It was the purpose of this study to investigate the effect of various concentrations of IAA on the nucleic acids of Chlorella pyrenoidosa TX 7-11-05. The time during the life cycle when the greatest effect occurred was investigated by the use of synchronous cultures.

Fungal infections are caused by a variety of fungi, and with a variety of clinical manifestations. Antifungal treatments are limited due to host toxicity and fungi gaining resistance. By utilizing the model organism Saccharomyces cerevisiae, we hope to elucidate the molecular mechanisms of fungal pathogenesis that we can then validate in the human pathogen Candida albicans, as well as explore options for novel therapies. Small molecule signaling is a method by which single-cell organisms can communicate with one another, enabling them to coordinate gene expression. This is a useful tool because it allows microbes to turn on phenotypes that are only valuable when done in large numbers, such as bioluminescence, or virulence traits. We have previously shown that the yeast Saccharomyces cerevisiae synthesizes the secondary metabolite indole-3-acetic acid (IAA) from tryptophan. IAA is secreted into the environment, where it acts as a signal. At low concentrations, the IAA signals yeast to induce virulence traits, while at high concentrations, it is lethal. The purpose of this thesis was to investigate the molecular mechanism of IAA (plant hormone auxin) regulation in fungi, specifically, Saccharomyces cerevisiae and the human pathogen Candida albicans. Towards this end, I first focused my efforts on evaluating the role of S. cerevisiae Grr1, as a putative IAA receptor. By evaluating the IAA response of several Grr1 mutants, I was able to show that the leucine-rich repeat region, while not required for function, likely plays a significant role in maintaining the structural integrity of the protein. Next, I evaluated IAA associated phenotypes, such as filamentation, surface adhesion and IAA uptake of the grr1 null mutant in the human pathogen Candida albicans. Together, these data support the hypothesis that GRR1 regulates IAA response, probably by regulating the IAA uptake carriers.

The work described in this thesis is in three parts:. Part I deals with the metabolism of 5-p-aminobenzene-sulphonamide- 3-methylisothiazole (sulphasomizole), 5-amino-3--methylisothiazole, sulphanilamide, and some of the acetyl derivatives. A marked species difference has been found in the metabolism of sulphasomizole.

The effects of polyamines, indole-3-acetic acid ( IAA ) and gibberellic acid ( GA3 ) on root elongation in radish ( Raphanus sativus L. cv. Luh Chin ) were studied. Incubation of radish seedlings in spermine or spermidine at 0.01 mM for 1hour, and then transferred to deionized water for 24 hours at 25¢J in the dark promoted root elongation as compared with concentration at 0.1 or 2 mM. When roots were treated with spermine or spermidine at 1 mM for 5 minutes, and then transferred to deionized water for 24 hours, root length increased significantly compared with controls. However, root length reduced gradually with increasing treatment times. Putrescine did not affect root elongation when treated in the same manner as spermine or spermidine. Exogenous spermidine synthesis inhibitor ( cyclohexylamine ) at 0.01, 0.1, 1 or 2 mM to the roots inhibited root elongation. The inhibition of root elongation was parallel to cyclohexylamine doses. Root length increased when spermine at 1 mM plus IAA at 10¡Â¹ ¡Ñ 6 nM was applied for 1 hour, and then transferred to deionized water for 24 hours compared with spermine at 1 mM plus IAA 10¡Â² or 1¡Ñ 6 nM. Root length was longer when treated with spermidine at 1 mM plus IAA at 10¡Â²¡Ñ 6 nM than at 10¡Â¹ or 1¡Ñ 6 nM. Root treated with spermine at 1 mM plus GA3 at 10¡Â²¡Ñ3 £gM Resulted in a longer root than treated with spermine at 1 mM plus GA3 at 10¡Â¹ or 1¡Ñ 3 £gM. Roots treated with spermidine at 1 mM plus GA3 at 10¡Â²¡Ñ3 £gM promoted root elongation. However, any treatments of spermine or spermidine in combination with IAA or GA3 significantly reduced the root length when compared with controls. Furthermore, either IAA or GA3 could not restore the inhibitory effects of root elongation caused by spermine or spermidine treatment at 1 mM for 1 hour and then transferred to deionized water for 24 hours. Endogenous spermidine and spermine contents after exogenous spermine plus GA3 treatment increased by increasing GA3 concentrations. But endogenous spermidine and spermine contents was the least in spermine 1 mM plus IAA 10¡Â¹ ¡Ñ 6 nM treatment. However, endogenous spermidine contents after exogenous spermidine plus IAA or GA3 application reduced significantly when compared with controls. But there is no significant difference of spermidine content between different exogenous IAA doses. In contrast, spermidine content maintained at a high level in spermidine at 1 mM plus GA3 at 10¡Â²¡Ñ3 £gM as compared with other spermidine plus GA3 combinations. However, endogenous spermine contents were not affected by exogenous spermidine plus IAA or GA3.

Cu-treated peanut seedlings not only showed a significant inhibition in peanut root growth, but also a decrease in endogenous indole-3-acetic acid (IAA) contents . The decline of IAA content in Cu-treated tissues is accompanied by an increase in cationic peroxidase activity. In addition, the increase in cationic peroxidase (pI 8.5) activity is correlated with an increase in cationic peroxidase transcripts. Cu might suppress the growth of peanut roots by inducing the synthesis of the cationic peroxidase isozyme that degrades endogenous IAA, causing the retardation of peanut root growth. The increase in activity of anionic peroxidases (pI 3.5) is also correlated with the rise in lignin content in Cu-treated roots. We suggest that the increase in anionic peroxidases (pI 3.5) induced by Cu might be responsible for lignin synthesis in peanut roots, and remove excess hydrogen peroxide, thus serving a detoxifying role during Cu treatment.

Not available / text

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

Thesis (M.S.)--Virginia Polytechnic Institute, 1961. / Vita. Abstract. Includes bibliographical references (leaves 83-89). Also available via the Internet.

Thesis (M.S.)--Ohio University, August, 2004. / Includes bibliographical references (p. 78-80).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1966. / Typescript. Vita. "The appendices of the thesis consist of a collection of scientific papers (preprints and reprints) which were co-authored with my research director, Professor W.J. Blaedel." eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.