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Induction of the Escherichia coli aidB gene under oxygen-limiting conditions requires a functional rpoS (katF) gene.

TitleInduction of the Escherichia coli aidB gene under oxygen-limiting conditions requires a functional rpoS (katF) gene.
Publication TypeJournal Article
Year of Publication1994
AuthorsVolkert, MR, Hajec, LI, Matijasevic, Z, Fang, FC, Prince, R
JournalJ Bacteriol
Volume176
Issue24
Pagination7638-45
Date Published1994 Dec
ISSN0021-9193
KeywordsAcetates, Alkylation, Alleles, Bacterial Proteins, DNA Mutational Analysis, DNA-Binding Proteins, Dose-Response Relationship, Drug, Escherichia coli, Escherichia coli Proteins, Gene Expression Regulation, Bacterial, Genes, Bacterial, Hydrogen Peroxide, Kanamycin Resistance, Mutagenesis, Insertional, Oxygen, Sigma Factor, Suppression, Genetic, Transcription Factors
Abstract

The Escherichia coli aidB gene is regulated by two different mechanisms, an ada-dependent pathway triggered by methyl damage to DNA and an ada-independent pathway triggered when cells are grown without aeration. In this report we describe our search for mutations affecting the ada-independent aidB induction pathway. The mutant strain identified carries two mutations affecting aidB expression. These mutations are named abrB (aidB regulator) and abrD. The abrB mutation is presently poorly characterized because of instability of the phenotype it imparts. The second mutation, abrD1, reduces the expression of aidB observed when aeration is ceased and oxygen becomes limiting. Genetic and phenotypic analysis of the abrD1 mutation demonstrates that it is an allele of rpoS. Thus, aidB is a member of the family of genes that are transcribed by a sigma S-directed RNA polymerase holoenzyme. Examination of aidB expression in an rpoS insertion mutant strain indicates that both rpoS13::Tn10 and abrD1 mutations reduce aidB expression under oxygen-limiting conditions that prevail in unaerated cultures, reduce aidB induction by acetate at a low pH, but have little or no effect on the ada-dependent alkylation induction of aidB.

Alternate JournalJ. Bacteriol.
PubMed ID8002588
PubMed Central IDPMC197221
Grant ListGM37052 / GM / NIGMS NIH HHS / United States