Thesis (M.S.)--University of Missouri-Columbia, 2004. / Typescript. Includes bibliographical references (leaves 84-89). Also available on the Internet.

Thesis (M.S.)--University of Missouri-Columbia, 2004. / Typescript. Includes bibliographical references (leaves 84-89). Also available on the Internet.

No description available.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2008. / Title from title screen (site viewed Feb. 17, 2009). PDF text: 93 p. : col. ill. ; 4 Mb. UMI publication number: AAT 3328257. Includes bibliographical references. Also available in microfilm and microfiche formats.

Mutations affecting the mitochondrial electron transport chain cause numerous neurodegenerative disorders in humans and affect longevity in other organisms. A natural model system to study the relationship between mitochondrial function and aging within an evolutionary or population genetic context has been lacking. Natural populations of Caenorhabditis briggsae nematodes were recently found to harbor mitochondrial genetic variation with likely functional consequences for aging. Specifically, C. briggsae isolates containing high frequencies of a deletion mutation affecting the mitochondrial NADH dehydrogenase 5 (ND5) gene were found to have reduced reproductive fitness and lifespan and elevated levels of mutagenic superoxide. Here, rates of growth and aging and aerobic respiratory capacity were evaluated in several isolates spanning the range of mitochondrial genetic variation in this species. There is considerable variation among isolates for all measured traits, although the observed relationships between isolate-specific trait means and ND5 deletion frequency did not always conform to my expectations. In an effort to determine whether the among-isolate phenotypic variation is due to mitochondrial rather than to nuclear genetic variation, inter-population hybrids of C. briggsae were created and compared to the progenitor isolates. Surprisingly, evidence for paternal mitochondrial inheritance was detected in many of these hybrid lines. Where mitochondrial genomes were maternally inherited as expected, intergenomic epistasis appears to contribute to fitness, longevity, and aging in this species.

No description available.

No / We have assessed the histological preservation of naturally degraded human hair shafts, and then assayed each for levels of amplifiable mitochondrial DNA and damage-associated DNA miscoding lesions. The results indicate that as sample histology is altered (i.e. as hairs degrade) levels of amplifiable mitochondrial DNA decrease, but no correlation is seen between histology and absolute levels of mitochondrial DNA miscoding lesions. Nevertheless, amplifiable mitochondrial DNA could be recovered across the complete range of the histological preservation spectrum. However, when template copy number is taken into consideration, a correlation of miscoding lesions with histology is again apparent. These relationships indicate that a potential route for the generation of misleading mitochondrial sequence data exists in samples of poor histology. Therefore, we argue that in the absence of molecular cloning, the histological screening of hair may be necessary in order to confirm the reliability of mitochondrial DNA sequences amplified from hair, and thus represents a useful tool in forensic mitochondrial DNA analyses.

No description available.

No description available.

No description available.