PMID:1317841: Difference between revisions
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''' | '''Wu, J and Weiss, B''' (1992) Two-stage induction of the soxRS (superoxide response) regulon of Escherichia coli. ''J. Bacteriol.'' '''174''':3915-20 | ||
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==EcoliWiki Links {{HelpIcon|Help:Literature}} == | ==EcoliWiki Links {{HelpIcon|Help:Literature}} == | ||
Latest revision as of 04:21, 15 September 2013
| Citation |
Wu, J and Weiss, B (1992) Two-stage induction of the soxRS (superoxide response) regulon of Escherichia coli. J. Bacteriol. 174:3915-20 |
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| Abstract |
soxR and soxS are adjacent genes that govern a superoxide response regulon. Previous studies revealed that induction of the regulon is accompanied by increased transcription of soxS, which can activate the target genes. Therefore, induction may occur in two stages: the soxR-dependent activation of soxS, followed by the soxS-dependent induction of other genes. However, the requirement for soxR was unproven because the only existing soxR mutations either were of the regulon-constitutive type or also involved soxS. Therefore, we produced an insertion mutation that was shown by complementation to inactivate only soxR. In confirmation of the two-stage model, soxR was required for the induction by paraquat of the target genes studied (nfo, zwf, and sodA), for paraquat resistance, and for the 47- to 76-fold induction of soxS-lacZ gene fusions. Paraquat did not affect the expression of soxR-lacZ gene fusions. In a soxRS deletion mutant, the regulon was constitutively activated by a runaway soxS+ plasmid. However, a lower-copy-number plasmid failed to activate nfo, zwf, or sodA but did increase the paraquat resistance of a soxRS mutant. Therefore, there is a differential response of the regulon genes to soxS overproduction. A soxR regulon-constitutive mutation was suppressed by a soxR+ plasmid, suggesting a competition between native and activated forms of SoxR. It is proposed that to enhance the sensitivity of the response, the cell minimizes such potential competition by manufacturing only a small amount of this sensor protein, thereby necessitating signal amplification via induction of soxS. |
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| Keywords |
Bacterial Proteins/genetics; Cloning, Molecular; Drug Resistance, Microbial/genetics; Escherichia coli/genetics; Escherichia coli Proteins; Gene Expression Regulation, Bacterial/drug effects; Gene Expression Regulation, Bacterial/physiology; Genetic Complementation Test; Mutation/genetics; Paraquat/pharmacology; Plasmids/genetics; Recombinant Fusion Proteins/genetics; Recombinant Fusion Proteins/metabolism; Superoxides/pharmacology; Trans-Activators; Transcription Factors/genetics |
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