Role of the supX gene in ultraviolet light-induced mutagenesis in Salmonella typhimurium.

Salmonella typhimurium strains with supX mutations are more sensitive than wild type to killing by ultraviolet (UV) irradiation. Studies with strains bearing the leuD21 mutation revealed that inactivation of the supX locus by a nonsense mutation or a deletion results in a complete lack of ability to produce induced Leu+ reversion mutations after UV irradiation. Suppression of the nonsense supX mutation or the presence of an Escherichia coli K-12 F'-borne supX+ allele restored the capacity for induced reversions and increased cell survival after UV irradiation. Introduction of plasmid pKM101 into supX mutant strains also restored their capacity for UV mutagenesis as well as increased survival. The possible nature of the supX gene product and mechanisms by which it may affect expression of the inducible SOS error-prone repair system are considered.     

Locations of the opp and supX genes of Salmonella typhimurium and Escherichia coli.

The chromosomal locations of the supX and opp loci of Salmonella typhimurium LT2 and Escherichia coli K-12 were identified and found to result in the same gene sequence in both species, namely, pyrF-cysB-supX-trpPOLEDCBA-tonB(chr)-opp. These results differ from a previously reported location of the opp gene on the E. coli chromosome. Evidence indicates that the opp gene lies between chr(tonB) and galU in S. typhimurium.     

New Class of Streptomycin-Resistant Mutants Incompatible with supX Suppressor Mutations in Salmonella typhimurium

Streptomycin-resistant colonies of Salmonella typhimurium appearing in platings of supX suppressors of strain leu-500 are less variegated in size than are those derived from strain leu-500 counterparts. Several of the streptomycin-resistant leu-500 clones, furthermore, yield suppressors and revertants of the leu-500 auxotrophy at unusually low rates, suggesting that they provide a genetic background inimicable to supX suppression. Two such "suppression-restrictive" leu-500 streptomycin-resistant (str) mutants, designated strains M(1) and M(4), were characterized as to their ability to receive the trp-supX-cysB linkage region by transduction. Coentry of a donor supX deletion mutation with the selected trp(+) marker was not observed even though these sites display more than 10% linkage in control experiments. This was demonstrably the result of nonviability of the combined supX mutant, M(1) or M(4) streptomycin-resistant genotype, rather than the lack of suppression of the leu-500 imparted auxotrophy. Both M(1)- and M(4)-type resistance was accompanied by pleiotropic effects resembling those caused by strB (nonribosomal)- rather than strA (ribosomal)-type resistance, but both restrictive mutants had a high upper limit of resistance corresponding to that of strA-type mutants. Transduction analyses indicated that the str character of neither the M(1) nor the M(4) strain was linked to the strA or the strB gene. These mutations define a previously undescribed locus, which we propose to designate strC, apparently related to streptomycin uptake rather than its intracellular action. Mutation at this locus is evidently incompatible with the inactivation or removal of the supX site, suggesting a functional association between products of the genes.     

Escherichia coli and Salmonella typhimurium supX genes specify deoxyribonucleic acid topoisomerase I.

Mutations of the Escherichia coli or Salmonella typhimurium supX genes eliminated deoxyribonucleic acid topoisomerase I. Suppression of a supX amber mutation partially restored the topoisomerase. Multicopy plasmids carrying supX+ caused overproduction of topoisomerase. Thus, these supX genes were identified as topA genes which specify deoxyribonucleic acid topoisomerase I.     

Dissymmetry of the origins of the roots of the spinal cord in the dog

The spinal cord in 25 non-inbred dogs has been studied macro-microscopically. The dissymmetry in the arrangement level in the right and left root bases on the dorsal surface of the spinal cord is much greater than on the ventral surface. The same as in the human being, the dissymmetry is the greatest in the thoracic part (as compared to other spinal parts). On the ventral surface of the spinal cord both along the anterior and posterior margin of the root bases, there is a right-sided dissymmetry (with cranial shift); on the dorsal surface it is present only at the roots along the posterior margin. The dissymmetry of the dog spinal cord is quantitatively estimated along its whole extension.