NEW TYPE OF STREPTOMYCIN RESISTANCE RESULTING FROM ACTION OF THE EPISOMELIKE MUTATOR FACTOR IN ESCHERICHIA COLI

Abstract

New type of streptomycin resistance resulting from action of the episomelike mutator factor in Escherichia coli. J. Bacteriol. 86:510-516. 1963.-Analyses have been performed to elucidate the genetic nature of the streptomycin resistance that results from the action of the previously described episomelike mutator factor in Escherichia coli. This streptomycin resistance has been found to differ from ordinary one-step streptomycin resistance. The new type of streptomycin resistance, "mutator resistance," can be lost, either spontaneously or by treatment with ultraviolet light and acriflavine. It is more stable in a K-12 strain than in the original E. coli strain 635. Mutator resistance segregates like a chromosomal marker in genetic crosses, and is located near the ordinary streptomycin locus. The locus for mutator resistance is

EVIDENCE FOR NON‐RIBOSOMAL LOCATION OF STREPTOMYCIN RESISTANCE IN ESCHERICHIA COLI CARRYING THE MU‐FACTOR

“…The normal gene for streptomycin sensitivity is present in the mutator-streptomycin resistant cells (81, a fact that might imply that their ribosomes are unchanged. The possibility of this resistance being due to a suppressor mechanism has formerly been suggested (8). This would result in a quantitative rather than a qualitative change, which is reconcilable with the present experimental data.…”

“…Bacterial strains: K12 T71, T71 str-r, T71Mu, T71Mu str-r and T71Mu thr his str-r have formerly been described (11,8). The bacteria were grown in Heart Infusion Broth (Difco).…”

“…Genetic evidence has been presented (8) indicating that the mutatorstreptomycin resistance is located a t the bacterial chromosome at a site distinct from that of the ordinary streptomycin locus, and apparently there is also a certain genetic distance between the two loci. The mutant T71Mu fhr his sfr-r has been employed in the present study because of its former use in the genetic mapping experiments.…”

“…When the Mu-factor is carried in its extrachromosomal state (11) the cells have a low level resistance to streptomycin ( 9 ) , the actual concentration of streptomycin tolerated depends upon the physiological state of the cells. In of the cells in such a population the chromosome is modified, possibly by an attachment of the Mu-factor to the bacterial chromosome, resulting in a significantly higher level of streptomycin resistance (11,8). Experiments on uptake of 14C-streptomycin (10) indicate that the low-level streptomycin resistance may be due to a decreased permeability of the drug.…”

Extrachromosomal inheritance in bacteria.

“…No unstable mutations or other plasmid-chromosome interactions have been observed that might be due to the effects of "controlling episomes" postulated by Dawson and Smith-Keary (53), nor have specific "mutator" episomes acting on specific chromosomal loci been seen. Two examples of elevated mutation frequency of specific loci thought to represent "mutator episome" effects both involved transmissible R factors (88,94,95) and can be interpreted as the occurrence of mutations whose effects are synergistic to R-linked resistance determinants, and whose occurrence is facilitated by residual growth of the R+ cells in the presence of the drug at a selective concentration (208).…”