confidence: 99%

The architecture of the pollen hoarding syndrome in honey bees: implications for understanding social evolution, behavioral syndromes, and selective breeding

Rueppell

2013

Apidologie

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Social evolution has influenced every aspect of contemporary honey bee biology, but the details are difficult to reconstruct. The reproductive ground plan hypothesis of social evolution proposes that central regulators of the gonotropic cycle of solitary insects have been coopted to coordinate social complexity in honey bees, such as the division of labor among workers. The predicted trait associations between reproductive physiology and social behavior have been identified in the context of the pollen hoarding syndrome, a larger suite of interrelated traits. The genetic architecture of this syndrome is characterized by a partially overlapping genetic architecture with several consistent, pleiotropic QTL. Despite these central QTL and an integrated hormonal regulation, separate aspects of the pollen hoarding syndrome may evolve independently due to peripheral QTL and additionally segregating genetic variance. The characterization of the pollen hoarding syndrome has also demonstrated that this syndrome involves many non-behavioral traits, which may be the case for numerous “behavioral” syndromes. Furthermore, the genetic architecture of the pollen hoarding syndrome has implications for breeding programs for improving honey health and other desirable traits: If these traits are comparable to the pollen hoarding syndrome, consistent pleiotropic QTL will enable marker assisted selection, while sufficient additional genetic variation may permit the dissociation of trade-offs for efficient multiple trait selection.

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“…Selecting for hygienic traits as a whole may therefore not be the best approach for developing a chalkbrood‐resistant strain. Rather, a more efficacious method for decreasing the effects of chalkbrood may be found by enhancing naturally occurring larva‐mediated resistance (Holloway et al ., ).…”

Section: Introductionmentioning

confidence: 99%

“…Holloway et al . () investigated the association between larva‐mediated chalkbrood resistance and regions on chromosomes 2 and 11 using QTL techniques. Although the mechanisms of chalkbrood resistance remain unclear, their results showed that two markers (est8471 and est8764) on chromosome 11 may be correlated with chalkbrood resistance (Holloway et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Larva‐mediated chalkbrood resistance‐associated single nucleotide polymorphism markers in the honey bee Apis mellifera

Liu

Yan

et al. 2016

Insect Molecular Biology

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Chalkbrood is a disease affecting honey bees that seriously impairs brood growth and productivity of diseased colonies. Although honey bees can develop chalkbrood resistance naturally, the details underlying the mechanisms of resistance are not fully understood, and no easy method is currently available for selecting and breeding resistant bees. Finding the genes involved in the development of resistance and identifying single nucleotide polymorphisms (SNPs) that can be used as molecular markers of resistance is therefore a high priority. We conducted genome resequencing to compare resistant (Res) and susceptible (Sus) larvae that were selected following in vitro chalkbrood inoculation. Twelve genomic libraries, including 14.4 Gb of sequence data, were analysed using SNP-finding algorithms. Unique SNPs derived from chromosomes 2 and 11 were analysed in this study. SNPs from resistant individuals were confirmed by PCR and Sanger sequencing using in vitro reared larvae and resistant colonies. We found strong support for an association between the C allele at SNP C2587245T and chalkbrood resistance. SNP C2587245T may be useful as a genetic marker for the selection of chalkbrood resistance and high royal jelly production honey bee lines, thereby helping to minimize the negative effects of chalkbrood on managed honey bees.

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Association of single nucleotide polymorphisms to resistance to chalkbrood inApis mellifera

Cited by 20 publications

References 16 publications

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

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

The architecture of the pollen hoarding syndrome in honey bees: implications for understanding social evolution, behavioral syndromes, and selective breeding

Larva‐mediated chalkbrood resistance‐associated single nucleotide polymorphism markers in the honey bee Apis mellifera

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