Cotransduction of strA and Ribosomal Protein Cistrons in Escherichia coli-Salmonella typhimurium Hybrids

Genetic mapping of ribosomal protein cistrons of Salmonella typhimurium and Escherichia coli was performed by phage P1 mediated, generalized transduction. From an E. coli hybrid strain which carried a S. typhimuirum F' factor, an E. coli strain was constructed which had integrated S. typhimurium genetic material including the region of the strA locus. Salmonella genetic material from this hybrid was transduced into E. coli recipients. The ribosomal protein electrophoretic patterns of these hybrid transductants were correlated with the presence of markers contributed by each parent.The results of these studies indicate that cistrons for at least three characteristic S. typhimurium and two E. coli 30S ribosomal proteins are closely linked to the strA locus on the genetic maps of both organisms. At least one cistron coding for a 50S ribosomal protein is also closely linked to this locus on both maps. These findings support the concept that cistrons coding for the ribosomal proteins are clustered in one area of the genome. Mutations to spectinomycin and streptomycin resistance are closely linked in S. typhimurium and are located at strA.     

The effect of strA mutation on symbiotic nitrogen fixation by Rhizobium meliloti.

Studies on 3H-dihydrostreptomycin accumulation and binding to ribosomes showed that ineffective strain CMts17 carries strB type mutation changing its membrane permeability to the drug. Introduction of high level streptomycin resistance of strA type into strain CMts17 was correlated with acquisition of effectiveness and membrane permeability to the drug. This suggests that changes in membrane permeability, responsible for ineffectiveness of strain CMts17, can be reversed by strA mutation.     

Increased loss of duplicated genes in streptomycin-resistant (strA) mutants of Escherichia coli k-12.

The recombination-dependent loss of a duplicated portion of the Escherichia coli chromosome is five- to tenfold greater in strains containing streptomycin resistance (strA) mutations than in the strA+ parental strain. Streptomycin (500 mug/ml) partially reverses the increase. These results suggest an interaction between strA mutations and recombination.     

Cloning, characterization, and DNA base sequence of the high-level streptomycin resistance gene strA1 of Haemophilus influenzae Rd.

The high-level streptomycin resistance strA1 gene of Haemophilus influenzae Rd was cloned in plasmid pAT4 as a 2.1-kbp EcoRI insert. It was later replaced in pAT4 by the wild-type strA+ gene. Plasmid pAT4 carrying the strA+ gene is highly unstable and renders chromosomally resistant recipients sensitive to streptomycin. The strA+ gene and the instability factor both reside on a 500-base HindIII-EcoRI subfragment. The two biological activities are also expressed in Escherichia coli. Both wild-type (strA+) and mutant (strA1) genes were sequenced. They show considerable nucleotide homology with the E. coli strA+ gene and its product.     

rpe, a cis-acting element from the strA region of the Haemophilus influenzae chromosome that makes plasmid establishment independent of recombination.

Plasmids that share homology with the Haemophilus influenzae chromosome transform wild-type cells more efficiently than they transform recombination-defective mutants. A 5.2-kilobase-pair chromosomal fragment containing the strA gene of H. influenzae was found to promote efficient plasmid establishment in recombination-defective mutants. A cis-acting element in the insert, called rpe for rec-less plasmid establishment, promoted plasmid transformation in rec-1 and rec-2 mutants without suppressing the recombination defects of these strains. The rpe locus increased plasmid transformation in wild-type cells without interfering with the pathway of plasmid establishment that is dependent on recombination functions.     

Effect of the transmission of a different type of mutation in the strA locus on the virulence of Sh. flexneri]

The authors noted a different influence upon the virulence of Sh. flexneri (determined by keratoconjunctival test) of transmission of different alleles of the strA-gene (A1, A2, A40, A60). There was revealed no correlation between the extent of the changes in virulence and the extent of capacity ot the limiting of suppression in donor strains.