Graduate Studies

 

First Advisor

Jessica Petersen

Degree Name

Doctor of Philosophy (Ph.D.)

Department

Animal Science

Date of this Version

7-2024

Document Type

Dissertation

Citation

A dissertation presented to the faculty of the Graduate College of the University of Nebraska in partial fulfillment of requirements for the degree of Doctor of Philosophy

Major: Animal Science

Under the supervision of Professor Jessica Petersen

Lincoln, Nebraska, July 2024

Comments

Copyright 2024, Rachel Renae Reith. Used by permission

Abstract

Heat stress is a major concern for livestock producers due to its negative impact on animal health and productivity. Heat stress does so by altering expression of genes through different regulatory mechanisms such as DNA methylation. Understanding how heat stress alters gene expression will help elucidate the genetic basis of physiological changes as well as identify targets for possible heat stress mitigation. The purpose of the first study was to understand how heat stress alters the adipose and skeletal muscle transcriptomes in zilpaterol-fed Brahman, as zilpaterol improves muscle growth and may mitigate the effects of heat stress. Differential expression and pathway analyses indicated that Brahman were overall resistant to effects of heat stress but may have experienced mitochondrial dysfunction and stress due to interaction of zilpaterol and heat stress. This contrasts prior results that indicated zilpaterol mitigated some effects of heat stress in Bos taurus cattle. The second study investigated the effects of heat stress on DNA methylation in Red Angus skeletal muscle. Heat stress altered methylation of genes and promoters involved in oxidative stress and inflammation, which was also predicted by RNA analysis. However, the methylated genes did not overlap with previously identified differentially expressed genes, suggesting DNA methylation was not the sole mechanism through which heat stress altered gene expression. The third study compares DNA methylation of Red Angus skeletal muscle at 48 hours of heat stress to the same animals five days post-heat stress. There were methylation changes in growth and inflammation genes, indicating possible anti-inflammatory mechanism and activation of growth pathways during recovery. Overall, these findings indicate heat stress alters expression of genes involved in inflammation and oxidative stress. However, results suggest altering DNA methylation is not the main mechanism for this.

The last two chapters investigate genetic defects in two cattle breeds: blindness in Herefords and bovine familial convulsions and ataxia in Angus. Whole-genome sequencing of affected and unaffected cattle revealed novel variants with predicted high impact on gene function. Pathohistological results and similarities to human genetic diseases support that the identified variants are likely causative in these cattle.

Advisor: Jessica Petersen

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