sdiA:Quickview
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| Quickview | Gene | Gene Product(s) | Expression | Evolution | On One Page |
| References | Suggestions |
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| Standard Name |
|---|
| Gene Synonym(s) |
| Product Desc. |
| Product Synonyms(s) |
| Knock-Out Phenotype |
| Regulation/Expression |
| Regulation/Activity |
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Notes
Suppresses inhibitory effect of the MinC/MinD division inhibitor. N-acyl homoserine lactones act as folding switches for SdiA. LuxR family. SdiA has other global transcription targets such as uvrY, csrB, recN and nei. E. coli makes an unknown weak auto-inducer when grown in rich media. Most phenotypic effects require overproduction of SdiA. sdiA mutants are more sensitive to fluoroquinolones and have reduced AcrB protein, but are not defective in cell division. An sdiA ydiV double mutant has twofold reduced cAMP levels than inhibits quorum sensing system 2 (Zhou, 2008).[1]
References