Abstract

BackgroundPhenotypic variation is determined by a combination of genotype, environment and their interactions. The realization that allelic diversity can be both genetic and epigenetic allows the environmental component to be further separated. Partitioning phenotypic variation observed among inbred lines with an altered epigenome can allow the epigenetic component controlling quantitative traits to be estimated. To assess the contribution of epialleles on phenotypic variation and determine the fidelity with which epialleles are inherited, we have developed a novel hypomethylated population of strawberry (2n = 2x = 14) using 5-azacytidine from which individuals with altered phenotypes can be identified, selected and characterized.ResultsThe hypomethylated population was generated using an inbred strawberry population in the F. vesca ssp. vesca accession Hawaii 4. Analysis of whole genome sequence data from control and hypomethylated lines indicate that 5-azacytidine exposure does not increase SNP above background levels. The populations contained only Hawaii 4 alleles, removing introgression of alternate F. vesca alleles as a potential source of variation. Although genome sequencing and genetic marker data are unable to rule out 5-azacytidine induced chromosomal rearrangements as a potential source of the trait variation observed, none were detected in our survey. Quantitative trait variation focusing on flowering time and rosette diameter was scored in control and treated populations where expanded levels of variation were observed among the hypomethylated lines. Methylation sensitive molecular markers indicated that 5-azacytidine induced alterations in DNA methylation patterns and inheritance of methylation patterns were confirmed by bisulfite sequencing of targeted regions. It is possible that methylation polymorphisms might underlie or have induced genetic changes underlying the observable differences in quantitative phenotypes.ConclusionsThis population developed in a uniform genetic background provides a resource for the discovery of new variation controlling quantitative traits. Genome sequence analysis indicates that 5-azacytidine did not induce point mutations and the induced variation is largely restricted to DNA methylation. Using this resource, we have identified new variation and demonstrated the inheritance of both variant trait and methylation patterns. Although direct associations remain to be determined, these data suggest epigenetic variation might be subject to selection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0936-8) contains supplementary material, which is available to authorized users.

Highlights

  • Phenotypic variation is determined by a combination of genotype, environment and their interactions

  • Genetic uniformity was verified among the F. vesca populations Since any genetic polymorphism is likely to complicate the effects resulting from induced epigenetic differences [66], in order to attribute any phenotypic variation observed in quantitative characters to epigenetic variation, it is necessary to perform the experiment using a genetically uniform population [14]

  • Studies have demonstrated the effect of epigenetic alterations on phenotypic variation taking advantage of the resources available in Arabidopsis, where Epigenetic Recombinant Inbred Lines (EpiRILs) derived from met1 mutants show increased trait variation [10]

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Summary

Introduction

Phenotypic variation is determined by a combination of genotype, environment and their interactions. The realization that allelic diversity can be both genetic and epigenetic allows the environmental component to be further separated. Partitioning phenotypic variation observed among inbred lines with an altered epigenome can allow the epigenetic component controlling quantitative traits to be estimated. Measuring the phenotypic variation observed among genetically uniform individuals allows the extent to which the environmental components affect quantitative traits to be estimated. Epigenetic variation has the potential to alter the magnitude of gene expression whereas genetic polymorphisms result from differences in the primary DNA sequence resulting in functional allelic variants. The development of tools that are able to detect and measure epigenetic variation in genetically uniform populations is allowing these issues to be resolved [9, 17]

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