SirR, a Novel Iron-Dependent Repressor inStaphylococcus epidermidis

Hill, Philip J.; Landers, Patrick; Morrissey, Julie A.; Sims, Catriona M.; Williams, Paul

doi:10.1128/.66.9.4123-4129.1998

Cited by 11 publications

(14 citation statements)

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“…The homologous region in S. aureus was likewise identified and referred to as MntABC and MntR (Horsburgh et al, 2002 ). Expression of sitABC / mntABC is controlled by the diphtheria toxin repressor (DtxR)-like homologue, SirR/MntR (Hill et al, 1998 ; Horsburgh et al, 2002 ; Ando et al, 2003 ). Transcription of sitABC is repressed by SirR in the presence of either Mn 2+ or Fe 2+ in S. epidermidis (Hill et al, 1998 ), although there is some contention over whether both Mn 2+ or Fe 2+ , or just Mn 2+ controls expression in S. aureus (Horsburgh et al, 2002 ; Ando et al, 2003 ).…”

Section: Control Of Iron-regulated Gene Expressionmentioning

confidence: 99%

“…Expression of sitABC / mntABC is controlled by the diphtheria toxin repressor (DtxR)-like homologue, SirR/MntR (Hill et al, 1998 ; Horsburgh et al, 2002 ; Ando et al, 2003 ). Transcription of sitABC is repressed by SirR in the presence of either Mn 2+ or Fe 2+ in S. epidermidis (Hill et al, 1998 ), although there is some contention over whether both Mn 2+ or Fe 2+ , or just Mn 2+ controls expression in S. aureus (Horsburgh et al, 2002 ; Ando et al, 2003 ). Like with Fur, transcription is blocked in the presence of these divalent metal ions because the metal ions facilitate the binding of SirR/MntR to a conserved SirR (or MntR) box (Figure 1A ), a region of dyad symmetry in the promoter/operator region of sitABC/mntABC (Hill et al, 1998 ; Ando et al, 2003 ).…”

Section: Control Of Iron-regulated Gene Expressionmentioning

confidence: 99%

“…Additionally, the extracellular release of lipoproteins during iron starvation, such as SitC, would further contribute to immunogenicity (Cockayne et al, 1998 ). Despite a proposed role in divalent metal uptake, the fact that expression of sitC is repressed in the presence of excess Mn 2+ or Fe 2+ (Hill et al, 1998 ), and that SitC is highly expressed in vivo , the substrate of SitC in S. epidermidis remains unknown.…”

Section: The Staphylococcal Irlps: Functions In Iron Acquisitionmentioning

confidence: 99%

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The iron-regulated staphylococcal lipoproteins

Sheldon¹,

Heinrichs²

2012

Front. Cell. Inf. Microbio.

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Lipoproteins fulfill diverse roles in antibiotic resistance, adhesion, protein secretion, signaling and sensing, and many also serve as the substrate binding protein (SBP) partner to ABC transporters for the acquisition of a diverse array of nutrients including peptides, sugars, and scarcely abundant metals. In the staphylococci, the iron-regulated SBPs are significantly upregulated during iron starvation and function to sequester and deliver iron into the bacterial cell, enabling staphylococci to circumvent iron restriction imposed by the host environment. Accordingly, this subset of lipoproteins has been implicated in staphylococcal pathogenesis and virulence. Lipoproteins also activate the host innate immune response, triggered through Toll-like receptor-2 (TLR2) and, notably, the iron-regulated subset of lipoproteins are particularly immunogenic. In this review, we discuss the iron-regulated staphylococcal lipoproteins with regard to their biogenesis, substrate specificity, and impact on the host innate immune response.

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Section: Control Of Iron-regulated Gene Expressionmentioning

confidence: 99%

Section: Control Of Iron-regulated Gene Expressionmentioning

confidence: 99%

Section: The Staphylococcal Irlps: Functions In Iron Acquisitionmentioning

confidence: 99%

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The iron-regulated staphylococcal lipoproteins

Sheldon¹,

Heinrichs²

2012

Front. Cell. Inf. Microbio.

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“…The transcriptional regulator sirR , a homologue of the staphylococcal iron regulator repressor and the basal transcription factor gene tfbF , were found to be induced by Lrp-overexpression (Fig. 7 ; Table 3 ) [ 39 ]. Lrp-overexpression produced induction of transporter genes, like pstC2 and phnC , which belong to phosphate transport operons (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The transcriptional regulator sirR , a homologue of the staphylococcal iron regulator repressor, was found to be induced by Lrp (Fig. 7 ; Table 3 ) [ 39 ]. SirR is described as a repressor of a putative Mn-dependent ABC-transporter in H. salinarum NRC-1 [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional control by two leucine-responsive regulatory proteins in Halobacterium salinarum R1

et al. 2010

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BackgroundArchaea combine bacterial-as well as eukaryotic-like features to regulate cellular processes. Halobacterium salinarum R1 encodes eight leucine-responsive regulatory protein (Lrp)-homologues. The function of two of them, Irp (OE3923F) and lrpA1 (OE2621R), were analyzed by gene deletion and overexpression, including genome scale impacts using microarrays.ResultsIt was shown that Lrp affects the transcription of multiple target genes, including those encoding enzymes involved in amino acid synthesis, central metabolism, transport processes and other regulators of transcription. In contrast, LrpA1 regulates transcription in a more specific manner. The aspB3 gene, coding for an aspartate transaminase, was repressed by LrpA1 in the presence of L-aspartate. Analytical DNA-affinity chromatography was adapted to high salt, and demonstrated binding of LrpA1 to its own promoter, as well as L-aspartate dependent binding to the aspB3 promoter.ConclusionThe gene expression profiles of two archaeal Lrp-homologues report in detail their role in H. salinarum R1. LrpA1 and Lrp show similar functions to those already described in bacteria, but in addition they play a key role in regulatory networks, such as controlling the transcription of other regulators. In a more detailed analysis ligand dependent binding of LrpA1 was demonstrated to its target gene aspB3.

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Iron and heme utilization inPorphyromonas gingivalis

et al. 2005

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Porphyromonas gingivalis is a Gram-negative anaerobic bacterium associated with the initiation and progression of adult periodontal disease. Iron is utilized by this pathogen in the form of heme and has been shown to play an essential role in its growth and virulence. Recently, considerable attention has been given to the characterization of various secreted and surface-associated proteins of P. gingivalis and their contribution to virulence. In particular, the properties of proteins involved in the uptake of iron and heme have been extensively studied. Unlike other Gram-negative bacteria, P. gingivalis does not produce siderophores. Instead it employs specific outer membrane receptors, proteases (particularly gingipains), and lipoproteins to acquire iron/heme. In this review, we will focus on the diverse mechanisms of iron and heme acquisition in P. gingivalis. Specific proteins involved in iron and heme capture will be described. In addition, we will discuss new genes for iron/heme utilization identified by nucleotide sequencing of the P. gingivalis W83 genome. Putative iron- and heme-responsive gene regulation in P. gingivalis will be discussed. We will also examine the significance of heme/hemoglobin acquisition for the virulence of this pathogen.

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SirR, a Novel Iron-Dependent Repressor inStaphylococcus epidermidis

Cited by 11 publications

References 0 publications

The iron-regulated staphylococcal lipoproteins

The iron-regulated staphylococcal lipoproteins

Transcriptional control by two leucine-responsive regulatory proteins in Halobacterium salinarum R1

Iron and heme utilization inPorphyromonas gingivalis

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