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A unicellular blue-green alga, Agmenellum quadruplicatum , and a filamentous blue-green alga, Lyngbya lagerheimíi , were grown heterotrophically in dim light with glucose as major source of carbon and possibly energy. The dim-light conditions did not support autotrophic growth. The two blue-green algae appeared to have the same metabolic block, namely an incomplete tricarboxylic acid cycle, as has been found in other obligately phototrophic blue-green algae. Under dim-light conditions, glucose made a greater contribution to cell constituents (amino acids) of A. quadruplicatum and L. lagerheimii than under high-light conditions.

Cell-free extract (crude extract) of Agrobacterium tumefaciens grown on d -glucuronate or d -glucarate converts d -glucarate and galactarate to a mixture of 2-keto-3-deoxy- and 4-deoxy-5-keto- d -glucarate. These compounds are then converted by partially purified crude extract to an intermediate tentatively identified as 2,5-diketoadipate. The same enzyme preparation further decarboxylates this intermediate to α-ketoglutarate semialdehyde, which is subsequently oxidized in a nicotinamide adenine dinucleotide-dependent reaction to α-ketoglutaric acid. Since A. tumefaciens converts d -glucuronic acid to d -glucarate, a pathway from d -glucuronate to α-ketoglutarate in A. tumefaciens was determined.

Two strains with mutations in the first structural gene of the histidine operon of Salmonella typhimurium were characterized. (The first structural gene specifies the first enzyme of histidine biosynthesis, phosphoribosyltransferase, which is sensitive to feedback inhibition by histidine.) One mutation, hisG3934 , results in a phosphoribosyltransferase which is no longer sensitive to feedback inhibition by histidine but is instead subject to inhibition by aspartic acid. The other mutation, hisG3935 , allows the histidine operon to be partially repressed by several amino acids, including aspartic acid. Analysis of hisG3935 is consistent with the hypothesis that phosphoribosyltransferase is directly involved in the regulation of the histidine operon.

The structural determinants for antigen 34 in the E group salmonella are glucosyl substituents on the galactosyl units of the O antigen which has a mannosylrhamnosylgalactose repeating sequence. The temperate bacteriophage ε 34 brings about the production of antigen 34. It has been shown here that glucose is transferred from uridine diphosphate glucose to the O antigen via a glucosyl-lipid intermediate in a two-step reaction. Glucose is linked through carbon 1 to the lipid by a phosphodiester bridge, the glucosyl bond having the β-anomeric configuration. The lipid is a C 55 -polyisoprenoid alcohol, each isoprene unit having one double bond. It is the same lipid which is involved in the synthesis of the O antigen repeating sequence.

Polyoma virus particles were purified by equilibrium centrifugation in CsCl. Particles from three regions of the density gradient were examined for infectivity, for their ability to induce expanded pools of deoxyribonucleic acid (DNA) precursors, and for their ability to stimulate the synthesis of DNA. The most infectious population of particles, the virions, having a buoyant density of 1.33 g/ml, gave the greatest stimulation of the DNA-synthesizing apparatus of mouse embryo cells. Empty particles at density 1.29 g/ml had no DNA stimulatory activity. A population of particles of intermediate density, referred to as pseudovirions, was also much less active than virions in stimulating DNA synthesis, and the limited stimulatory activity of the latter fraction may be accounted for by its measured contamination with infective particles.

Zygorhynchus vuilleminii , a nonmelanin-containing fungus, was not lysed by mycolytic actinomycetes. Several enzymes and Streptomyces enzyme preparations digesting walls of other fungi were without appreciable activity on walls of Zygorhynchus species. A bacterium able to solubilize a portion of the Zygorhynchus wall released little or no reducing sugars from these structures. Fractions of Z. vuilleminii walls were resistant to glucanase hydrolysis, but certain fractions were digested by chitinase and microbial enzyme preparations. The walls and several wall fractions were not readily susceptible to degradation by a soil community. Walls of lysis-resistant Zygorhynchus species contained glucosamine, fucose, glucuronic acid, and galactose but little or no glucose. Resistant wall fractions were rich in uronic acid and fucose, whereas the readily degradable fractions contained abundant glucosamine. Cultural conditions affected the extent of digestion and composition of the walls. Possible reasons for the resistance of Zygorhynchus to lysis in nature are discussed.

Preparations of purified cell walls from Staphylococcus aureus were shown to contain small amounts of phospholipid and glycerol teichoic acid. Since these are components of the cell membrane, it is probable that the wall itself contains no lipid, but does retain fragments of membrane because of physical connections between wall and membrane. In walls of S. aureus strain 52A5, which completely lacks ribitol teichoic acid, the only phosphorylated compound identified as a genuine wall component was a phosphorylated derivative of murein that gave rise to muramic acid phosphate on acid hydrolysis. Muramic acid phosphate was also identified in hydrolysates of walls from S. aureus H and strain 52A2.

Novobiocin-supersensitive (NS) mutants which could not grow on plates containing 40 μg or less of novobiocin per ml were isolated from Escherichia coli strain JE1011 (derived from E. coli K-12). Most of these NS mutants were found to have incomplete lipopolysaccharides (LPS), and they lack phosphate diester bridges in their backbone structure, with or without total loss of heptose, to which the phosphate diester is linked, and consequently lack external outer-core oligosaccharides. The phosphate diester bridges in the LPS backbone are apparently very important in forming a cell surface structure resistant to the penetration of antibiotics such as novobiocin, spiramycin, and actinomycin D. NS mutants, with incomplete LPS, lacking phosphates in their backbone structure were found to be resistant to phage T4, and those which also lacked heptose were resistant to phages T4 and T7. In contrast to the generally accepted idea that resistances to phages T3, T4, and T7 are linked genetically, no NS mutant was found to be resistant to T3. The possible structures of the receptors for T4 and T7 are discussed. The positions of novobiocin-supersensitive genes on the chromosome of several of the NS mutants defective in LPS were mapped. The genes were designated lpcA (between ara and lac ) and lpcB (between 55 min and 60 min). The latter seemed to be a group of several related genes.