The proU locus in Escherichia coli encodes an important osmoregulatory function which mediates the growth-promoting effect of L-proline and glycine betaine in high-osmolarity media. This locus was cloned, in contiguity with a closely linked Tn10 insertion, onto a multicopy plasmid directly from the E. coli chromosome. For a given level of osmotic stress, the magnitude of osmoresponsive induction of a single-copy proU::lac fusion was reduced in strains with multiple copies of the proU+ genes; in comparison with haploid proU+ strains, strains with the multicopy proU+ plasmids also exhibited enhanced osmotolerance in media supplemented with 1 mM L-proline or glycine betaine. Experiments involving subcloning, Tn1000 mutagenesis, and interplasmid complementation in a deletion mutant provided evidence for the presence at this locus of two cistrons, both of which are necessary for the expression of ProU function. We propose the designations proU for the gene originally identified by the proU224::Mu d1(lac Ap) insertion and proV for the gene upstream (that is, counterclockwise) of proU.

A series of monomeric and dimeric cationic surfactants with tuned polarity was synthesized. Oil solubilization capacity, thermotropic liquid crystalline properties, and minimum inhibitory concentration (MIC) of novel hydroxylated cationic surfactants using selected gram positive and gram negative bacteria were examined. Antibacterial activity and the propensity of gemini surfactants for oil solubilization were observed to be better than those of corresponding monomeric surfactants. Pseudo ternary phase diagrams for these surfactants, methyl methacrylate (MMA), and water clearly showed, that microemulsions can be easily formulated with all these surfactants. Solubilization and foam studies of mixed surfactant systems were also examined. Molecular architecture like the tail length, head group area, and presence of ethanolic goups in the surfactant affect the performance properties. Unlike conventional gemini surfactants the synthesized gemini surfactants also show thermotropic liquid crystalline properties (smectic-A, L a phase).

Summary The well‐known role of antibiotics in killing sensitive organisms has been challenged by the effects they exert at subinhibitory concentrations. Unfortunately, there are very few published reports on the advantages these molecules may confer to their producers. This study describes the construction of a genetically verified deletion mutant of Streptomyces flaviscleroticus unable to synthesize chromomycin. This mutant was characterized by a rapid loss of viability in stationary phase that was correlated with high oxidative stress and altered antioxidant defences. Altered levels of key metabolites in the mutant signalled a redistribution of the glycolytic flux toward the PPP to generate NADPH to fight oxidative stress as well as reduction of ATP‐phosphofructokinase and Krebs cycle enzymes activities. These changes were correlated with a shift in the preference for carbon utilization from glucose to amino acids. Remarkably, chromomycin at subinhibitory concentration increased longevity of the non‐producer and restored most of the phenotypic features’ characteristic of the wild type strain. Altogether these observations suggest that chromomycin may have antioxidant properties that would explain, at least in part, some of the phenotypes of the mutant. Our observations warrant reconsideration of the secondary metabolite definition and raise the possibility of crucial roles for their producers.

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A new chromosomal mutation (cpeA), that causes increased expression of plasmid-borne genes in Escherichia coli, was identified and mapped to the sbcB locus. The effect of the mutation on plasmid transcription was non-specific with respect to the various promoters that were studied, but was more pronounced for an IncW low-copy-number plasmid than for ColE1- or p15A-based, high-copy-number plasmids. The mutant phenotype was observed even in recB+C+D+ strains, but not in recA mutants. The increased-expression phenotype was also observed in sbcB15 but not in xonA1 (another sbcB allele) mutants, suggesting that the expression of this phenotype is mediated by genes of the so-called RecF pathway family. Consistent with this interpretation was the observation that the cpeA mutant phenotype was less pronounced in recF, recJ and recO mutants. The increased-expression phenotype was also correlated with increased recovery of plasmid DNA from the cpeA/sbcB mutant strains, but there was no evidence for the occurrence of linear plasmid multimers in these strains.