Azaserine resistance in Escherichia coli: chromosomal location of multiple genes

Abstract

Resistance to azaserine in Escherichia coli is the result of mutations in at least three different loci. All spontaneously arising azaserine-resistant mutants harbor a lesion in the aroP gene. However, a lesion in this gene is not solely responsible for resistance. All spontaneously arising intermediate-level azaserine-resistant mutants also harbor a lesion in a gene designated azaA, which lies near min 43 on the chromosome. High-level resistant mutants harbor lesions in the aroP and azaA genes and in a third gene designated azaB, which lies near min 69 on the chromosome. Transport studies demonstrate that mutants harboring lesions in the azaA gene are not defective in the transport of the aromatic amino acids, but that mutants which harbor lesions in the azaB gene are defective in phenylalanine transport but not in tyrosine or tryptophan transport.

Cloning and sequencing of the pheP gene, which encodes the phenylalanine-specific transport system of Escherichia coli

“…1) confirmed that the cloned fragment indeed was derived from that region. It differs from the azaB gene described by Williams et al, which was mapped near min 69 on the chromosome and was reported also to be involved in the transport of phenylalanine (43).…”

Amplifiable resistance to tetracycline, chloramphenicol, and other antibiotics in Escherichia coli: involvement of a non-plasmid-determined efflux of tetracycline

“…Chromosomal resistances are often expressed from single genes, but occasional cooperativity between loci has been demonstrated (36,38). Azaserine resistance in E. coli involves mutations at three loci that arise spontaneously and sequentially and promote independent or additive resistance (38). Low-level resistance to tetracycline, chloramphenicol, and penicillin G in Neisseria gonorrhoeae has been linked to interactive chromosomal loci (36).…”

“…More than one resistance phenotype may be elaborated by a single gene; many unlinked loci have been identified, and these are Pl transducible to sensitive strains by direct' and indirect selection (33,34). These chromdsomal mutations include cmlA (resistance to, chloramphenicol [34]), cmlB (resistance to chloramphenicol and tetracycline [33]), lon (resistance to chloramphenicol and tetracycline [33]), and several other loci that have not been precisely mapped or identified, but promote low-level resistance to one or several antibiotics (33,38).…”

The LIV-I/LS system as a determinant of azaserine sensitivity of Escherichia coli K-12

“…Williams et al [16,17] isolated and characterized two types of azaserine-resistant mutants; one exhibiting moderate-level resistance and the other high-level resistance. While both mutants had aroP lesions, the presence of additional mutation(s) in the high-level resistant strain was deduced since it showed a severe deficiency in the accumulation of phenylalanine in cells as compared to the moderate-resistant one [16,17].…”

“…Williams et al [16,17] isolated and characterized two types of azaserine-resistant mutants; one exhibiting moderate-level resistance and the other high-level resistance. While both mutants had aroP lesions, the presence of additional mutation(s) in the high-level resistant strain was deduced since it showed a severe deficiency in the accumulation of phenylalanine in cells as compared to the moderate-resistant one [16,17]. Because the uptake of phenylalanine into E. coli had been considered to be performed by AroP and PheP (phenylalanine/tyrosine transporter) [18][19][20][21], a mutation in the pheP gene was speculated; however, the location of the mutation in the high-level resistant strain was found to be far from pheP, although precise mapping was not possible [17].…”