Defense Date


Document Type


Degree Name

Master of Science



First Advisor

Dr. Erich Damm


Notable progress has been made in understanding the development of the neural crest (NC). Neural crest cells (NCCs) can be divided into 4-5 subpopulations. A major lineage among trunk NC derivatives are sympathoadrenal (SA) cells, which give rise to the sympathetic nervous system (SNS). Trunk NCCs follow a ventromedial migration pathway where signals derived from the dorsal aorta instruct migrating NCCs to a SA cell fate. Defects in NC development can result in syndromes known as neurocristopathies. Neuroblastoma is one of the most common forms of pediatric cancer affecting nearly 800 infants each year in the United States (Takita et al., 2021). This neurocristopathy is characterized by extracranial solid tumors caused by malignancy of the SNS, specifically SA precursor cells. In high-risk neuroblastoma, EMP3 is highly methylated, correlating with low levels of EMP3 mRNA and protein expression (Wang et al., 2017) suggesting a potential tumor suppressor function. However, other studies have shown that the overexpression of EMP3 promotes proliferation and migration but suppresses cell adhesion in urinary cancer (Wang et al., 2017). EMP3 signaling has been studied in the context of cancer, but its role in embryonic development has not been described. Here I examine the role of emp3b during SNS development in zebrafish. Overall, my work suggests when emp3b is knocked down, SA progenitor cells do not differentiate into the SNS. Through further investigation I found that normal NC migration is disrupted in emp3b morphants. In conclusion this study demonstrates a potential mechanism by which emp3b regulates SNS development and NC migration through erbb3b regulation. EMP3 signaling is highly complex and misunderstood. Therefore, additional investigation is required to clarify the factors that regulate EMP3 expression and activity to understand its involvement in NC migration and SNS development.


© Jessica M. White

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Available for download on Friday, May 10, 2024