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. 1967 Jun;93(6):1925–1937. doi: 10.1128/jb.93.6.1925-1937.1967

Transformation and Transduction in Recombination-defective Mutants of Bacillus subtilis

J A Hoch 1, M Barat 1, C Anagnostopoulos 1
PMCID: PMC276712  PMID: 4960898

Abstract

The effects on transformation and transduction of an ultraviolet sensitivity (uvr−) and two ultraviolet sensitivity-recombination deficiency (rec-1− and rec-2−) mutations in isogenic strains of Bacillus subtilis were investigated. Transformation frequency in the rec-1− and rec-2− strains was reduced to approximately 5 and 25%, respectively, of the parental strains. Normal kinetics of deoxyribonucleic acid dose response in transformation were found for the rec-1+ and rec-2− strains. Biphasic curves were obtained with the rec-1− strains. Transduction frequency with bacteriophage SP-10 decreased parallel to transformation frequency in the rec-1− and rec-2− strains. This result suggests that transformation and SP-10 transduction share a common mechanism for genetic recombination. It also indicates that the reduction in transformation frequency of these strains was not due to altered competence. Transduction frequency with bacteriophage PBS-1 or 3NT, on the contrary, was not diminished in rec-1− strains. This frequency was reduced in rec-2− strains but not as severely as that of transformation or SP-10 transduction. Several hypotheses to interpret these differences are presented. Recombination frequency between linked markers was reduced more than 50% in transformation by the presence of the rec-1− mutation. Linkage was unaffected in the rec-2− strains. Neither the rec-1− nor the rec-2− mutation had an effect on linkage in PBS-1 or 3NT transduction. The uvr− strains were transformed at a frequency equal to or greater than that of the parental strains. These strains were transduced by all bacteriophage systems at frequencies about twofold higher than those of parental strains.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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