Date of Award


Publication Type

Doctoral Thesis

Degree Name



Great Lakes Institute for Environmental Research

First Advisor

Daniel D. Heath


DNA methylation, epigenetics, evolution, genetic architecture, maternal effects, population genetics



Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.


DNA methylation has been proposed as an epigenetic, evolutionary mechanism for acclimation, transgenerational plasticity, and local adaptation without changes in DNA sequence. In this thesis, I assess the highly targeted evolutionary nature of DNA methylation in Chinook salmon from the tissue to the population level, with important implications for organism survival and evolution. First, I developed a PCR-based bisulfite assay for Next-Generation sequencing for genes involved in growth, development, immune function, stress response, and metabolism (Chapter 2). Locus- and tissue-specific methylation was assessed in inbred and outbred Chinook salmon at two developmental stages (fry and yearling). This chapter established DNA methylation as a mechanism targeted to specific loci, tissues, levels of inbreeding, and developmental stages/environmental contexts. I assessed the role of DNA methylation in the propagation of maternal effects at three early developmental stages (egg, alevin, and fry; Chapter 3). Two 6x6 fully factorial Chinook salmon breeding crosses were used to estimate maternal effects. DNA methylation was assessed using bisulfite sequencing and both locus-specific and CpG-specific maternal effects were identified. This chapter established DNA methylation as a potential mechanism for the transmission of maternal effects, which can have important influences on offspring development and fitness. I quantified the effects of early environment on the genetic architecture of DNA methylation using 6x6 factorial crosses reared in two environments: a hatchery and a semi-natural channel (Chapter 4). Additive, non-additive, and maternal variance components, combined with environmental and GxE effects for DNA methylation were calculated. Rearing environment caused gene-specific plasticity in methylation, as well as differences in the genetic architecture of methylation. This chapter identified the importance of both genetic and environmental variation in controlling methylation, with important implications for methylation as an acclimation or adaptive mechanism. Finally, I characterized differences in locus-specific methylation among eight populations of Chinook salmon (Chapter 5). The significant population differences in locus-specific methylation were tested for correlation with environmental variables from natal streams, and pairwise FST estimates (microsatellite and SNP data). I identified no effects of rearing environment, but a weak among-population correlation between methylation and microsatellite FST indicating that genetic drift is influencing methylation. Population-level differences in DNA methylation suggest methylation may contribute to local adaptation and is certainly an important additional source of phenotypic variation. In conclusion, my doctoral research evaluated the role of DNA methylation from the tissue to the population level. My results support DNA methylation as a novel, potentially adaptive mechanism, contributing to normal organism function, transgenerational plasticity through maternal effects, plasticity, and population-level acclimation or adaptation.

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