Transformation and transfection in lysogenic strains of Bacillus subtilis: evidence for selective induction of prophage in competent cells.
Lysogenic strains of Bacillus subtilis 168 were reduced in their level of transformation as compared to non-lysogenic strains. The level of transformation decreased even further if the competent lysogenic cells were allowed to incubate in growth media prior to selection on minimal agar. This reduction in the frequency of transformation was attributable to the selective elimination of transformed lysogenic cells from the competent population. Concurrent with the decrease in the number of transformants from a lysogenic competent population was the release of bacteriophage by these cells. The lysogenic bacteria demonstrated this dramatic release of bacteriophage only if the cells were grown to competence. Both the selective elimination of transformed lysogens and the induction of prophage was prevented by the inhibition of protein synthesis. Additionally, competent lysogenic cells released significantly higher amounts of exogenous donor transforming deoxyribonucleic acid than did competent non-lysogenic cells or competent lysogenic cells incubated with erythromycin. These data establish that the induction of the prophage from the competent lysogenic cells was responsible for the selective elmination of the lysogenic transformants. A model is presented that accounts for the induction of the prophage from competent lysogenic bacteria via the induction of a repair system. It is postulated that a repair system is induced or derepressed by the accumulation of gaps in the chromosomes of competent bacteria. This hypothetical enzyme(s) is ultimately responsible for the induction of the prophage and the selective elimination of transformants.
D001391:Azo Compounds; D001412:Bacillus subtilis / Q000254:growth & development / Q000378:metabolism; D001435:Bacteriophages / Q000254:growth & development; D002701:Chloramphenicol / Q000494:pharmacology; D003470:Culture Media; D004260:DNA Repair; D004267:DNA Viruses; D004269:DNA, Bacterial; D004279:DNA, Viral; D004917:Erythromycin / Q000494:pharmacology; D008242:Lysogeny; D008954:Models, Biological; D009154:Mutation; D011995:Recombination, Genetic; D012293:Rifampin / Q000494:pharmacology; D014170:Transformation, Genetic / Q000187:drug effects; D014364:Tryptophan / Q000096:biosynthesis; D014498:Uracil / Q000031:analogs & derivatives / Q000494:pharmacology; D014779:Virus Replication
D001391:Azo Compounds; D003470:Culture Media; D004269:DNA, Bacterial; D004279:DNA, Viral; D014498:Uracil; D004917:Erythromycin; D002701:Chloramphenicol; D014364:Tryptophan; D012293:Rifampin