Deletion mutant collections allow for the systematic study of gene function by linking a genotype to a phenotype. Furthermore, these collections permit the parallel and quantitative study of phenotypes, which is the foundation of functional genomics. I begin by summarizing the methods used and data derived from the field of functional genomics using the Baker’s yeast Saccharomyces cerevisiae, and provide important background information on the origins of the filamentous growth-competent S.cerevisiae strain Σ1278b, and the developmental process of fungal dimorphism. I describe my efforts in creating a complete deletion mutant collection in the filamentous growth-competent S.cerevisiae strain Σ1278b, and the subsequent phenotypic analysis of that deletion mutant collection. By quantitatively measuring mutant phenotypes of cells undergoing haploid invasive growth, biofilm mat formation and diploid pseudohyphal growth, I studied the clinically relevant developmental process of fungal dimorphism. I present the first genome-wide and quantitative phenotypic analysis of fungal dimorphism and identify a novel transcription factor encoded by the open reading frame YDL233W, which I named FMR1for Filamentation Master Regulator 1. By performing genetic, cell biological, biochemical, and expression analysis, I demonstrate that Ydl233w acts by forming a protein complex with the DNA-binding transcription factors Flo8 and Mss11 and this complex binds to a specific element within the promoter of the surface adherence mediating gene FLO11. I directly compare the essential gene sets between the Σ1278b deletion collection and the reference deletion collection made in the S288c genetic background completed by the Yeast Deletion Consortium in 2002. I find that most essential genes are shared between these two strains but a number of genes are essential for viability in only one genetic background, a phenomenon termed conditional essentiality. I describe the genetic basis of conditional essentiality as a consequence of the complex inheritance of background-specific alleles. Lastly, I summarize the scientific advancements of my research using the Σ1278b deletion collection, and highlight some potential applications for both the data derived from my research and the deletion mutant collection itself. The Σ1278b deletion collection provides a valuable resource for yeast geneticists, evolutionary biologists, researchers of fungal disease, and researchers interested in modeling the genetics that underlie complex traits and diseases.

Compounds belonging to the vitamin K family possess anti-hemorrhagic property, and are used in treating patients suffering from hypoprothrombinemia and obstructive jaundice. Some of these compounds also exhibit marked antimicrobial activity toward various microorganisms. Vitamin K₅, 4-amino-2-methyl- 1-naphthol hydrochloride, a water-soluble analog of vitamin K has been shown to possess such an antimicrobial activity toward many bacteria, molds, and yeasts. Much of the work reported in literature is on its use as a possible food preservative, and little information is available on the mechanism of its action on the microorganisms. In this study, the mode of action of vitamin K₅ on Saccharomyces cerevisiae was investigated. Its effect on yeast cells, with and without sodium chloride; its color reactions with trisodium pentacyanoaminoferroate; its influence on certain enzyme systems of the yeast cell as indicated by 2, 3, 5-triphenyltetrazolium chloride; and the antagonistic effect of cysteine hydrochloride toward it were studied. In addition, the sulfhydryl groups of yeast cells were estimated by amperometric titration, and carbon dioxide production by yeast cells from different substrates was determined manometrically. The results showed that vitamin K₅ did not inhibit the yeast cells immediately on coming into contact with them. Vitamin K₅, with sodium chloride, produced 76 percent inhibition of yeast cells in 50 minutes as compared to 50 percent inhibition produced during the same time when used alone. Cysteine hydrochloride reacted with vitamin K₅ and stopped it from producing a blue color with trisodium pentacyanoaminoferroate. Cysteine hydrochloride also antagonized the antifungal activity of vitamin K₅, since in its presence vitamin K₅ failed to stop the reduction of 2, 3, 5-triphenyltetrazolium chloride by dehydrogenase systems. The yeast cells which had previously been inhibited by vitamin K₅ could not be revived by treatment with cysteine hydrochloride. These cells had developed a dark pink color which could not be removed by repeated washings. The sulfhydryl groups of yeast cells were reduced quantitatively when they were exposed to vitamin K₅. The reduction was not immediate and followed the same pattern as in case of total counts. Higher concentrations of vitamin K₅ inhibited carbon dioxide production by yeast cells to a greater extent in the three substrates used in this study. The action of vitamin K₅ is not immediate, the coloration picked up by the cells cannot be washed off, and its action is hastened in the presence of sodium chloride. All these seem to indicate that permeability of the cell is involved in some manner in the inhibition process. Higher concentrations of vitamin K₅ produce greater inhibition which shows that this compound also combines with sulfhydryl groups of the yeast cells. These findings suggest that the mode of action of vitamin K₅ is most likely due to an alteration of cell permeability as well as by combining with sulfhydryl groups of the yeast cells. / Graduation date: 1963

v, 100 leaves : ill., graphs, tables ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.1976) from the Dept. of Genetics, University of Adelaide

1 v. (various paging) : photos, graphs, tables ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Oral Biology, 1980

Thesis (Ph. D.)--University of Chicago, 1921. / "Private edition, distributed by the University of Chicago libraries, Chicago, Illinois." "Reprinted from the Journal of biological chemistry, vol. XLIV, no. I, October 1920 and vol. XLVIII, no. 2, October 1921." Also available on the Internet.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2007. / Title from title screen (site viewed Mar. 27, 2008). PDF text: xxiii, 235 p. : ill. (some col.) ; 3 Mb. UMI publication number: AAT 3284719. Includes bibliographical references. Also available in microfilm and microfiche formats.

Thesis (Ph.D. 1976) from the Department of Genetics, University of Adelaide.

Thesis (Ph.D.) -- University of Adelaide, Department of Oral Biology, 1980.

Thesis (M.Sc.) --University of Adelaide, 1953. / Typewritten copy.

Thesis (Ph.D.) -- University of Adelaide, Dept. of Plant Science, 2000. / Bibliography : leaves 74-92.