|Dataset Name||Affymetrix data for EvgA overexpression.|
|Short Description||Effect of the overexpression of EvgA response regulator.|
|Reference||Masuda, N.; Church, G.M.; Escherichia coli Gene Expression Responsive to the Levels of Response Regulator EvgA J. Bacteriol. 184(22): 6225-6234 (2002)|
|Strains||There are four comparisons of experimental strains with baseline strains, see Long Description for genotype details.|
|Conditions||exponentially grown in Luria-Bertani broth|
|Date Added to ExpressDB||Jan 9 2002 3:06:10:933PM|
|Number of Measures on ExpressDB||44 (here to download dataset and view measure details)|
|Long Description||The four pairs of strains that were compared are as follows:
Comparison 1: delta evgAS/pUCevgA (experimental strain) vs delta evgAS/pUC19 (baseline strain),
Comparison 2: delta evgAS/pQEevgA with IPTG (experimental strain) vs delta evgAS/pQEevgA without IPTG (baseline strain),
Comparison 3: delta acrB delta evgAS/pUCevgA (experimental strain vs delta acrB delta evgAS/pUC19 (baseline strain),
Comparison 4: delta acrB delta evgAS/pQEevgA with IPTG (experimental strain) vs delta acrB delta evgAS/pQEevgA without IPTG (baseline strain).
Abstract from published paper:
To investigate the function of the EvgA response regulator, we compared the genome-wide transcription profile of EvgA-overexpressing and EvgA-lacking Escherichia coli strains by oligonucleotide microarrays. The microarray measurements allowed the identification of at least 37 EvgA-activated genes, including acid resistance-related genes gadABC and hdeAB, efflux pump genes yhiUV and emrK, and 21 genes with unknown function. EvgA overexpression conferred acid resistance to exponentially growing cells. This acid resistance was abolished by deletion of ydeP, ydeO, or yhiE, which was induced by EvgA overexpression. These results suggest that ydeP, ydeO, and yhiE are novel genes related to acid resistance and that EvgA regulates several acid resistance genes. Furthermore, the deletion of yhiE completely abolished acid resistance in stationary-phase cells, suggesting that YhiE plays a critical role in stationary-phase acid resistance. The multidrug resistance in an acrB deletion mutant caused by EvgA overexpression was completely abolished by deletion of yhiUV, while the emrKY deletion had no effect on the increase in resistance by EvgA overexpression. In addition, EvgA overexpression did not confer resistance in a tolC-deficient strain. These results suggest that YhiUV induced by EvgA overexpression is functionally associated with TolC and contributes to multidrug resistance.
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Copyright (c) 2006 by Wayne Rindone and the President and Fellows of Harvard University