Thesis (Ph. D.)--University of Wisconsin--Madison, 1949. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Bibliography: leaves 46-47.

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To investigate the lineage relationships that are postulated to underlie the origins of phenotypically different neurons, Thy-1.1 $ leftrightarrow$ Thy-1.2 and hNF-L $ leftrightarrow$ +/+ mouse chimeras were examined for the distribution of the two neuron genotypes. Throughout the nervous system, a finely variegated pattern of mosaicism was always observed and, in each chimera, similar genotype proportions were found in all analysed neuronal populations of the peripheral and central nervous system. These findings require that the chimera neuroectoderm was a homogeneous mix of the two genotypes and that different neuronal phenotypes do not arise clonally from a small number of prespecified progenitors. Rather it would seem that all progenitors contribute daughter cells to all of the neuronal subpopulations at each level of the neuroaxis.

Thesis (M.S.)--Bowling Green State University, 2008. / Document formatted into pages; contains x, 75 p. : ill. Includes bibliographical references.

In diabetes the body lacks the mechanism for producing insulin. This disease is one of the most prevalent in the world, causing a tremendous loss of health, life and economy. Thus, there is a need for developing novel therapies effective in control of diabetes. In an effort to develop such a therapy we have targeted G-protein coupled receptors (GPCRs) to stimulate 13-cells for insulin secretion. GPCRs are membrane bound receptors which respond to a variety of external signals and mediate intracellular signal Stransduction. GPCRs, therefore, are the targets of many current therapeutic drugs. The objective of this study was to generate chimeric receptors containing portions of two closely related GPCRs to identify domains important in binding various ligands to stimulate increased secretion of insulin by f3-cells of the pancreas. In this collaborative research with Kelly Wilbur of Eli Lilly, domains of receptors GPR40 and GPR41 were exchanged at different regions to construct two chimeric receptors (GPR40.431_41.459 and GPR40.567 41.547) using two separate cloning steps to insert these fragments sequentially into the cloning vector, pcDNA3.1. Construction of the chimeric receptors was carefully planned to include specific amino acid residues important in ligand binding. Priority was given to locate the joining section of the two receptor portions at the transmembrane region and to maintain full length of the receptor. This was to maintain the integrity of external and internal loops of the receptors important in ligand binding and signal transduction. Following transformation of the chimeras into E. coli to obtain sufficient DNA, construction of the desired chimeric receptors was verified by agarose gel electrophoresis for size and by PCR for the presence of the correct portions of each receptor. The two constructs were sent to Eli Lilly for sequencing. One construct was found to be appropriately constructed (GPR40.431_GPR41.459) but the other one was unstable and had undergone recombination as is often seen in cloned membrane proteins which can be toxic to E. coli. In the future, Human Embryonic Kidney cells will be transfected with the chimeric receptor and a FLIPR analysis will be performed to assess the activity of the receptor when stimulated by ligands of interest to Eli Lilly. Construction of additional chimeras will be needed in the future to fully understand the specific regions responsible for ligand binding and activation of GPR40 to aid in the design of drugs to stimulate insulin secretion by 03-cells. / Department of Biology

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In sexually reproducing individuals, intraorganismal genetic heterogeneity (IGH) or mosaicism is thought to occur infrequently while genetic homogeneity is presumed the norm. In organisms that undergo modular development, such as long-lived plants, IGH has been substantially documented. In Arabidopsis thaliana we have shown that non-parental DNA that is inherited at low but detectable rates can also manifest on single plants as genotypically distinct somatic sectors suggesting that even short-lived annual plants show IGH. The underlying mechanism responsible for generating this type of IGH remains unknown. In order to better understand this phenomenon I have tested the hypothesis that among genome changes that occur in response to stress, these putative triggers also up-regulate IGH. Metabolic stress, cold stress, mechanical damage and ROS exposure were examined. To test for IGH, transgene markers and polymorphic molecular markers were used. Also, presented in this thesis is work investigating the effect of in vitro propagation through tissue culture on IGH frequencies. Regenerated plants as well as undifferentiated callus tissue were genotyped and assayed for sequence reversions. Molecular genotyping revealed an outcome contrary to that predicted by the initial hypothesis showing instead that a high frequency of restoration occurred in the progeny of un-treated control plants. With the exception of samples passed through tissue culture, molecular marker changes, including single and double reversions of alleles, were detected in every line at some low level Furthermore, many of the revertants were found to be genetic mosaics. DNA sequence analyses revealed that sequences flanking three molecular markers that had undergone reversion were near identical to the great-grandparent of the sequenced individual. These results suggest that stress is perhaps an inhibitor of restoration. Although there may be other explanations for the results described in this thesis, the evidence implicates genome restoration as a mechanism for generating IGH.

Thesis (M.S.)--Ball State University, 2009. / Title from PDF t.p. (viewed on Nov. 30, 2009). Includes bibliographical references (p. [59]-63).

Thesis (M.S.)--West Virginia University, 2001. / Title from document title page. Document formatted into pages; contains vi, 41 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 39-41).

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