[Show abstract][Hide abstract] ABSTRACT: Pseudomonas chlororaphis strain PA23 is a biocontrol agent able to suppress growth of the fungal pathogen Sclerotinia sclerotiorum. This bacterium produces an arsenal of exometabolites including pyrrolnitrin (PRN), phenazine (PHZ), hydrogen cyanide (HCN), and degradative enzymes. Production of these compounds is controlled at both the transcriptional and posttranscriptional levels by the Gac-Rsm system, RpoS, PsrA, and the Phz quorum-sensing system. Beyond pathogen-suppression, the success of a biocontrol agent is dependent upon its ability to establish itself in the environment where predation by bacterivorous organisms, including nematodes, may threaten persistence. The focus of this study was to investigate whether PA23 is able to resist grazing by Caenorhabditis elegans and to define the role played by exoproducts in the bacterial-nematode interaction. We discovered that both PRN and HCN contribute to fast- and slow-killing of C. elegans. HCN is well-established as having lethal effects on C. elegans; however, PRN has not been reported to be nematicidal. Exposure of L4 stage nematodes to purified PRN reduced nematode viability in a dose-dependent fashion and led to reduced hatching of eggs laid by gravid adults. Because bacterial metabolites can act as chemoattractants or repellents, we analyzed whether PA23 exhibited attractant or repulsive properties towards C. elegans. Both PRN and HCN were found to be potent repellents. Next we investigated whether the presence of C. elegans would elicit changes in PA23 gene activity. Co-culturing the two organisms increased expression of a number of genes associated with biocontrol, including phzA, hcnA, phzR, phzI, rpoS and gacS. Exoproduct analysis showed that PHZ and autoinducer signals were upregulated, consistent with the gene expression profiles. Collectively, these findings indicate that PA23 is able to sense the presence of C. elegans and it is able to both repel and kill the nematodes, which should facilitate environmental persistence and ultimately biocontrol.
PLoS ONE 04/2015; 10(4):e0123184. DOI:10.1371/journal.pone.0123184 · 3.23 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The environmental organism Serratia marcescens is one of the primary causes of numerous nosocomial outbreaks and opportunistic infections. Multi-drug resistance is now a common feature among S. marcescens clinical isolates complicating the efficacy of treatment. Recent reports have attributed antibiotic resistance to altered porin expression as well as perturbation of the intrinsic AmpC beta-lactamase production pathway. In this study, we aim to genetically correlate the absence of OmpF and OmpC classical porins with increased antibiotic resistance. In generating isogenic porin mutant strains, we avoided incorporating additional resistance through the use of antibiotic cassette in gene replacement and adopted an alternate strategy in creating clean unmarked mutant strains. We found that lack of OmpF, but not OmpC, significantly increased antibiotic minimum inhibitory concentration (MIC) values to the beta-lactam drugs such as ampicillin and cefoxitin as well as to nitrofurantoin. Furthermore, we found that cefoxitin did not induce intrinsic AmpC beta-lactamase production indicating that the increased MIC values was a result of reduced permeability of cefoxitin due to the lack of OmpF. Genetic deletion of both ompF and ompC did not compromise the integrity of the bacterial cell envelope in optimal growth conditions suggesting that other outer membrane porins may function in a compensatory role to facilitate nutrient uptake and cell envelope integrity. Taken together, to our knowledge this is the first study that genetically correlates increased antibiotic resistance with altered porin expression in S. marcescens.
