Proteomic Analysis of the Pseudomonas aeruginosa Iron Starvation Response Reveals PrrF Small Regulatory RNA-Dependent Iron Regulation of Twitching Motility, Amino Acid Metabolism, and Zinc Homeostasis Proteins.

Iron is a critical nutrient for most microbial pathogens, and the immune system exploits this requirement by sequestering iron. The opportunistic pathogen exhibits a high requirement for iron yet an exquisite ability to overcome iron deprivation during infection. Upon iron starvation, induces the expression of several high-affinity iron acquisition systems, as well as the PrrF small regulatory RNAs (sRNAs) that mediate an iron-sparing response.

The human innate immune protein calprotectin induces iron starvation responses in .

Most microbial pathogens have a metabolic iron requirement, necessitating the acquisition of this nutrient in the host. In response to pathogen invasion, the human host limits iron availability. Although canonical examples of nutritional immunity are host strategies that limit pathogen access to Fe(III), little is known about how the host restricts access to another biologically relevant oxidation state of this metal, Fe(II).

The Pseudomonas aeruginosa PrrF1 and PrrF2 Small Regulatory RNAs Promote 2-Alkyl-4-Quinolone Production through Redundant Regulation of the mRNA.

is an opportunistic Gram-negative pathogen that requires iron for growth and virulence. Under low-iron conditions, transcribes two highly identical (95%) small regulatory RNAs (sRNAs), PrrF1 and PrrF2, which are required for virulence in acute murine lung infection models. The PrrF sRNAs promote the production of 2-akyl-4(1)-quinolone metabolites (AQs) that mediate a range of biological activities, including quorum sensing and polymicrobial interactions.

Sequence-Specific Affinity Chromatography of Bacterial Small Regulatory RNA-Binding Proteins from Bacterial Cells.

Bacterial small RNA molecules (sRNAs) are increasingly recognized as central regulators of bacterial stress responses and pathogenesis. In many cases, RNA-binding proteins are critical for the stability and function of sRNAs. Previous studies have adopted strategies to genetically tag an sRNA of interest, allowing isolation of RNA-protein complexes from cells.

AlgR Phosphorylation Status Differentially Regulates Pyocyanin and Pyoverdine Production.

employs numerous, complex regulatory elements to control expression of its many virulence systems. The AlgZR two-component regulatory system controls the expression of several crucial virulence phenotypes. We recently determined, through transcriptomic profiling of a PAO1 Δ mutant strain compared to wild-type PAO1, that and are cotranscribed and show differential iron-dependent gene expression.

PAMDB: a comprehensive Pseudomonas aeruginosa metabolome database.

The Pseudomonas aeruginosaMetabolome Database (PAMDB, http://pseudomonas.umaryland.edu) is a searchable, richly annotated metabolite database specific to P.

The Pseudomonas aeruginosa PrrF Small RNAs Regulate Iron Homeostasis during Acute Murine Lung Infection.

is a Gram-negative opportunistic pathogen that requires iron for virulence. Iron homeostasis is maintained in part by the PrrF1 and PrrF2 small RNAs (sRNAs), which block the expression of iron-containing proteins under iron-depleted conditions. The PrrF sRNAs also promote the production of the quinolone signal (PQS), a quorum sensing molecule that activates the expression of several virulence genes.

Regulation of Pseudomonas aeruginosa Virulence by Distinct Iron Sources.

is a ubiquitous environmental bacterium and versatile opportunistic pathogen. Like most other organisms, requires iron for survival, yet iron rapidly reacts with oxygen and water to form stable ferric (FeIII) oxides and hydroxides, limiting its availability to living organisms. During infection, iron is also sequestered by the host innate immune system, further limiting its availability.

Dual-seq transcriptomics reveals the battle for iron during Pseudomonas aeruginosa acute murine pneumonia.

Determining bacterial gene expression during infection is fundamental to understand pathogenesis. In this study, we used dual RNA-seq to simultaneously measure P. aeruginosa and the murine host's gene expression and response to respiratory infection.

Cystic Fibrosis Isolates of Pseudomonas aeruginosa Retain Iron-Regulated Antimicrobial Activity against Staphylococcus aureus through the Action of Multiple Alkylquinolones.

Cystic fibrosis (CF) is a hereditary disease that predisposes individuals to pulmonary dysfunction and chronic infections. Early infection of the CF lung with Staphylococcus aureus is common, while Pseudomonas aeruginosa becomes dominant as disease progresses. Emergence of P.

