Properties of Mutants in Galactose Taxis and Transport

beta-Methylgalactoside (mgl) permease mutants of Escherichia coli, which are defective in three genes, mglA, mglB, and mglC, were assayed for galactose taxis and galactose transport. The mglB product is the galactose-binding protein. Previous evidence, supported by our new findings, shows that the galactose-binding protein is the recognition component for galactose taxis as well as for galactose transport. Most mutants defective in mglB showed strong effects on both chemotaxis and transport; however, a couple showed effects chiefly on one process or the other, thus allowing a separation of chemotaxis and transport. The mglA and mglC products have not yet been identified, but they must be components of the galactose transport machinery since mutants defective in mglA or mglC, or both, showed strongly reduced transport. Although some of these mutants showed little chemotaxis, most gave close to wild-type chemotactic responses. Thus, transport is not required for galactose taxis. The bacteria detect changes in the fraction of binding protein associated with galactose, not changes in the rate of transport.     

Antibacterial Action of Essential Oils of Artemisia as an Ecological Factor: II. Antibacterial Action of the Volatile Oils of Artemisia tridentata (Big Sagebrush) on Bacteria from the Rumen of Mule Deer

Rumen microorganisms of wild and captive deer were subjected to increasing amounts of volatile oils. The oils had a marked antibacterial effect on the rumen bacteria when the concentration reached approximately 16 muliters of oil per 10 ml of rumen fluid nutrient broth. The gross reactions of rumen bacteria obtained from wild, as well as captive, deer to the volatile oils seemed to be of the same magnitude; thus no adaptation by the bacteria to the oils was apparent.     

Interferon Production in Mice by Cell Wall Mutants of Salmonella typhimurium

The interferon response elicited by Salmonella typhimurium mutants in mice is not dependent on the presence of a complete cell wall lipopolysaccharide. In fact, a mutant (G30/C21) which has lost all the polysaccharide side chains and sugars of the O antigen and contains only 2-keto-3-deoxyoctonate and lipid is indistinguishable in its interferon-stimulating ability from the wild type which possesses a complete O antigen with polysaccharide side chains.     

Purification and Chemistry of Bacteriophage ?

From a stock of varkappa phage grown on Salmonella, a host-range mutant which attacks Escherichia coli was isolated. As in the case of Salmonella, only motile strains of E. coli are sensitive to varkappa. The phage shows an eclipse period of 35 min and a minimal latent period of 52 min. The adsorption rate constant is 3 x 10(-9) ml/min. Adsorption shows a marked dependence on temperature. Bacteriophage varkappa was purified by differential centrifugation and CsCl density gradient centrifugation. It contains deoxyribonucleic acid (DNA) which is double-stranded. The DNA has a molecular weight of 42 million and a guanine plus cytosine content of 57%. Of 68 molecules of DNA inspected, 7 were circular. The phage particle weight is about 90 million.     

α1-Adrenergic Receptor Mediates Arachidonic Acid Release in Spinal Cord Neurons Independent of Inositol Phospholipid Turnover

The alpha 1-adrenergic receptor has been shown to mediate the release of arachidonic acid in FRTL5 thyroid cells and MDCK kidney cells. In primary cultures of spinal cord cells, norepinephrine stimulated release of arachidonic acid (from neurons only) and turnover of inositol phospholipids (from neurons and glia) via alpha 1-adrenergic receptors. These two responses were dissociated by treatment with phorbol ester and pertussis toxin, which inhibited production of inositol phosphates with no appreciable effect on release of arachidonic acid. Extracellular calcium was required for release of arachidonic acid, but not for production of inositol phosphates. The calcium channel blockers nifedipine and verapamil inhibited release of arachidonic acid only. However, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), a compound that blocks intracellular calcium release, diminished production of inositol phosphates, but had little effect on release of arachidonic acid. These results suggest that alpha 1-adrenergic receptors couple to release of arachidonic acid in primary cultures of spinal cord cells by a mechanism independent of activation of phospholipase C, possibly via the activation of phospholipase A2.