Date of Award

Spring 5-2025

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Pharmaceutical Sciences

First Advisor

Cintia E. Citterio, PhD

Second Advisor

Jennifer Totonchy, PhD

Third Advisor

Ajay Sharma, PhD

Abstract

Vertebrate life is unsustainable without thyroid hormones. The only known precursor for thyroid hormone synthesis is thyroglobulin (Tg), composed of upstream regions I-II-III and a C-terminal cholinesterase-like (ChEL) domain, which bears 47% similarity to acetylcholinesterase (AChE). Mutations in Tg cause congenital hypothyroidism, the most common congenital endocrinopathy affecting 1 in 2,000-4,000 newborns, with a varying degree of phenotypic manifestations. Tg protein, regulated by TSH, is secreted to the lumen of thyroid follicles, where thyroxine (T4) is formed primarily at the N-terminus, and triiodothyronine (T3) is formed primarily in the ChEL domain. Previous in vitro studies indicated that the isolated ChEL domain (following a signal peptide) is competent for dimerization, secretion, iodination, and T3 generation, but little to no T4 generation. However, the in vivo biological relevance of the Tg-ChEL domain (in the absence of the remaining Tg molecule) is entirely unknown. Furthermore, the functional effects of several Tg-ChEL mutations responsible for congenital hypothyroidism remain to be elucidated. This project has two main objectives. Objective 1 examines the thyroid histological characteristics of a genetically engineered mouse model built for selective expression of the Tg-ChEL domain. Objective 2 establishes an in vitro system using recombinant AChE as a reporter to enable future functional testing of ChEL domain mutations linked to congenital hypothyroidism. A deeper understanding of the functional role of the Tg’s ChEL domain could shed light on the spectrum of congenital hypothyroidism phenotypes, allowing for genotype-phenotype correlations for the future improvement of the disease diagnosis and treatment.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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