The effect of various nutritional conditions on the levels of Krebs cycle enzymes in Bacilllus subtilis, B. licheniformiiis, and Escherichia coli was determined. The addition of glutamate, a-ketoglutarate, or compounds capable of being catabolized to glutamate, to a minimal glucose medium resulted in complete repression of aconitase in B. slibtilis and B. lichenifortunis. The synthesis of fumarase, succinic dehydrogenase, malic dehydrogenase, and isocitric dehydrogenase was not repressed by these compounds. It is postulated that glutamate or a-ketoglutarate is the true corepressor for the repression of aconitase. A rapidly catabolizable carbon source and a-ketoglutarate or glutamate must be simultaneously present for complete repression of the formation of aconitase. Conditions which repress the synthesis of aconitase in B. subtilis restrict the flow of carbon in the sequence of reactions leading to ae-ketoglutarate but do not prevent glutamate oxidation in vivo. The data indicate that separate and independent mechanisms regulate the activity of the anabolic and catabolic reactions of the Krebs cycle in B. slubtilis and B. lichenijbrm7lis. The addition of glutamate to the minimal glucose medium results in the repression of aconitase, isocitric dehydrogenase, and fumarase, but not malic delhydrogenase in E. coli K-38.
then the recombination to d2-la+•. and d2-la,+• followed by the back electron transfer probably from A"• furnishes the degenerate rearrangement. The fact that 1 did not isomerize to the thermodynamically more stable isomers, l-(diphenylmethylene)cyclopropane, may suggest that 72-2a+• may be a bisected species in which the pivot carbon does not enter the allylic system because of steric restrictions. Molecular oxygen13 then captures d2-2a+• faster than recombination,10 giving d2-5a+•, 72-6a+•, and 72-6a,+•, and the cyclization followed by the back electron transfer gives dioxolanes (Scheme III).Further experiments are continuing on the photosensitized (electron-transfer) sigmatropic rearrangements and will be reported soon.
The biological methylation of arsenic was first recognized during several poisoning episodes in the early nineteenth century (1).Several individuals succumbed in their sleep to arsenic poisoning, the cause of which was not immediately recognized. Initially it was attributed to the presence of particles of arsenic in the room air originating from wallpaper pigments.Others thought biological activity might have reduced these arsenic pigments to arsine which was the toxic agent.An experimental approach ultimately determined the cause of gas formation when an Italian scientist, Gosio, isolated and characterized some volatile arsenic-producing fungi.He exposed potato pulp containing arsenic trioxide to the air and soon detected growth of molds accompanied by a garlic-type odor. From these cultures he isolated a mold Penicillium brevicaule (Scopulariopsis brevicaulis) which produced copious quantities of gas with a garlic-like odor. Gosio trapped samples of the gas from this culture and converted it to arsenic proving that the metal had truly been volatilized by the fungus (2). An associate, Bignelli, performed an elemental analysis on the gaseous material and incorrectly deduced the structure of diethylarsine (3).It wasn't for another thirty years that the structure of "Gosio gas" was determined by Challenger's group in England. A great deal of research on biological methylation of metals was performed by Challenger and associates over twenty odd years beginning with the methylation of arsenic compounds (1,4).These researchers cultured several strains of S. brevicaulis on bread crumbs containing arsenic trioxide and the gas produced was precipitated in aqueous solutions as either the mercuric chloride,
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.