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Abstract
Growth Differentiation Factor 11 (GDF11) serves vital roles in the developing embryo, governing organogenesis and axial patterning, yet surprisingly little is known about its function or genetic regulation in the adult mammal. Over the past several years, some studies have suggested that GDF11 has a rejuvenative effect on the heart by suppressing and even reversing cardiac hypertrophy. However, it is unclear whether those effects are actually due to its homolog, myostatin, which is structurally similar and signals through the same pathways. The work presented in this thesis outlines a translational systems approach to define the genetics of GDF11 better understand its true role in disease pathology. Importantly, the approach has underscored novel genes and pathways that will form the foundation for future GDF11 research.