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At least 19 recordsLinked to original sources

Prophage type of recombinants produced by cell fusion between various combinations of lysogenic or non-lysogenic substrains from two Staphylococcus aureus L-forms.

Streptomycin (SM)- or erythromycin (EM)-resistant lysogenic and non-lysogenic substrains were produced from two Staphylococcus aureus L-form strains lysogenic for different prophages, namely, EMT-L (prophage alpha) and 209P (prophage beta). Cells of these L-form substrains were fused in various combinations using polyethylene glycol (PEG), and the frequency of recombinants selected as double resistance to both SM and EM and the prophage types of these recombinants were examined. In all the combinations, the frequency of recombinants was greater when the cells were treated with PEG than when they were not, and the difference was statistically significant (p less than 0.01) in 13 combinations. Combination between the lysogenic SM-resistant EMT-L substrain [EMT(Smr-alpha)] and lysogenic EM-resistant 209P-L substrain [209P(Emr-beta)] and the reverse combination, between 209P(Smr-beta) and EMT(Emr-alpha), resulted in a majority of recombinants harboring prophage beta. The former combination yielded recombinants that all held both prophage alpha and beta.

Bacteriolysis↗

[Characteristics of the mutants of the temporate actinophage phiC31 with a disordered lysogenicity and that overcome the immunity of lysogenic cultures].

The study of c- and cts-mutants of the temperate actinophage phiC31, affecting the lysogenization process in Streptomyces coelicolor showed the interallelic negative complementation. This fact implies the protein nature of the repressor synthesized under the control of gene C and its multiunit structure. Transdominant c- and cts-mutants were partly virulent being able to overcome the immunity of lysogens with effecting of plating (eop) about 5. Virulent mutants infecting lysogens with an eop 1 were detected. Differences in behaviour of virulent mutants isolated from transdominant mutant (v) stock and those containing a recessive mutation in the gene C (vd- and vdt-mutants) are shown. It is demonstrated that vd-mutants unlike v-mutants are not capable of growing without phage-helper (presumably prophage) and use many prophage gene products marked by ts- and host-range-mutations to form progeny. Common to all isolated virulent mutants are their ability to promote the prophage induction in lysogens and inability to display virulent phenotype in the absence of a mutation in the gene C.

Bacteriophages↗

[Lysogeny and lysogenic conversion in methylotrophic bacteria. II. Lysogenic conversion in facultative methanol-assimilating Acetobacter strains].

The lysogenic state of the methylotrophic strain Acetobacter MB 58/1 is completely demonstrated by curing and lysogenization experiments. During these investigations we found that some phenotypic characteristics are modified by the presence or loss of the prophage MO 1. It could be shown that changes of the serological behaviour, the adsorption of the phages and the sensitivity against oxytetracycline are caused by lysogenic conversion. The phenotypic alterations of the bacterial cells induced by the phage genome are the result of modifications of the lipopolysaccharide structures on the cell surface. In the case of oxytetracycline resistance, interactions between the modified lipopolysaccharide structures and specific transport proteins of the cell membranes must be assumed.

Acetobacter↗

Appearance of new phage types and new lysogenic strains after adaptation of lysogenic B. megatherium to ammonium sulfate culture medium.

1. Lysogenic B. megatherium 899a was adapted to growth in a minimal ammonium sulfate medium (ASCM). 2. Adaptation took place slowly and the following changes in the culture occurred: (a) The growth rate increased from 0.5 to 1.5-2.0/hr. (b) The culture changed from diffuse to mucoid. (c) The total phage titer, and the gelatinase concentration decreased to 1/100 or less. (d) The types of phage produced changed from >99 per cent T (wild type) to 30 to 60 per cent miscellaneous clear types. The original T phage was replaced by a different smaller t, never observed in the original 899a culture. (e) Several new colony types also appeared, but the colony morphology was not correlated with the phage types produced. None of the colony types was stable on repeated transfer either in peptone or ASCM, but continued to disassociate into different colony types (cf. Ivánovics, 1955). 3. Control experiments showed that these changes in phage production and colony types could not be brought about by growing sensitive B. megatherium in the presence of the various new phages, in ASCM. It is therefore unlikely that the changes observed in adapted culture were due to infection of a sensitive cell with phage. 4. Continued growth of the ASCM-adapted strain in peptone resulted in increasing the total phage titer, and also the gelatinase concentration. The growth rate returned to its original value and the ability to grow rapidly in ASCM was soon lost. The phage types, however, remained the same as in the ASCM. 5. An improved cell for steady state growth is described.

Ammonium Sulfate↗

In vivo lysogenic conversion of Tox(-) Streptococcus pyogenes to Tox(+) with Lysogenic Streptococci or free phage.

Temperate bacteriophage can transfer toxin-encoding genes between bacteria, often resulting in acquired pathogenicity. However, little is known regarding the effects of the eukaryotic host on the phage-pathogen interaction. Using Streptococcus pyogenes as a model, we demonstrate, both in vitro and in vivo, that the eukaryote mediates the efficient induction of toxin-encoding temperate phage and the resultant conversion of Tox(-) flora to Tox(+). Furthermore, we show that both phage induction and subsequent conversion need not happen in the same mammalian host, as host-to-host phage transmission can result in toxigenic conversion within the secondary host. Ultimately, our findings demonstrate that the eukaryotic host serves as an essential component in the phage-mediated evolution of virulence within the microbial population.

Animals↗