Abstract
BackgroundIntersexual genomic conflict sometimes leads to unequal expression of paternal and maternal alleles in offspring, resulting in parent-of-origin effects. In honey bees reciprocal crosses can show strong parent-of-origin effects, supporting theoretical predictions that genomic imprinting occurs in this species. Mechanisms behind imprinting in honey bees are unclear but differential DNA methylation in eggs and sperm suggests that DNA methylation could be involved. Nonetheless, because DNA methylation is multifunctional, it is difficult to separate imprinting from other roles of methylation. Here we use a novel approach to investigate parent-of-origin DNA methylation in honey bees. In the subspecies Apis mellifera capensis, reproduction of females occurs either sexually by fertilization of eggs with sperm, or via thelytokous parthenogenesis, producing female embryos derived from two maternal genomes.ResultsWe compared genome-wide methylation patterns of sexually-produced, diploid embryos laid by a queen, with parthenogenetically-produced diploid embryos laid by her daughters. Thelytokous embryos inheriting two maternal genomes had fewer hypermethylated genes compared to fertilized embryos, supporting the prediction that fertilized embryos have increased methylation due to inheritance of a paternal genome. However, bisulfite PCR and sequencing of a differentially methylated gene, Stan (GB18207) showed strong allele-specific methylation that was maintained in both fertilized and thelytokous embryos. For this gene, methylation was associated with haplotype, not parent of origin.ConclusionsThe results of our study are consistent with predictions from the kin theory of genomic imprinting. However, our demonstration of allele-specific methylation based on sequence shows that genome-wide differential methylation studies can potentially confound imprinting and allele-specific methylation. It further suggests that methylation patterns are heritable or that specific sequence motifs are targets for methylation in some genes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2506-8) contains supplementary material, which is available to authorized users.
Highlights
Intersexual genomic conflict sometimes leads to unequal expression of paternal and maternal alleles in offspring, resulting in parent-of-origin effects
Violations of Mendelian inheritance can arise when the genetic interests of the mother and father diverge [2, 3]. Males benefit if their offspring can secure more resources from the offspring’s mother, whereas females normally benefit if their offspring are provisioned regardless of paternity. These sexual conflicts can lead to parent-of-origin effects, arising from genomic imprinting, where offspring phenotype is altered depending on whether an allele is inherited from a mother or a father [4]
To examine whether the remaining non-CG sites corresponded to actual Capensis CG sites that are absent from the Amel2.0 reference genome, we examined the Single nucleotide polymorphism (SNP) present from our Capensis2.0 alignment derived from Wallberg et al [57]
Summary
Intersexual genomic conflict sometimes leads to unequal expression of paternal and maternal alleles in offspring, resulting in parent-of-origin effects. Violations of Mendelian inheritance can arise when the genetic interests of the mother and father diverge [2, 3] Males benefit if their offspring can secure more resources from the offspring’s mother, whereas females normally benefit if their offspring are provisioned regardless of paternity. These sexual conflicts can lead to parent-of-origin effects, arising from genomic imprinting, where offspring phenotype is altered depending on whether an allele is inherited from a mother or a father [4]. Mice embryos derived from two maternal genomes or two paternal genomes via pronuclear transfers are non-viable due to parent-specific imprinting [6, 7]
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