The dimorphic yeast <i>Candida albicans</i> is capable of growth in a budding yeast form and in a mycelial form. Growing in the yeast form in the digestive and vaginal tracts it normally presents no problems to the host; however, when the dimorphic transition takes place and mycelial growth is initiated, symptoms of candidiasis manifest in the host tissues. This thesis studies the control of the dimorphic response and investigates some of the cellular changes which accompany it. Germ tube formation was induced in a defined amino acids/salts medium. Temperature, pH and culture density were critical factors in stimulating the dimorphic response. Different percentages of term tube formation were recorded for eight different strains of <i>C. albicans</i>. Each strain also acidified the growth medium to a different extent; this was correlated to the extent of filamentation of each strain. Internal pH changes were monitored using the weak and technique and ³¹P nuclear magnetic resonance spectroscopy during bud and germ tube formation. In mycelial cells there was an initial increase in internal pH from 6.8 to around 8.0, followed by a gradual decrease to neutrality at the actual time of germ tube emergence. Cells in the budding form of growth did not exhibit such a marked increase in cytoplasmic alkalinisation. Mutant strains which were unable to produce germ tubes did not show cytoplasmic alkalinisation under conditions which would normally promote mycelial growth. Activation of the plasmamembrane ATPase may account for this increase in internal pH since diethylstilboestrol inhibited cytoplasmic alkalinisation and germ tube formation without affecting cell viability. Weak bases induced artificially, a rise in internal pH which was accompanied by germ tube formation. Potassium ions were found to enter cells as protons were expelled at the initiation of mycelial growth. Lactic acid prevented any rise in internal pH during germ tube formation. It also collapsed the ΔpH of the cells preventing growth by bud or germ tube formation. This may relate to the observation that endogenous <i>Lactobacilli</i> compete with <i>C. albicans</i> in the vagina and may explain why topically applied live yoghurt cultures soothe vaginal candidiasis. Transport of methionine was found not to be significantly different in cells induced to the budding or mycelial form. Transport or arginine and glutamate was induced by growing cells in the presence of these amino acids. The amino acid pool levels changed during the dimorphic process in <i>C. albicans</i>. A rapid increase in the pool level was shown within the first hour of both bud and hyphal growth followed by a gradual decrease. Little or no evidence was found in support of the hypothesis that the formation of hyphae is a response to nutrient starvation.

Thesis (Ph. D.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 101-137).

Thesis--Wisconsin. / Vita. Includes bibliographical references (leaves 103-113).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1975. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1908. / Reprinted from The Journal of Morphology, vol. XX, no. 2. Includes bibliographical references (p. 291-295).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1926. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Luteinizing hormone (LH), one of the two gonadotropin hormones released from the anterior pituitary gland, binds to its receptor (LHR) in the gonads to stimulate steroid hormone production, in addition to ovulation and gametogenesis. Mutations of the receptors amino acid sequence have the ability to either constitutively activate or inactivate it. All activating mutations result in male-limited precocious puberty. Males with this condition undergo puberty around 4 years of age, and have a premature elevation in testosterone levels and premature skeletal development. In order to understand how chronic ligand-mediated activation of the LHR affects gonadal development and function, a mouse model expressing a yoked hormone-receptor (YHR) complex, engineered by covalently linking the hormone human chorionic gonadotropin to the rat LHR, has been studied. YHR+ males have prepubertally elevated testosterone and decreased gonadotropin levels, smaller testis, and smaller average seminiferous tubule diameters when compared to wild type (WT) animals. In a preliminary breeding study it was shown that YHR+ males were sub-fertile. Based the phenotype exhibited by the YHR+ mice, it was hypothesized that increased levels of testosterone in addition to decreased gonadotropin hormone levels in neonatal and prepubertal mice that results from premature activation of the luteinizing hormone receptor causes spermatogenesis to be impaired. The first objective of this study was to determine if there was a difference in the testicular germ cell and Sertoli cell populations in the WT and YHR+ animals using flow cytometry and systematic Sertoli cell counting, respectively. There was no difference in the Sertoli cell population between YHR+ animals and WT controls, but there were significantly fewer total germ cells in YHR+ animals at 10 days and from 4 weeks through adulthood. The second objective was to calculate the daily sperm production in the testis and epididymis of WT and YHR+ animals in order to determine if there is a further decrease in the total sperm count due to an epididymal dysfunction. Interestingly, there were significantly fewer sperm calculated in the caput/corpus region of the epididymis in YHR+ males at 12 weeks of age, but not in the testis and cauda epididymis. Furthermore, the daily sperm production in WT and YHR+ mice at 16 weeks of age were not significantly different. The final objective was to determine if the decrease in germ cells observed in YHR+ animals is the result of decreased proliferation or an increase in either germ cell or Sertoli cell apoptosis. Quantification of germ cell and Sertoli cell proliferation revealed no significant difference between the WT and YHR+ animals. Similar findings were found after quantification of apoptotic germ cell and Sertoli cells. Taken together, these data suggest that premature elevation in testosterone and persistently lower levels of circulating follicle stimulating hormone (FSH) are affecting Sertoli cell function, which is causing a reduced germ cell to Sertoli cell ratio in the YHR+ mice. These data suggest that the decrease in testis weight and seminiferous tubule diameter in YHR+ mine is due to a decrease in germ cell rather than Sertoli cell number.

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LD2668 .T4 1941 D61 / Master of Science