Genetic Basis of Colicin E Susceptibility in Escherichia coli I. Isolation and Properties of Refractory Mutants and the Preliminary Mapping of Their Mutations

Colicin E-resistant mutants were isolated in Escherichia coli K-12 which, although still apparently possessing the E receptor and adsorbing colicin, were nevertheless insensitive (refractory) to its effect. Eight phenotypic groups were obtained, but some mutants from three of these groups were all shown to map at gal, whereas a second refractory locus, giving resistance to E1 alone, mapped close to thy. It is suggested that the successful fixation of any of the three distinct colicins of group E may involve a dual role for the cell surface "receptor," the first for the binding of the protein and the second for the correct orientation of the bound molecule relative to the cytoplasmic membrane. The majority of the refractory mutants isolated may derive from changes in components concerned with the second of these receptor functions. Two groups of mutants, however, refractory to only E1 or E2, probably reflect changes in the intracellular transmission systems which specifically mediate the effects of these two colicins, the changes not allowing transmission through the cytoplasmic membrane to the respective targets of the colicins. The E1 adsorption site was shown to be distinct from that for E2 and E3, indicating an early separation of the colicin E transmission systems.     

Agreement Between Deoxyribonucleic Acid Base Composition and Taxometric Classification of Gram-Positive Cocci.

Silvestri, L. G. (Università Statale, Milan, Italy), and L. R. Hill. Agreement between deoxyribonucleic acid base composition and taxometric classification of gram-positive cocci. J. Bacteriol. 90:136-140. 1965.-It had been previously proposed, from taxometric analyses, that gram-positive, catalase-positive cocci be divided into two subgroups. Thirteen strains, representative of both subgroups, were examined for deoxyribonucleic acid (DNA) base composition, determined from melting temperatures. Per cent GC (guanine + cytosine/total bases) values fell into two groups: 30.8 to 36.5% GC and 69 to 75% GC. Strains with low per cent GC values belonged to the Staphylococcus aureus-S. saprophyticus-S. lactis taxometric subgroups, and those with high per cent GC values belonged to the S. roseus-S. afermentans subgroup. The hypothetical nature of any classification is emphasized, and, in the present work, the hypothesis derived from taxometric analyses of division into two subgroups is confirmed by the study of DNA base ratios. The two subgroups correspond, respectively, to the genera Staphylococcus and Micrococcus.     

Effect of dark repair on ultraviolet sensitivity of bacteriophage-infected bacteria

Feiner, R. R. (Columbia University, New York, N.Y.), and R. F. Hill. Effect of dark repair on ultraviolet sensitivity of bacteriophage-infected bacteria. J. Bacteriol. 91:1239-1247. 1966.-Changes in ultraviolet (UV) sensitivity of phage-host complexes during phage development have been studied for the following systems: T1 and Escherichia coli B, T1 and E. coli K-12S, lambda and E. coli K-12S. Complexes were formed with bacterial strains differing in ability to dark-repair UV damage to deoxyribonucleic acid and, after irradiation, were plated on bacteria differing similarly. In the first half of the latent period, the resistance of complexes formed with nonrepairing bacteria increased considerably; with T1 and E. coli B hcr(-), in 4 min the resistance became the same as that of complexes formed with repairing bacteria. The repair ability of plating bacteria affected survival curves only upon irradiation in the second half of the latent period after mature phages were present in the initial complex. Use of nonrepairing bacteria both for initial infection and for plating of late complexes resulted in a series of survival curves showing for all three systems the same pattern of change originally reported for T2-E. coli B complexes. Thus, a hitherto unexplained difference between radiation survival curves for T-even and T-odd phages seems due to repair of T-odd phages by the host.