Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Derivatives of Myxococcus xanthus FB(t) resistant to chloramphenicol (25 mug/ml) arose spontaneously with a frequency of approximately 10(-7). One of these organisms (FB(t)Cam(1) (r)) was characterized. FB(t)Cam(1) (r) showed a unique type of phenotypic instability. After transfer from medium containing chloramphenicol to medium lacking the drug, resistance was lost after approximately one generation. The loss resulted in a sharp drop in the total number of chloramphenicol-resistant organisms and was not due to segregation of chloramphenicol-susceptible organisms during growth. Cell-free extracts of strain FB(t)Cam(1) (r) converted chloramphenicol to acetyl chloramphenicols in a fashion implicating activity of chloramphenicol acetyltransferase. This activity was lost simultaneously with the loss of chloramphenicol resistance after removal of the drug from cultures. Organisms with a similar phenotype to FB(t)Cam(1) (r) could be produced at high frequencies when strain FB(t) was exposed to low concentrations of chloramphenicol (2 to 5 mug/ml), to 3-acetylchloramphenicol (25 mug/ml), or to 1,3-diacetylchloramphenicol (25 mug/ml). Since strain FB(t) is capable of deacetylating acetyl chloramphenicols, these effects are probably all due to low concentrations of chloramphenicol. In the presence of chloramphenicol, FB(t)Cam(1) (r) produced fruiting bodies and myxospores on fruiting agar; however, glycerol-induced myxospore formation was inhibited. In the absence of the antibiotic, chloramphenicol resistance was maintained by glycerol-induced myxospores.
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PMID:Chloramphenicol resistance in Myxococcus xanthus. 80 62

We have constructed a small, transposition-defective derivative of the transposon Tn10 that carries the chloramphenicol acetyltransferase gene of pACYC184. This new genetic element, Tn10d-Cam, transposes when Tn10 transposase is provided from a multi-copy plasmid. Transposon insertion mutagenesis of Salmonella typhimurium was performed by using a strain carrying a Tn10d-Cam insertion in an Escherichia coli F' episome as the donor in transductional crosses into recipients that carried a plasmid expressing Tn10 transposase. Tn10d-Cam insertion mutations were also generated by complementation in cis of Tn10d-Cam by a cotransducible Tn10 element that overproduces transposase. Here, transposase was provided only transiently, and the Tn10d-Cam insertion mutations were recovered in a transposase-free strain. Cis complementation was used for mutagenesis of a plasmid target. The site specificity of insertion and the effect of insertions on expression of a downstream gene were investigated, using Tn10d-Cam insertions in a plasmid carrying a segment of the histidine operon.
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PMID:Characterization of Tn10d-Cam: a transposition-defective Tn10 specifying chloramphenicol resistance. 284 6

The transcription rates of the rat serine protease inhibitor 2.3 and 2.1 genes (spi 2.3 and spi 2.1), which are normally very low and high, respectively, are inversely modulated during inflammation. Two growth-hormone-response elements (GHRE-I and GHRE-II) maintain the spi 2.1 gene under the stringent control of growth hormone [Le Cam, A., Pantescu, V., Paquereau, L., Legraverend, C., Fauconnier, G. & Asins, G. (1994) J. Biol. Chem. 269, 21532-21539], whereas spi 2.3 appears to escape control by this hormone, despite the presence in its promoter of a functional GHRE-I. A major difference between these two otherwise very similar genes is the presence in spi 2.3 of a specific 348-bp extension of the 3' untranslated region (3' UTR). Inserting this 3' UTR element downstream of the polyadenylation signal or upstream of the spi 2.3 promoter in constructs containing the chloramphenicol acetyltransferase gene strongly decreases basal transcription and inhibits growth-hormone-stimulated transcription, but poorly affects transcriptional stimulation by dexamethasone or interleukin-6. The spi 2.3 3' UTR extension also inhibits, basal and growth-hormone-induced transcription from the spi 2.1 promoter. Repressor activity appears to be distributed throughout the specific extension of the 3' UTR and seems to involve interactions with two types of 5' cis-acting promoter elements. The first is the GAGA box, a key control spi promoter element, whose mutation faithfully reproduces the effects of the 3' UTR silencer on spi 2.1 and spi 2.3 promoters. The second is represented by CCAAT enhancer-binding-protein-(C/EBP)-binding sites, whose functions are severely impaired by the spi 2.3-specific 3' UTR extension. The presence of this silencer in the spi 2.3 gene very likely accounts for the lack of basal of transcription in vivo and for induction of the gene during acute inflammation.
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PMID:Transcriptional repression, a novel function for 3' untranslated regions. 764 61