[Show abstract][Hide abstract] ABSTRACT: BackgroundA one-step skin disinfection method containing 2% chlorhexidine-gluconate (CHG) and 70% isopropyl alcohol (IPA) is currently used by blood suppliers worldwide. Reports of bacterially contaminated platelet concentrates (PCs) indicate that skin disinfection is not fully effective. Approximately 20% of skin microflora exist as surface-attached aggregates (biofilms), known for displaying increased resistance to disinfectants. This study was aimed at determining whether skin microflora biofilm-positive Staphylococcus epidermidis and Staphylococcus capitis are resistant to CHG and/or IPA.Study Design and Methods
Free-floating cells and mono or dual (1 : 1 ratio) biofilms of S. epidermidis and S. capitis were exposed to CHG, IPA, or CHG/IPA for 30 seconds, simulating skin disinfection practices. Residual viable cells were quantified by colony counting. Morphology of disinfectant-treated S. epidermidis biofilms was examined by scanning electron microscopy. Treated S. epidermidis and S. capitis biofilms were inoculated into PCs and bacterial concentrations were determined on Days 0 and 5 of storage.ResultsTreatment of staphylococcal biofilm cells with all disinfectants caused cell damage and significant reduction in viability, with CHG/IPA being the most effective. However, biofilms were significantly more resistant to treatment than free-floating cells. Disinfectant-treated S. epidermidis proliferated better in PCs than S. capitis, especially when grown as monospecies biofilms.Conclusion
Although CHG/IPA is effective in reducing the viability of S. epidermidis and S. capitis biofilms, these organisms are not completely eliminated. Furthermore, disinfectant-treated staphylococcal biofilms multiply well in PCs. These results demonstrate that the biofilm-forming capability of the skin microflora reduces the bactericidal efficiency of blood donor skin disinfectants.
[Show abstract][Hide abstract] ABSTRACT: Pseudomonas sp. DF41 is able to suppress the fungal pathogen Sclerotinia sclerotiorum through production of a lipopeptide called sclerosin. The aim of this study was to isolate the DF41 QS locus and characterize its role in fungal antagonism. Through screening of a fosmid library, one clone was selected that tested positive for AHL production. Sequence analysis revealed the presence of two QS genes: pdfR and pdfI, encoding a LuxR transcriptional activator and an AHL synthase, respectively. Downstream of pdfI lays a gene encoding a transcriptional activator called RfiA followed by pdfC, comprising part of an efflux locus. Characterization of an AHL-deficient strain revealed it to be phenotypically identical to the wild type. Conversely rfiA, which is co-transcribed with pdfI, is essential for both AF activity and sclerosin production. Using a pdfI-lacZ fusion analysis, we discovered that pdfI is positively autoregulated. Additionally, pdfI expression was markedly increased in the rfiA mutant and quantification of AHL levels revealed elevated intracellular signal accumulation. We hypothesize that RfiA is a positive activator of the downstream efflux pump which serves to export both sclerosin and AHL signals. In a gacS mutant, pdfI-lacZ activity was decreased; however, plasmid-borne rsmZ was able to restore expression. Collectively, our findings indicate that: (i) QS indirectly controls DF41 suppression of Sclerotinia through RfiA; and (ii) pdfI expression and AHL signal production are positively regulated by the Gac–Rsm system. Identification of the PdfRI QS system, RfiA and RsmZ add to the increasingly complex network overseeing expression of DF41 biocontrol factors.
Biological Control 02/2014; 69:82–89. DOI:10.1016/j.biocontrol.2013.11.005 · 1.64 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The platelet (PLT) storage environment triggers the formation of surface-attached aggregates known as biofilms by the common PLT contaminant Staphylococcus epidermidis. The biofilm matrix is largely composed of polysaccharide intercellular adhesin (PIA) mediated by the icaADBC operon. However, PIA-negative S. epidermidis has been reported to form biofilms in PLT concentrates (PCs). Since biofilm formation is associated with increased virulence, this study was aimed at determining if PIA-negative S. epidermidis grown in PCs presents enhanced virulence using the nematode Caenorhabditis elegans as a host model for bacterial pathogenesis.
Biofilm-positive S. epidermidis ATCC 35984 and 9142, which carry the icaADBC operon, and biofilm-negative S. epidermidis ATCC 12228 and 9142 ΔicaA were grown in regular media and in PCs and biofilm formation was quantified using a crystal violet assay. The virulence of these strains after passage through PCs was tested using nematode killing assays. Nematode survival was calculated using the Kaplan-Meier method and statistical differences were determined by log-rank analysis.
All S. epidermidis strains were able to form biofilms in PCs. Although persistence of a biofilm-positive phenotype in the biofilm-negative strains grown in PCs was not observed after passage in regular medium, the virulence of all strains was significantly increased as demonstrated by shortened life spans of the nematodes in C. elegans killing assays.
Our findings highlight the potential of an increased risk of nosocomial infections caused by S. epidermidis in transfusion recipients since PC storage conditions promote biofilm formation, and possibly pathogenicity, of strains traditionally known to be attenuated for virulence.
