Difference between revisions of "PMID:15687217"
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| + | !align=left align='left' bgcolor='#CCCCFF' |Citation | ||
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| + | '''Pérez-Capilla, T, Baquero, MR, Gómez-Gómez, JM, Ionel, A, Martín, S and Blázquez, J''' (2005) SOS-independent induction of dinB transcription by beta-lactam-mediated inhibition of cell wall synthesis in Escherichia coli. ''J. Bacteriol.'' '''187''':1515-8 | ||
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| + | !align=left align='left' bgcolor='#CCCCFF' |Abstract | ||
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| + | Transcription of the dinB gene, encoding DNA polymerase IV, is induced by the inhibition of cell wall synthesis at different levels. Using the beta-lactam antibiotic ceftazidime, a PBP3 inhibitor, as a model, we have shown that this induction is independent of the LexA/RecA regulatory system. Induction of dinB transcription mediated by ceftazidime produces an increase in the reversion of a +1 Lac frameshift mutation. | ||
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| + | !align=left align='left' bgcolor='#CCCCFF' |Links | ||
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| + | [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15687217 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC545630 PMC545630] | ||
| + | Online version:[http://dx.doi.org/10.1128/JB.187.4.1515-1518.2005 10.1128/JB.187.4.1515-1518.2005] | ||
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| + | !align=left align='left' bgcolor='#CCCCFF' |Keywords | ||
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| + | Adenosine Triphosphatases/physiology; Bacterial Proteins/physiology; Ceftazidime/pharmacology; Cell Wall/metabolism; DNA Helicases/physiology; Enzyme Inhibitors/pharmacology; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli Proteins/genetics; Frameshift Mutation; Gene Expression Regulation, Bacterial/drug effects; SOS Response (Genetics); Serine Endopeptidases/physiology; Transcription, Genetic; beta-Galactosidase/analysis; beta-Galactosidase/genetics | ||
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| + | ==Main Points of the Paper == | ||
| + | {{LitSignificance}} | ||
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| + | == Materials and Methods Used == | ||
| + | {{LitMaterials}} | ||
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| + | ==Phenotype Annotations== | ||
| + | {{AnnotationTableHelp}} | ||
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| + | !|Phenotype of!!Taxon Information!!Genotype Information (if known)!!Condition Information!!OMP ID!!OMP Term Name!!ECO ID!!ECO Term Name!!Notes!!Status | ||
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| + | ==Notes== | ||
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| + | ==References== | ||
| + | {{RefHelp}} | ||
| + | <references/> | ||
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| + | [[Category:Publication]] | ||
Latest revision as of 15:32, 25 June 2015
| Citation |
Pérez-Capilla, T, Baquero, MR, Gómez-Gómez, JM, Ionel, A, Martín, S and Blázquez, J (2005) SOS-independent induction of dinB transcription by beta-lactam-mediated inhibition of cell wall synthesis in Escherichia coli. J. Bacteriol. 187:1515-8 |
|---|---|
| Abstract |
Transcription of the dinB gene, encoding DNA polymerase IV, is induced by the inhibition of cell wall synthesis at different levels. Using the beta-lactam antibiotic ceftazidime, a PBP3 inhibitor, as a model, we have shown that this induction is independent of the LexA/RecA regulatory system. Induction of dinB transcription mediated by ceftazidime produces an increase in the reversion of a +1 Lac frameshift mutation. |
| Links |
PubMed PMC545630 Online version:10.1128/JB.187.4.1515-1518.2005 |
| Keywords |
Adenosine Triphosphatases/physiology; Bacterial Proteins/physiology; Ceftazidime/pharmacology; Cell Wall/metabolism; DNA Helicases/physiology; Enzyme Inhibitors/pharmacology; Escherichia coli/genetics; Escherichia coli/metabolism; Escherichia coli Proteins/genetics; Frameshift Mutation; Gene Expression Regulation, Bacterial/drug effects; SOS Response (Genetics); Serine Endopeptidases/physiology; Transcription, Genetic; beta-Galactosidase/analysis; beta-Galactosidase/genetics |
| edit table |
Main Points of the Paper
Please summarize the main points of the paper.
Materials and Methods Used
Please list the materials and methods used in this paper (strains, plasmids, antibodies, etc).
Phenotype Annotations
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<protect>
| Phenotype of | Taxon Information | Genotype Information (if known) | Condition Information | OMP ID | OMP Term Name | ECO ID | ECO Term Name | Notes | Status |
|---|---|---|---|---|---|---|---|---|---|
| edit table |
</protect>
Notes
References
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