The initial studies reported in this dissertation were attempts to induce mutations in those genes which control dissociation in cells of Nei sseria gonorrhoeae. These studies led to an investigation of survival curves of cells grown in liquid media. Instead of survival curves reflecting the diploid nature of gonococci, multiple cell kinetics were observed. It was found that large clumps contained a predominance of cells of the T2 type and that when these clumps were dispersed by DNAase, it appeared that dissociation of T2 was inhibited. The notion of a mechanism of T2 to T4 dissociation being due to genetic transformation was disspelled by these data.

When Y-1 mouse adrenal tumor cells were treated with sodium orthovanadate, an intermediate filament (IF) inhibitor in BHK21-F cells, there was no change in the amount of 20α-dihydroprogesterone produced. A neurofilament inhibitor, β, β'-iminodipropionitrile (IDPN), enhanced the ability of Y-1 cells to produce steroid in response to ACTH by acting on the plasma membrane. Electron microscopy of Y-1 cells extracted with Triton X-100 revealed that both vanadate and IDPN caused the aggregation of cytoskeletal and granular structures in the perinuclear area. The steroidogenic effects of IDPN suggest that the perinuclear aggrergation of cytoskeletal structures may result from the detachment of IF from the plasma membrane, while the reason for the cytoskeletal changes by vanadate is unknown.

Using cultured Y-1 mouse adrenal tumor cells which produce the steroid 20(-hydroxypregn-4-en-3-one (20-DHP), it was found that 10-5 M corticosterone and deoxycorticosterone increased basal and inhibited ACTH-induced 20-DHP production. The steroid effects were concentration-dependent, reversible, and specific since six other steroids did not stimulate steroidogenesis and varied in their ability to inhibit ACTH-induced steroidogenesis. Cytochalasin D inhibited steroid-stimulated 20-DHP production, suggesting a mechanism of steroid stimulation similar to that of ACTH. Steroidogenesis stimulated by cholera toxin, (Bu) 2 cAMP, or pregnenolone was not inhibited by exogenous steroid; corticosterone increased basal and inhibited ACTH-induced intracellular cAMP production. Steroids altered cell surface morphology. These findings suggest that steroids alter adrenal steroidogenesis by acting within the plasma membrane.

The purpose of this study was to search for the substrates utilized by Azotobacter vinelandii in dialysed soil media. Also, we sought to determine the relationship between these substrates and the growth and morphological variations of A. vinelandii. p-Hydroxybenzoic acid was shown to be used as the carbon and energy source by A. vinelandii in dialysed soil medium. The amount of this compound in the soil dialysed soil medium ranged from 14 to 21 micrograms per gram of soil. In a dialysed soil medium, p-hydroxybenzoic acid induced A. vinelandii to form minute bodies, similar to the filtrable forms reported by Gonzalez and Vela, although no growth of minute bodies was detected.