[Show abstract][Hide abstract] ABSTRACT: Legionella pneumophila, an intracellular parasite of protozoa, possesses a distinct dimorphic life cycle that alternates between the vegetative replicative form and the resilient but highly infectious cyst form. Previously, temporally expressed heterodimeric IHF was shown to be required for differentiation into the cyst form. However, the precise regulatory mechanisms controlling the expression of IHF have not been identified. Microplate kinetic assays with GFP reporter promoter fusion constructs in wild-type, Δihf, ΔrpoS and ΔletA mutant strain backgrounds were employed to assess differences in expression levels of ihfA, ihfB, rsmY and rsmZ. Loss of IHF, RsmY and RsmZ expression in various mutant strain backgrounds was confirmed by quantitative PCR. Here we report that the stationary phase sigma factor RpoS is a positive regulator of IHF whereas IHF appears to act as a positive autoregulator assisting RpoS. Bioinformatic analyses identified a set of IHF binding sites upstream of one RpoS binding sites in the promoter region for both ihfA and ihfB. Recombinant IHF protein bound ihfA and ihfB promoter regions in vitro confirming the functionality of these IHF binding sites that may assist in the bending of the promoter DNA to facilitate transcription activation of ihfA and ihfB by RpoS. Interestingly, the consensus binding site for IHF is very similar to that of the two component response regulator LetA. LetA negatively regulates transcription of ihfA and ihfB implying titrational regulatory control by LetA and IHF. Along with LetA, IHF was found to positively regulate expression of the non-coding regulatory RNAs RsmY and RsmZ responsible for the de-repression of CsrA-repressed transcripts associated with cyst formation and coordinated post-exponential virulent phenotypes. Taken together, these observations indicate that IHF may have more of an integral role in the global regulatory system governing the transition from replicative to cyst forms than previously thought.
[Show abstract][Hide abstract] ABSTRACT: Caenorhabditis elegans can serve as a simple genetic host to study interactions between Legionellaceae and their hosts, and to examine the contribution of specific gene products to virulence and immunity. C. elegans nematodes have several appealing attributes as a host organism; they are inexpensive, have robust genetic analysis tools, have a simple anatomy yet display a wide range of complex behaviors, and, as invertebrates, do not require animal ethics protocols. Use of C. elegans as a host model complements cell-based models, providing additional support and consistency of the experimental data obtained from multiple models. The C. elegans innate immune system functions similarly to that of the alveolar macrophage including the apoptosis [e.g. programmed cell death (PCD)] pathway located within the germline. The digestive tract of C. elegans is a primary interface between the innate immune system and bacterial pathogens. Thus, the C. elegans host model provides an alternative approach to investigate Legionella pneumophila immunopathogenesis.
[Show abstract][Hide abstract] ABSTRACT: Pseudomonas sp. strain DF41 produces a lipopeptide, called sclerosin that inhibits the fungal pathogen Sclerotinia sclerotiorum . The aim of the current study was to deduce the chemical structure of this lipopeptide and further characterize its bioactivity. Mass spectrometry analysis determined the structure of sclerosin to be CH(3)-(CH(2))(6)-CH(OH)-CH(2)-CO-Dhb-Pro-Ala-Leu/Ile-Ala-Val-Val-Dhb-Thr-Val-Leu/Ile-Dhp-Ala-Ala-Ala-Val-Dhb-Dhb-Ala-Dab-Ser-Val-OH, similar to corpeptins A and B of the tolaasin group, differing by only 3 amino acids in the peptide chain. Subjecting sclerosin to various ring opening procedures revealed no new ions, suggesting that this molecule is linear. As such, sclerosin represents a new member of the tolaasin lipopeptide group. Incubation of S. sclerotinia ascospores and sclerotia in the presence of sclerosin inhibited the germination of both cell types. Sclerosin also exhibited antimicrobial activity against Bacillus species. Conversely, this lipopeptide demonstrated no zoosporicidal activity against the oomycete pathogen Phytophthora infestans . Next, we assessed the effect of DF41 and a lipopeptide-deficient mutant on the growth and development of Caenorhabditis elegans larvae. We discovered that sclerosin did not protect DF41 from ingestion by and degradation in the C. elegans digestive tract. However, another metabolite produced by this bacterium appeared to shorten the life-span of the nematode compared to C. elegans growing on Escherichia coli OP50.
