• Source: Scopus
20042021

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Research in the Lawson Lab addresses important questions about the genotype – phenotype relationship that must be answered to understand variation in dietary obesity-related metabolic traits. Questions such as: Are particular metabolic traits more genetically or epigenetically controlled? How does diet affect the relative contribution of genetics or epigenetics? Do differences in genetic and epigenetic modes of regulation result in discordance among metabolic traits? Answers to these questions are critical to understanding why some individuals with metabolic complications respond to lifestyle modifications while others require therapeutic interventions. Further, understanding how diet modifies genetic and epigenetic effects might shed light on why some obese individuals develop metabolic complications while others remain metabolically normal.

We have found prevalent complex parent-of-origin effects on dietary obesity-related metabolic traits. However, there is currently no way to predict these epigenetic effects on phenotype from DNA sequence. The ability to predict such effects would be a step towards personalized medicine and towards understanding how associations among metabolic traits evolved. We integrate whole-genome sequence data with phenotypic data to understand the molecular mechanisms underlying the genetic architecture of metabolic traits. We work with mouse models, which allow experimental manipulations of genotype and environmental factors under controlled conditions. Our research aims to: 1) learn under what context(s) parent-of-origin influences phenotype; 2) understand how diet affects relationships among obesity-related traits; and 3) translate results found in our discovery research to human datasets.

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