Abstract
When HfrC strain (str-s) was mated with an acriflavine-sensitive (acrA) mutant (str-r) recipient in PGY medium and plated onto D-lactose plus streptomycin (200μg per ml) medium, the yield of lac+ met+ str-r recombinant decreased. This effect was more remarkable when the mating and incubation of the plates were done at 30°C than 37°C. However, the recombinant yield was restored to a considerable extent or even completely (i) when the mating mixture was plated onto D-lactose medium (without addition of streptomycin), (ii) when acriflavine-resistant revertants of acrA mutant were used as the recipients, and (iii) when F13-prime (lac+-purE+) strain was used as the donor. Under the conditions used, the str-s gene of the donor was transferred only 0.0 to 0.4% of the lac+ gene to the recipients. The streptomycin was not a selective killer to the acrA mutant cell. No lethal zygosis occurred under the present conjugational conditions. From these results, it is concluded that the streptomycin effect on the recombination in the acrA mutant recipient was due to a certain deficiency of the recombinational reaction sequence. However, such streptomycin effect was the case also when donor strains contained the acriflavine-sensitive (acrA) mutations. And the effect was not observed when acriflavine-resistant revertants of these acrA mutants were used as the donor. Therefore, it is apparent that the acrA mutation, perhaps a substance produced by its allele, hindered the recombinational reactions. No difference in streptomycin uptake by the cells was found between the acrA and acrA+ strains.
