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theses

Genetic diseases arise from a mutation in a globin protein in humans in hemoglobinopathies, one of the most common diseases that can be inherited. The types of hemoglobinopathy range from structural hemoglobin variants to hemoglobin synthesis disorders. Globins in general are a conserved protein family that is characterized by its 6-8 alpha helices with an oxygen-interacting heme group and exist in all the kingdoms of life. The comprehensive study of globins are critical for more than just hemoglobin; they include myoglobin, neuroglobin, cytoglobin, androglobin, globin E, globin X, and globin Y in vertebrates. Neuroglobin, myoglobin, and cytoglobin have been studied the most out of the vertebrate globins. Caenorhabditis elegans globins offer the ability to understand globin protein function at a more fundamental level due to the large number and variety of globins, number of displayed phenotypes, sexual dimorphism, and ease of separating internal and external factors on protein function without inducing lethality. Despite these advantages, only 6 out of 34 globins have been characterized in the nematode C. elegans. It is still unknown why a nematode would have so many globins compared to more complex organisms which have fewer globins. I recently discovered that glb-28, one of the uncharacterized 34 globins of C. elegans, is endogenously expressed in extracellular vesicle-releasing neurons (EVNs) and oxygen sensing neurons. Currently, glb-28 is the only globin found in EVNs and it is required in male mating behavior. I will utilize CRISPR/Cas9 mediated genome editing to investigate the function of glb-28 in mating behavior, oxygen sensing neurons and EVNs. Results from this thesis may a novel connection with glb-28 between EVNs.

ETD_10672

M.S.

Includes bibliographical references

doi:10.7282/t3-jj48-fd39

ETD graduate

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