Canadian Journal of Microbiology 08/2012; 58(8):1027-34. DOI:10.1139/w2012-079 · 1.22 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Carbapenem-resistant Enterobacteriaceae (CRE) have emerged as major causes of health care-associated infections worldwide. This diverse collection of organisms with various resistance mechanisms is associated with increased lengths of hospitalization, costs of care, morbidity, and mortality. The global spread of CRE has largely been attributed to dissemination of a dominant strain of Klebsiella pneumoniae producing a serine β-lactamase, termed K. pneumoniae carbapenemase (KPC). Here we report an outbreak of KPC-producing CRE infections in which the degree of horizontal transmission between strains and species of a promiscuous plasmid is unprecedented. Sixteen isolates, comprising 11 unique strains, 6 species, and 4 genera of bacteria, were obtained from 14 patients over the first 8 months of the outbreak. Of the 11 unique strains, 9 harbored the same highly promiscuous plasmid carrying the KPC gene blaKPC. The remaining strains harbored distinct blaKPC plasmids, one of which was carried in a strain of Klebsiella oxytoca coisolated from the index patient and the other generated from transposition of the blaKPC element Tn4401. All isolates could be genetically traced to the index patient. Molecular epidemiological investigation of the outbreak was aided by the adaptation of nested arbitrary PCR (ARB-PCR) for rapid plasmid identification. This detailed molecular genetic analysis, combined with traditional epidemiological investigation, provides insights into the highly fluid dynamics of drug resistance transmission during the outbreak.
[Show abstract][Hide abstract] ABSTRACT: We investigated whether nematodes contribute to the persistence, differentiation and amplification of Legionella species in soil, an emerging source for Legionnaires' disease. Here we show that Legionella spp. colonize the intestinal tracts of Caenorhabditis nematodes leading to worm death. Susceptibility to Legionella is influenced by innate immune responses governed by the p38 mitogen-activated protein kinase and insulin/insulin growth factor-1 receptor signalling pathways. We also show that L. pneumophila colonizes the intestinal tract of nematodes cultivated in soil. To distinguish between transient infection and persistence, plate-fed and soil-extracted nematodes-fed fluorescent strains of L. pneumophila were analysed. Bacteria replicated within the nematode intestinal tract, did not invade surrounding tissue, and were excreted as differentiated forms that were transmitted to offspring. Interestingly, the ultrastructural features of the differentiated bacterial forms were similar to cyst-like forms observed within protozoa, amoeba and mammalian cell lines. While intestinal colonization of L. pneumophila dotA and icmT mutant strains did not alter the survival rate of nematodes in comparison to wild-type strains, nematodes colonized with the dot/icm mutant strains exhibited significantly increased levels of germline apoptosis. Taken together, these studies show that nematodes may serve as natural hosts for these organisms and thereby contribute to their dissemination in the environment and suggest that the remarkable ability of L. pneumophila to subvert host cell signalling and evade mammalian immune responses evolved through the natural selection associated with cycling between protozoan and metazoan hosts.
[Show abstract][Hide abstract] ABSTRACT: Members of the family Enterobacteriaceae including Klebsiella have re-emerged as major pathogens in solid organ transplantation. The recent appearance and dissemination of carbapenemase-producing Enterobacteriaceae in Europe and the northeastern United States represents a major challenge to the treatment of enteric gram-negative bacterial infections in immunocompromised patients; however, few reports have detailed the outcomes of such infections. Here we report 2 cases of Klebsiella pneumoniae carbapenemase (KPC)-producing Klebsiella infections in orthotopic liver transplant recipients, which were the index case and initial secondary case for an outbreak of KPC-producing Enterobacteriaceae in our institution. In both instances, the pathogens were initially misidentified as being carbapenem sensitive, the infections recurred after cessation of directed therapy, and the patients ultimately succumbed to their infections.
