Operator sequences of the aerobactin operon of plasmid ColV-K30 binding the ferric uptake regulation (fur) repressor

Abstract

The promoter region of the pColV-K30-encoded operon specifying biosynthesis and transport of the siderophore aerobactin was subjected to deletion analysis to determine the smallest DNA sequence affording iron regulation of a iucA'-'lacZ gene fusion. A 78-base-pair (bp) region containing the main (P1)

The flavohaemoglobin (HMP) of Escherichia coli generates superoxide in vitro and causes oxidative stress in vivo

“…Under the aerobic growth conditions employed here, FNR is unlikely to be active [23] and will not contribute to soda regulation. We could detect no 'iron box' (GATAATGAT A ATCATTATC) for binding FUR [24] in the hmp promoter region. A third represser of sodA is Integration Host Factor (IHF), product of the himA gene [25].…”

Growth and siderophores production in Alcaligenes faecalis is regulated by metal ions

“…Exogenous regulatory signal(s) activate LemA, a membrane-bound sensor kinase, which in turn regulates the production of bacterial autoinducers that control the biosynthesis of antifungal metabolites like siderophore/antibiotics [24] and the transcription of iron-regulated gene is under the negative control of protein [repressor] with Fe 2+ as an essential co-repressor. Increase in the concentration of iron in cell cytoplasm cause iron toxicity to the cell [22,25]. 2+ in the intracellular control of siderophores synthesis and are responsible for repressing siderophore synthesis [26].…”

Expression of the Iron-ActivatednspAandsecYGenes inNeisseria meningitidisGroup B by Fur-Dependent and -Independent Mechanisms

“…In its most basic state, Fur forms a dimer together with divalent cations, such as ferrous iron, and binds to a consensus sequence (the Fur box) that overlaps the promoters of iron-regulated genes to prevent their transcription. Recent studies indicate that in some organisms, Fur may also function as a positive regulator of gene transcription, together with iron (8,(9)(10)(11)(12)24), although the mechanism of iron activation by Fur is not well elucidated. Our recent studies of N. meningitidis group B, using a combination of microarray technology, computational analysis, and in vitro binding studies, revealed that a large number of genes are activated during growth in the presence of iron and that a number of these iron-activated genes have putative Fur-binding sequences to which Fur was demonstrated to bind (17).…”