Animal Science Department


First Advisor

Dr. Jessica L. Petersen

Date of this Version



A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science, Major: Animal Science, Under the Supervision of Professor Jessica L. Petersen. Lincoln, Nebraska: April 2021

Copyright © 2021 Renae L. Sieck


Beta-adrenergic agonists (β-AA) are widely used supplements in livestock production to improve feed efficiency and increase lean muscle mass. Heat stress is one of the largest economic burdens to the livestock industry due to production efficiency losses and morbidity and mortality of animals. Both β-AA and catecholamines released in response to heat stress bind to β-adrenoceptors on the skeletal muscle cell surface to activate downstream signaling pathways. The purpose of this study was to determine if β-AA supplementation and heat stress have an additive effect on the skeletal muscle transcriptome. 3’ RNA sequencing of samples of the longissimus dorsiwas performed to quantify gene expression and identify genes differentially expressed due to treatment. No additive effects were observed, but instead β-AA supplementation mediated the heat-stress induced oxidative stress response in skeletal muscle. Therefore, the objective of the second study was to identify the influence of β-AA on mitochondrial function in skeletal muscle satellite cells of cattle, sheep, and pigs. Real-time measurements of oxygen consumption rates were recorded using intracellular flux analysis. Incubation of bovine cells with β-AA increased maximal respiration and spare respiratory capacity (P

The third study identified genomic variation underlying a congenital facial deformity in Hereford cattle termed Mandibulofacial Dysostosis (MD). Affected calves shared hallmark features of a variably shortened and/or asymmetric lower mandible and bilateral skin tags caudal to the commissure of the lips. Whole genome sequencing led to the discovery of a missense variant (Chr26 g. 14404993T>C) in CYP26C1 associated with MD. We postulate that this recessive missense mutation impacts the catalytic activity of the encoded enzyme, leading to the observed MD phenotype.

Advisor: Jessica L. Petersen