[Show abstract][Hide abstract] ABSTRACT: Legionella pneumophila is an intracellular parasite of protozoa that differentiates late in infection into metabolically dormant cysts that are highly infectious. Regulation of this process is poorly understood. Here we report that the small DNA binding regulatory proteins integration host factor (IHF) and HU are reciprocally expressed over the developmental cycle, with HU expressed during exponential phase and IHF expressed postexponentially. To assess the role of these regulatory proteins in development, chromosomal deletions were constructed. Single (ihfA or ihfB) and double deletion (Deltaihf) IHF mutants failed to grow in Acanthamoeba castellanii unless complemented in trans when expressed temporally from the ihfA promoter but not under P(tac) (isopropyl-beta-d-thiogalactopyranoside). In contrast, IHF mutants were infectious for HeLa cells, though electron microscopic examination revealed defects in late-stage cyst morphogenesis (thickened cell wall, intracytoplasmic membranes, and inclusions of poly-beta-hydroxybutyrate), and were depressed for the developmental marker MagA. Green fluorescent protein promoter fusion assays indicated that IHF and the stationary-phase sigma factor RpoS were required for full postexponential expression of magA. Finally, defects in cyst morphogenesis noted for Deltaihf mutants in HeLa cells correlated with a loss of both detergent resistance and hyperinfectivity compared with results for wild-type cysts. These studies establish IHF and HU as markers of developmental stages and show that IHF function is required for both differentiation and full virulence of L. pneumophila in natural amoebic hosts.
[Show abstract][Hide abstract] ABSTRACT: Legionella pneumophila expresses two peroxide-scavenging alkyl hydroperoxide reductase systems (AhpC1 and AhpC2D) that are expressed differentially during the bacterial growth cycle. Functional loss of the postexponentially expressed AhpC1 system is compensated for by increased expression of the exponentially expressed AhpC2D system. In this study, we used an acrylamide capture of DNA-bound complexes (ACDC) technique and mass spectrometry to identify proteins that bind to the promoter region of the ahpC2D operon. The major protein captured was an ortholog of OxyR (OxyR(Lp)). Genetic studies indicated that oxyR(Lp) was an essential gene expressed postexponentially and only partially complemented an Escherichia coli oxyR mutant (GS077). Gel shift assays confirmed specific binding of OxyR(Lp) to ahpC2D promoter sequences, but not to promoters of ahpC1 or oxyR(Lp); however, OxyR(Lp) weakly bound to E. coli OxyR-regulated promoters (katG, oxyR, and ahpCF). DNase I protection studies showed that the OxyR(Lp) binding motif spanned the promoter and transcriptional start sequences of ahpC2 and that the protected region was unchanged by treatments with reducing agents or hydrogen peroxide (H(2)O(2)). Moreover, the OxyR(Lp) (pBADLpoxyR)-mediated repression of an ahpC2-gfp reporter construct in E. coli GS077 (the oxyR mutant) was not reversed by H(2)O(2) challenge. Alignments with other OxyR proteins revealed several amino acid substitutions predicted to ablate thiol oxidation or conformational changes required for activation. We suggest these mutations have locked OxyR(Lp) in an active DNA-binding conformation, which has permitted a divergence of function from a regulator of oxidative stress to a cell cycle regulator, perhaps controlling gene expression during postexponential differentiation.
Journal of bacteriology 06/2008; 190(10):3444-55. DOI:10.1128/JB.00141-08 · 2.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The inactivation of TcaA contributes to intrinsic teicoplanin resistance in experimental and clinical isolates of glycopeptide-intermediate resistant Staphylococcus aureus. PhoA fusions confirmed that TcaA is a transmembrane protein with a short intracellular N-terminal domain containing a C-4 zinc finger binding motif, a single membrane-spanning domain, and a large extracellular C-terminal domain. The region conferring teicoplanin susceptibility was narrowed down to the transmembrane part and the first third of the extracellular domain of TcaA, suggesting that neither the C-4 zinc finger binding motif nor the C terminus contributed to teicoplanin susceptibility. TcaA belongs to the cell wall stress stimulon, which comprises a set of genes universally upregulated by cell wall damage. Induction of tcaA was shown to be fully dependent on the two-component regulatory system VraSR. A 66-bp region upstream of the transcriptional start site, which contained an inverted repeat partially covering the promoter box, was shown to be essential for VraSR-mediated induction by cell wall stress. Interestingly, the induction or overexpression of tcaA did not contribute further to teicoplanin susceptibility, suggesting that small amounts of TcaA, such as those present under normal uninduced conditions, were sufficient for TcaA-mediated teicoplanin susceptibility. The strong attenuation of tcaA deletion mutants in a Caenorhabditis elegans survival assay suggested that TcaA may, in addition to affecting glycopeptide susceptibility, also play a role in virulence.
