Disease relevance of soxS

• 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 [1].
• The SoxR protein of Escherichia coli responds to redox signals by activating the transcription of soxS, which encodes another transcription activator that directly stimulates oxidative stress genes [2].

High impact information on soxS

• The kinetic analysis also revealed that an oxidative stress-linked decrease in soxS mRNA stability contributes to the rapid attainment of a new steady state after SoxR activation [3].
• The in vivo kinetics of SoxR [2Fe-2S] cluster oxidation and reduction exactly paralleled the increase and decrease of transcription of soxS, the target gene for SoxR [3].
• We found that 4-nitroquinoline-N-oxide (4NQO) is a powerful inducer of soxS, > 10-fold more potent than paraquat [4].
• Several mutations in the dimerization domain of SoxR disrupted intersubunit communication, and the resulting proteins were unable to propagate redox signals to the soxS promoter [5].
• SoxR transcriptional activity, but not DNA binding, is completely dependent on the [2Fe-2S] clusters; apo-SoxR prepared in vitro binds the soxS promoter with unchanged affinity but does not have transcription activity [6].

Chemical compound and disease context of soxS

• Expression of the marA or soxS genes is induced by exposure of Escherichia coli to salicylate or superoxides, respectively [7].

Biological context of soxS

• Organisms lacking all three transcription factors (triple knockouts) were significantly less virulent than parental strains, and complementation studies demonstrated that the addition of marA, soxS and rob individually restored wild-type virulence in the triple-knockout strain [1].
• Activated SoxR turns on transcription of a single gene, soxS, which encodes a transcriptional regulator that activates a regulon that includes dozens of oxidative stress response genes [8].
• However, it displayed a soxS-dependent induction by paraquat (methyl viologen), and the fldB gene is preceded by two overlapping regions that resemble known soxS binding sites [9].
• Instead of a soxS homolog, ORFs encoding an unknown hypothetical protein and soxR are arranged divergently with their 5' ends separated by a 78 bp region containing a sequence homologous to the SoxR-binding soxS promoter [10].

Other interactions of soxS

• Deletion of soxS or rob alone was more detrimental than the removal of marA [1].

Analytical, diagnostic and therapeutic context of soxS

• Western blot analysis failed to demonstrate overexpression of MarA, and Northern blot analysis did not detect overexpression of soxS RNA in any of the clinical strains [11].

References