Disease relevance of sulI

• A sulfathiazole-resistant dihydropteroate synthase (DHPS) present in two different laboratory strains of Escherichia coli repeatedly selected for sulfathiazole resistance was mapped to folP by P1 transduction [1].

High impact information on sulI

• We have cloned the plasmid-quinolone resistance gene, termed qnr, and found it in an integron-like environment upstream from qacE Delta 1 and sulI [2].
• Genes for spectinomycin resistance, aadA1 [ant (3")-Ia], and sulfonamide resistance, sulI, were located downstream of dfrXV in a manner identical to that in pLMO229 [3].
• PCR mapping of the aac(6')-Im [corrected] gene environment in these isolates indicated that the gene was located within a sulI-type integron; the insert region is 1,700 bases long and includes two genes cassettes, the second being ant (3")-Ib [4].
• In strains with sulfamethizole MICs > 2048 mg/L, 97% carried sulI, sulII or both genes, with sulII being the most common [5].
• Among the sulI gene-positive strains, 96% were intI 1 gene positive [5].

Biological context of sulI

• To further investigate the structure of these integrons, the DNA sequence of the segment located between the two sulI genes was determined [6].
• DNA sequence of direct repeats of the sulI gene of plasmid pSa [7].
• A selection of multiresistant bacterial isolates were further genetically characterized by hybridization with probes specific for the antibiotic resistance genes; sulI, sulII, dfrI, dfrIIb, dfrIX, and the class A, B, C, and D tetracycline resistance determinants [8].
• The informative nature of these models opens up avenues for structure-based drug design approaches toward the development of alternative and more effective inhibitors of P. falciparum PPPK-DHPS [9].
• The active site residues of DHPS are highly conserved in S. cerevisiae, M. tuberculosis, E. coli, S. aureus, and B. anthracis, an attribute also shared by P. falciparum DHPS [9].

Associations of sulI with chemical compounds

• ORF4, whose product lacks the C-terminal 16 amino acids of the ORF1 protein, may have evolved by the interruption of ORF1 from the insertion of a DNA segment carrying a sulI sulfonamide resistance determinant [10].
• Site-specific recombination promotes linkage between trimethoprim- and sulfonamide resistance genes. Sequence characterization of dhfrV and sulI and a recombination active locus of Tn21 [11].
• They were identical for 1065 bp and contained the entire coding sequence of the sulfanilamide resistance gene, sulI [7].
• Class 1 integrons containing sulI (sulfonamide resistance), aadA1a (streptomycin resistance), or dfrA1 (trimethoprim resistance)-aadA1a gene cassettes were detected in 28 strains [12].
• Elucidation of sulfadoxine resistance with structural models of the bifunctional Plasmodium falciparum dihydropterin pyrophosphokinase-dihydropteroate synthase [9].

Other interactions of sulI

• The aadA, tetA, and sulI genes were most commonly detected in bacteria resistant to streptomycin, tetracycline and sulfonamide, respectively [13].
• Further study indicated that the ampicillin resistance gene probe reacted with the gene for TEM-1 beta-lactamase and that the gene probe for sulphonamide resistance reacted with the gene for type II dihydropteroate synthase [14].

References