Linked Life Data

12492863

Source:http://linkedlifedata.com/resource/pubmed/id/12492863

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-12-20
pubmed:abstractText
IclR is a repressor for the Escherichia coli aceBAK operon, which encodes isocitrate lyase (aceB), malate synthase (aceA) and isocitrate dehydroge-nase kinase/phosphorylase (aceK) in the glyoxylate bypass. IclR also represses the expression of iclR in an autogenous manner. DNase I footprinting and in vitro transcription assays indicated that IclR binds to an IclR box (-21 to +14), which overlaps the iclR promoter and thus competes with the RNA polymerase for DNA binding, leading to transcription repression. In the case of the aceBAK operon, IclR binds to IclR box II between -52 and -19 of the aceB promoter and interferes with binding of the RNA polymerase to this promoter. A secondary IclR binding site (IclR box I) was identified between -125 and -99 of the aceB promoter. IclR binds to this IclR box I even after formation of the aceB promoter open complex and, moreover, induces disassembly of the open complex, leading to repression of aceB transcription. In parallel, the location of the C-terminal domain of the RNA polymerase alpha subunit (alphaCTD) on DNA is shifted close to the IclR box I, indicating that direct interaction between the alphaCTD and the IclR box I-associated IclR caused the repression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
183-94
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Two different modes of transcription repression of the Escherichia coli acetate operon by IclR.
pubmed:affiliation
Department of Molecular Genetics, National Institute of Genetics, Mishima, Shizuoka 411-8504, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't