Interactions between Pseudomonas aeruginosa and Staphylococcus aureus during co-cultivations and polymicrobial infections.

Pseudomonas aeruginosa and Staphylococcus aureus are versatile bacterial pathogens and common etiological agents in polymicrobial infections. Microbial communities containing both of these pathogens are shaped by interactions ranging from parasitic to mutualistic, with the net impact of these interactions in many cases resulting in enhanced virulence. Polymicrobial communities of these organisms are further defined by multiple aspects of the host environment, with important implications for disease progression and therapeutic outcomes.

Iron Depletion Enhances Production of Antimicrobials by Pseudomonas aeruginosa.

Unlabelled: Cystic fibrosis (CF) is a heritable disease characterized by chronic, polymicrobial lung infections. While Staphylococcus aureus is the dominant lung pathogen in young CF patients, Pseudomonas aeruginosa becomes predominant by adulthood. P.

Spoils of war: iron at the crux of clinical and ecological fitness of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a versatile environmental microorganism that also causes life-threatening opportunistic infections. At the root of this bacterium's ability to survive in such diverse environments is its large suite of iron acquisition systems. More recently, studies have highlighted the ability of P.

The prrF-encoded small regulatory RNAs are required for iron homeostasis and virulence of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an opportunistic pathogen that requires iron to cause infection, but it also must regulate the uptake of iron to avoid iron toxicity. The iron-responsive PrrF1 and PrrF2 small regulatory RNAs (sRNAs) are part of P. aeruginosa's iron regulatory network and affect the expression of at least 50 genes encoding iron-containing proteins.

Sibling rivalry: related bacterial small RNAs and their redundant and non-redundant roles.

Small RNA molecules (sRNAs) are now recognized as key regulators controlling bacterial gene expression, as sRNAs provide a quick and efficient means of positively or negatively altering the expression of specific genes. To date, numerous sRNAs have been identified and characterized in a myriad of bacterial species, but more recently, a theme in bacterial sRNAs has emerged: the presence of more than one highly related sRNAs produced by a given bacterium, here termed sibling sRNAs. Sibling sRNAs are those that are highly similar at the nucleotide level, and while it might be expected that sibling sRNAs exert identical regulatory functions on the expression of target genes based on their high degree of relatedness, emerging evidence is demonstrating that this is not always the case.

A method for in vivo identification of bacterial small RNA-binding proteins.

Small bacterial regulatory RNAs (sRNAs) have gained immense appreciation over the last decade for their roles in mediating posttranscriptional gene regulation of numerous physiological processes. Several proteins contribute to sRNA stability and regulation, most notably the Hfq RNA-binding protein. However, not all sRNAs rely on Hfq for their stability.

Adaptation of iron homeostasis pathways by a Pseudomonas aeruginosa pyoverdine mutant in the cystic fibrosis lung.

Cystic fibrosis (CF) patients suffer from chronic bacterial lung infections, most notably by Pseudomonas aeruginosa, which persists for decades in the lungs and undergoes extensive evolution. P. aeruginosa requires iron for virulence and uses the fluorescent siderophore pyoverdine to scavenge and solubilize ferric iron during acute infections.

The complex interplay of iron, biofilm formation, and mucoidy affecting antimicrobial resistance of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is a Gram-negative opportunistic bacterial pathogen that is refractory to a variety of current antimicrobial therapeutic regimens. Complicating treatment for such infections is the ability of P. aeruginosa to form biofilms, as well as several innate and acquired resistance mechanisms.

Iron-responsive bacterial small RNAs: variations on a theme.

For most living organisms, iron is both essential and potentially toxic, making the precise maintenance of iron homeostasis necessary for survival. To manage this paradox, bacteria regulate the acquisition, utilization, and storage of iron in response to its availability. The iron-dependent ferric uptake repressor (Fur) often mediates this iron-responsive regulation by both direct and indirect mechanisms.

Characterization of a heme-regulated non-coding RNA encoded by the prrF locus of Pseudomonas aeruginosa.

Pseudomonas aeruginosa, an opportunistic pathogen, requires iron for virulence and can obtain this nutrient via the acquisition of heme, an abundant source of iron in the human body. A surplus of either iron or heme can lead to oxidative stress; thus, the Fur (ferric uptake regulator) protein blocks expression of genes required for iron and heme uptake in iron-replete environments. Fur also represses expression of two nearly identical genes encoding the 116- and 114-nucleotide (nt) long PrrF1 and PrrF2 RNAs, respectively.