Disease relevance of soxS

• Overexpression of the marA or soxS regulatory gene in clinical topoisomerase mutants of Escherichia coli [1].
• The Pseudomonas putida genome did not reveal a clear soxS homolog [2].
• In conclusion, polyamines protect against paraquat-induced toxicity but downregulate soxS expression, suggesting that the protective role of polyamines against oxidative damage induced by paraquat results in soxS downregulation [3].
• We engineered fusions of the Escherichia coli soxS promoter to the luciferase structural genes (luxAB) from Vibrio harveyi [4].
• Clinical Escherichia coli isolates, and isogenic strains lacking marA, soxS and rob, were studied in a murine model of ascending pyelonephritis, which is a clinically relevant model of urinary tract infection [5].

High impact information on soxS

• The hmp promoter is more sensitive to SNP and S-nitroso-N-penicillamine (SNAP) than is the soxS promoter, consistent with the role of Hmp in protection from reactive nitrogen species [6].
• Genomics of the marA/soxS/rob regulon of Escherichia coli: identification of directly activated promoters by application of molecular genetics and informatics to microarray data [7].
• Purified SoxR protein is a homodimer containing a pair of [2Fe-2S] centers essential for soxS transcription in vitro . The [2Fe-2S] centers are thought to be anchored by a C-terminal cluster of four cysteine residues in SoxR [8].
• To facilitate purification and characterization of SoxS, we constructed a fusion of soxS to malE, which encodes maltose-binding protein, and demonstrated that the in vivo expression of the MalE-SoxS fusion protein can provide SoxS function to a soxRS deletion mutant [9].
• These genes, named soxR and soxS, are arranged divergently with their 5' ends separated by only 85 bp [10].

Chemical compound and disease context of soxS

• Four of five clinical E. coli strains which overexpressed marA or soxS also showed enhanced triclosan resistance [11].

Biological context of soxS

• Here, we identify directly activated promoters of the overlapping marA, soxS and rob regulon(s) of Escherichia coli by applying informatics, genomics and molecular genetics to microarray data obtained by others [7].
• These functions were revealed by studies in which the sequence of the 1.1-kb soxR-soxS region was determined, the 5' ends of the mRNAs were mapped, and complementation tests were performed with soxRS plasmids containing deletions of known sequence [12].
• Constitutive expression of marA of the multiple antibiotic resistance (mar) locus or of the soxS or robA gene product produced tolerance to cyclohexane [13].
• In this paper it is shown that a physical agent, such as ultraviolet radiation with a wavelength of 312 nm (UVB) can induce soxS gene expression [14].
• In the absence of oxidative stress, the [2Fe-2S] centres are in the reduced form and the protein is inactive, although it still binds the soxS promoter [15].

Anatomical context of soxS

• After incubation with murine macrophages, soxS expression was induced in the phagocytosed bacteria up to approximately 30-fold after an 8-h exposure [16].

Associations of soxS with chemical compounds

• Multicopy expression of mar, soxS, or robA induced cyclohexane tolerance in strains with a deleted or inactivated chromosomal mar, soxRS, or robA locus; thus, each transcriptional activator acts independently of the others [13].
• In contrast, growth inhibition of the mutant by paraquat was relieved, and soxS was no longer induced by exogenous putrescine (1 mmol/L) [3].
• Putrescine and spermidine downregulate the expression of soxS induced by paraquat in a concentration-dependent manner [3].
• Several other superoxide-generating agents also trigger soxR(+)-dependent soxS expression, and the inductions by paraquat and phenazine methosulfate were dependent on the presence of oxygen [17].
• We report here that overexpression of the multidrug efflux pump locus acrAB, or of marA or soxS, both encoding positive regulators of acrAB, decreased susceptibility to triclosan 2-fold [11].

Other interactions of soxS

• It has been shown that mutations giving rise to increased expression of the transcriptional activators marA and soxS affect the expression of a variety of different genes, including ompF and acrAB [18].
• This increase could be explained by transcription of soxS gene in a rpoS-dependent pathway [14].

References