Of 24 strains of P . pestis tested, all but one produced pesticin. A mutant of P. pseudotuberculosis which was resistant to pesticin produced by one strain of P. pestis was found to be resistant to pesticin produced by all the other strains.
Genetic analysis and molecular characterization of plasmid deoxyribonucleic acid (DNA) was performed in a toxigenic isolate ofStaphylococcus aureus strain DU4916. Elimination, transduction, and transformation experiments provided us with a series of derivatives similar except for the presence or absence of genes mediating resistance to penicillin (penr), methicillin (mecr), and tetracycline (tetr) and enterotoxin type B (SEB) production (entB+). The derivatives were examined for the presence of a plasmid species which encodes for SEB production. Two distinct species of covalently closed circular DNA of about 2.8 x 106 and 0.75 x 106 daltons were identified in an ethidium bromide-cured, penicillinase-negative (pens) isolate, SN109 (mecr tetr emtB+). Further segregation of either methicillin resistance or tetracycline resistance or of both together resulted in the loss of SEB production and the disappearance of both plasmids. Transduction from strain SN109 showed that determinants for tetracycline resistance are carried by the 2.8 x 106f-dalton plasmid. Transformation with covalently closed circular DNA from strain SN109 yielded mecs tetr entBtransformants harboring the tetracycline resistance plasmid alone and mecr tetr entB+ transformants harboring both the tetracycline resistance and the 0.75 x 106dalton plasmid. Further segregation of methicillin resistance in transformants was not associated with any change in plasmid DNA. The results indicate that a genetic determinant for SEB production is carried by the 0.75 x 106-dalton plasmid. It is possible, however, that this plasmid cannot be maintained in the host independently from the tetracycline resistance plasmid. Methicillin resistance in the strains examined could not be ascribed to any of the covalently closed circular DNA components resolved in strain DU4916.
The functional R6K alpha origin is composed of two DNA elements, one of 580 bp carrying the alpha origin sequences and the other of 277 bp containing the seven 22 bp direct repeats previously identified as also required for gamma and beta origin activity. These two genetic elements are separated by approximately 3,000 bp of R6K sequences which are dispensable for alpha origin activity. The function of the alpha origin depends on the presence in cis of the 580 bp and the 277 bp fragments and requires that they be oriented as in the intact R6K. Activation of the alpha origin depends on the R6K replication initiation protein pi. Within the 580 bp of the alpha origin, there is a sequence of 98 bp which appears as an inverted repeat of 96 bp in the beta replicon. Deletion of the 96 bp or 98 bp results in inactivation of the alpha and the beta origins respectively. These long repeats are palindromic and it is suggested that these may serve as the recognition signals for initiation of DNA replication in the alpha and the beta origins of R6K. DNA homology analysis performed on alpha, beta and gamma origin sequences, also reveals 10-23 bp sequences in the alpha and the beta origins that are related to the family of 22 bp direct repeats in the gamma origin which were shown previously to be binding sites for the pi protein.
Cellular functions of a double mutant ofEscherichia coliK 12 deficient in recombination (recA) and defective in excision of pyrimidine dimers (uvrB) have been compared to those of isogenicrecAoruvrBsingle mutants and ‘wild type’ bacteria. A combined effect of the two mutations on cell survival both under normal conditions of growth and after exposure to ultraviolet light or mitomycin C was demonstrated. The ratio of optical density to the number of colony formers in growing cultures of the double mutant is three times greater than in similar cultures of therecAsingle mutant and 9 times greater than in eitheruvrBor in ‘wild type’ cultures. The doubling time in growingrecA uvrBcultures is 90 min, compared to 60 min, for therecAsingle mutant and 40 min for theuvrBsingle mutant and ‘wild type’ bacteria. Growing cultures ofrecA uvrB(λcI857) bacteria contain a substantial fraction of cells which are unable to form colonies at 32 °C, but produce phage when heated to 42 °C. No such cells were found in cultures of the single mutants or the ‘wild type’ bacteria lysogenic for λc1857. The double mutant is 10 times more sensitive to ultraviolet light and twice more sensitive to mitomycin C than therecAsingle mutant. In contrast torecAbacteria, exposure of the double mutant to mitomycin C induces little additional breakdown of cellular DNA. Induction of the prophage by mitomycin C is, however, prevented in bothrecA uvrB(λ) andrecA(λ) bacteria. Exposure to mitomycin C creates conditions which render the prophage inducible by a newly transducedree Agene. This effect of mitomycin C persists and can be revealed in complete medium at 37 °C after 100 min of incubation. The decay of the prophage, in cells exposed to mitomycin C, proceeds at a similar rate in both the double mutant and therecAsingle mutant. The inability ofrecAlysogens to be induced to phage production is discussed in the light of the present findings.
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.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.