[Show abstract][Hide abstract] ABSTRACT: Legionella pneumophila displays a biphasic developmental cycle in which replicating forms (RFs) differentiate postexponentially into highly infectious,
cyst-like mature intracellular forms (MIFs). Using comparative protein profile analyses (MIFs versus RFs), we identified a
20-kDa protein, previously annotated as “Mip-like” protein, that was enriched in MIFs. However, this 20-kDa protein shared
no similarity with Mip, a well-characterized peptidyl-prolyl isomerase of L. pneumophila, and for clarity we renamed it MagA (for “MIF-associated gene”). We monitored MagA levels across the growth cycle (in vitro
and in vivo) by immunoblotting and established that MagA levels increased postexponentially in vitro (∼3-fold) and nearly
10-fold during MIF morphogenesis in HeLa cells. DNA sequence analysis of the magA locus revealed an upstream divergently transcribed gene, msrA, encoding a peptide methionine sulfoxide reductase and a shared promoter region containing direct and indirect repeat sequences
as well as −10 hexamers often associated with stationary-phase regulation. While MagA has no known function, it contains a
conserved CXXC motif commonly found in members of the thioredoxin reductase family and in AhpD reductases that are associated
with alkylhydroperoxide reductase (AhpC), suggesting a possible role in protection from oxidative stress. MIFs from L. pneumophila strain Lp02 containing a magA deletion exhibited differences in Giménez staining, as well as an apparent increase in cytopathology to HeLa cells, but otherwise
were unaltered in virulence traits. As demonstrated by this study, MagA appears to be a MIF-specific protein expressed late
in intracellular growth that may serve as a useful marker of development.
Journal of Bacteriology 06/2004; 186(10):3038-45. DOI:10.1128/JB.186.10.3038-3045.2004 · 2.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The response regulator CtrA controls chromosome replication by binding to five sites, a, b, c, d, and e, inside the Caulobacter crescentus replication origin (Cori). In this study, we demonstrate that integration host factor (IHF) binds Cori over the central CtrA binding site c. Surprisingly, IHF and CtrA share DNA recognition sequences. Rather than promoting cooperative
binding, IHF binding hinders CtrA binding to site c and nearby site d. Unlike other CtrA binding sites, DNA mutations in the
CtrA c/IHF site uniquely impair autonomous Cori plasmid replication. These mutations also alter transcription from distant promoters more than 100 bp away. When the CtrA
c/IHF site was deleted from the chromosome, these cells grew slowly and became selectively intolerant to a CtrA phosphor-mimic
allele (D51E). Since CtrA protein concentration decreases during the cell cycle as IHF protein concentration increases, we
propose a model in which IHF displaces CtrA in order to bend Cori and promote efficient chromosome replication.
Journal of Bacteriology 10/2003; 185(18):5563-72. DOI:10.1128/JB.185.18.5563-5572.2003 · 2.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Nucleotide sequence analysis of an approximately 80-kb genomic region revealed an approximately 65-kb locus that bears hallmarks of a pathogenicity island. This locus includes homologues of a type IV secretion system, mobile genetic elements, and known virulence factors. Comparative studies with other Legionella pneumophila strains and serogroups indicated that this approximately 65-kb locus is unique to L. pneumophila serogroup 1 Philadelphia-1 strains.
Journal of Bacteriology 09/2003; 185(15):4630-7. DOI:10.1128/JB.185.15.4630-4637.2003 · 2.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: CzcR is the Rickettsia prowazekii homolog of the Caulobacter crescentus global response regulator CtrA. CzcR expression partially compensates for developmental defects in ctrA mutant C. crescentus cells, and CzcR binds to all five CtrA binding sites in the C. crescentus replication origin. Conversely, CtrA binds to five similar sites in the putative R. prowazekii replication origin (oriRp). Also, Escherichia coli IHF protein binds over a central CtrA binding site in oriRp. Therefore, CtrA and IHF regulatory proteins have similar binding patterns in both replication origins, and we propose that
CzcR is a global cell cycle regulator in R. prowazekii.
Journal of Bacteriology 11/2002; 184(20):5789-99. DOI:10.1128/JB.184.20.5789-5799.2002 · 2.81 Impact Factor