Loren Wipf

Document Type

Thesis - University Access Only

Award Date


Degree Name

Master of Science (MS)

Department / School

Biology and Microbiology

First Advisor

Nels H. Granholm


The objective of this project was to determine the concentrations of the differently-acetylated αMSH species (des-Ac-αMSH, N-Ac-αMSH, and N,O-di-Ac-αMSH) in three tissues of C57BL/6J mice possessing the lethal yellow ( experimental) and nonagouti black ( control) mutations of the agouti locus. Three tissues of interest were the pituitary gland (because the intermediate lobe of the pituitary is a known source of significant quantities of αMSH), serum (the transporter which this peptide would utilize in inducing ubiquitous effects), and hair bulb-containing preparations from the inner surface of dorsal skins (follicular melanocytes are known to possess MSH receptors and can be induced by αMSH). It was important to include measurements of di-Ac-αMSH in these studies because di-Ac-αMSH is probably the major melanotropic product of the intermediate pituitary of mice, as it is of the rat pituitary (Glembotski, 1982; Rudman et al., 1979; Browne et al., 1981). Confirmation of decreased acetylation of ACTH(1-13)NH2 (des-Ac-αMSH) in AY/a mice as compared to a/a mice would support Bray and Shimizu's observations regarding the endocrinologic status of viable yellow mice (Bray et al., 1988; Shimizu et al., 1989a). Conversely, a finding of no significant difference in the acetylation of αMSH, in comparing the tissues of AY/a and a/a mice, would suggest that faulty acetylation of αMSH is neither a cause nor an effect of any characteristic of the lethal yellow syndrome.

Library of Congress Subject Headings

Mice -- Genetics
MSH (Hormone)
Lethal mutation




South Dakota State University



Rights Statement

In Copyright