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dc.contributor.authorLandini, Paolo
dc.contributor.authorVolkert, Michael R.
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:49Z
dc.date.available2022-08-23T16:52:49Z
dc.date.issued1995-09-01
dc.date.submitted2008-07-09
dc.identifier.citationEMBO J. 1995 Sep 1;14(17):4329-35.
dc.identifier.issn0261-4189 (Print)
dc.identifier.pmid7556074
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42130
dc.description.abstractThe ada and aidB genes are part of the adaptive response to DNA methylation damage in Escherichia coli. Transcription of the ada and the aidB genes is triggered by binding of the methylated Ada protein (meAda) to a specific sequence located 40-60 base pairs upstream of the transcriptional start, which is internal to an A/T-rich region. In this report we demonstrate that the Ada binding site is also a binding site for RNA polymerase. RNA polymerase is able to bind the -40 to -60 region of the ada and the aidB promoters in the absence of meAda, and its binding is mediated by the alpha subunit. This region resembles the UP element of the rrnB P1 promoter in location, sequence and mechanism of interaction with RNA polymerase. We discuss the function of UP-like elements in positively controlled promoters and provide evidence that Ada does not act by enhancing RNA polymerase binding affinity to the promoter region. Instead, Ada stimulates transcription by modifying the nature of the RNA polymerase-promoter interaction, allowing RNA polymerase to recognize the core promoter -35 and -10 elements in addition to the UP-like element.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=7556074&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC394517/?tool=pubmed
dc.subjectBacterial Proteins
dc.subjectBase Sequence
dc.subjectBinding Sites
dc.subjectDNA, Bacterial
dc.subjectDeoxyribonuclease I
dc.subjectEscherichia coli
dc.subject*Escherichia coli Proteins
dc.subject*Genes, Bacterial
dc.subjectMacromolecular Substances
dc.subjectMolecular Sequence Data
dc.subjectO(6)-Methylguanine-DNA Methyltransferase
dc.subject*Promoter Regions (Genetics)
dc.subjectRNA Polymerase I
dc.subjectRestriction Mapping
dc.subject*Trans-Activation (Genetics)
dc.subjectTranscription Factors
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleRNA polymerase alpha subunit binding site in positively controlled promoters: a new model for RNA polymerase-promoter interaction and transcriptional activation in the Escherichia coli ada and aidB genes
dc.typeArticle
dc.source.journaltitleThe EMBO journal
dc.source.volume14
dc.source.issue17
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/505
dc.identifier.contextkey544987
html.description.abstract<p>The ada and aidB genes are part of the adaptive response to DNA methylation damage in Escherichia coli. Transcription of the ada and the aidB genes is triggered by binding of the methylated Ada protein (meAda) to a specific sequence located 40-60 base pairs upstream of the transcriptional start, which is internal to an A/T-rich region. In this report we demonstrate that the Ada binding site is also a binding site for RNA polymerase. RNA polymerase is able to bind the -40 to -60 region of the ada and the aidB promoters in the absence of meAda, and its binding is mediated by the alpha subunit. This region resembles the UP element of the rrnB P1 promoter in location, sequence and mechanism of interaction with RNA polymerase. We discuss the function of UP-like elements in positively controlled promoters and provide evidence that Ada does not act by enhancing RNA polymerase binding affinity to the promoter region. Instead, Ada stimulates transcription by modifying the nature of the RNA polymerase-promoter interaction, allowing RNA polymerase to recognize the core promoter -35 and -10 elements in addition to the UP-like element.</p>
dc.identifier.submissionpathoapubs/505
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.source.pages4329-35


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