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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asymmetric localization of proteins is essential to many biological functions of bacteria. Shigella IcsA, an outer membrane protein, is localized to the old pole of the bacillus, where it mediates assembly of a polarized actin tail during infection of mammalian cells. Actin tail assembly provides the propulsive force for intracellular movement and intercellular dissemination. Localization of IcsA to the pole is independent of the amino-terminal signal peptide (Charles, M., Perez, M., Kobil, J.H., and Goldberg, M.B., 2001, Proc Natl Acad Sci USA 98: 9871-9876) suggesting that IcsA targeting occurs in the bacterial cytoplasm and that its secretion across the cytoplasmic membrane occurs only at the pole. Here, we characterize the mechanism by which IcsA is secreted across the cytoplasmic membrane. We present evidence that IcsA requires the SecA ATPase and the SecYEG membrane channel (translocon) for secretion. Our data suggest that YidC is not required for IcsA secretion. Furthermore, we show that polar localization of IcsA is independent of SecA. Finally, we demonstrate that while IcsA requires the SecYEG translocon for secretion, components of this apparatus are uniformly distributed within the membrane. Based on these data, we propose a model for coordinate polar targeting and secretion of IcsA at the bacterial pole.
Mol Microbiol 2003 Oct
PMID:IcsA, a polarly localized autotransporter with an atypical signal peptide, uses the Sec apparatus for secretion, although the Sec apparatus is circumferentially distributed. 1450 62

In Shigella and enteroinvasive Escherichia coli (EIEC), the etiologic agents of shigellosis in humans, the determinants responsible for entry of bacteria into and dissemination within epithelial cells are encoded by a virulence plasmid. To understand the evolution of the association between the virulence plasmid and the chromosome, we performed a phylogenetic analysis using the sequences of four chromosomal genes (trpA, trpB, pabB, and putP) and three virulence plasmid genes (ipaB, ipaD, and icsA) of a collection of 51 Shigella and EIEC strains. The phylogenetic tree derived from chromosomal genes showed a typical "star" phylogeny, indicating a fast diversification of Shigella and EIEC groups. Phylogenetic groups obtained from the chromosomal and plasmidic genes were similar, suggesting that the virulence plasmid and the chromosome share similar evolutionary histories. The few incongruences between the trees could be attributed to exchanges of fragments of different plasmids and not to the transfer of an entire plasmid. This indicates that the virulence plasmid was not transferred between the different Shigella and EIEC groups. These data support a model of evolution in which the acquisition of the virulence plasmid in an ancestral E. coli strain preceded the diversification by radiation of all Shigella and EIEC groups, which led to highly diversified but highly specialized pathogenic groups.
J Mol Evol 2003 Aug
PMID:The evolutionary history of Shigella and enteroinvasive Escherichia coli revised. 1456 58

Diarrheal diseases caused by microorganisms and their toxins are a major cause of mortality and morbidity throughout the world. Acute diarrhea is mainly caused due to increased intestinal secretion, commonly as a result of infection with enterotoxin producing organisms (enterotoxigenic Escherichia coli, Vibrio cholera) or due to decreased intestinal absorption from infection with organisms that damage the intestinal epithelium (enteropathogenic E. coli sp., Shigella sp., Salmonella sp.) The studies of the impact of enteric pathogens and their virulence factors exert their effect by producing toxins, called bacterial toxins. The protein toxins are produced by diverse group of bacteria. Most of the bacterial toxins exert their effect through involvement of ADP-ribosylation proteins; otherwise essential for several cellular functions while other toxins involve guanylate cyclase systems or calcium and protein kinases for their ultimate action.
Mol Cell Biochem 2003 Nov
PMID:Modulation of gut physiology through enteric toxins. 1461 51

In the human enteropathogen Shigella transcription of virF, the primary regulator of the invasion functions, is strictly temperature-dependent and is antagonistically mediated by H-NS and FIS, which bind to specific sites on the virF promoter. Here we report on the relevance of DNA geometry to the thermoregulation of virF and demonstrate that the virF promoter hosts a major DNA bend halfway between two H-NS sites. The bent region has been mutagenized in vitro to mimic temperature-induced changes of DNA curvature. Functional analysis of curvature mutants and of promoter constructs in which the two H-NS sites are phased-out by a half-helix turn reveals that modifying the spatial relationships between these sites severely affects the interaction of H-NS with the virF promoter, as well as its in vivo and in vitro temperature-dependent activity. The role of promoter curvature as thermosensor is also compatible with the present observation that, with increasing temperature, the virF bending centre moves downstream at a rate having its maximum around the transition temperature, abruptly unmasking a binding site for the transcriptional activator FIS.
Mol Microbiol 2004 Jan
PMID:The virF promoter in Shigella: more than just a curved DNA stretch. 1475 91

In bacteria, the evolution of pathogenicity seems to be the result of the constant arrival of virulence factors (VFs) into the bacterial genome. However, the integration, retention, and/or expression of these factors may be the result of the interaction between the new arriving genes and the bacterial genomic background. To test this hypothesis, a phylogenetic analysis was done on a collection of 98 Escherichia coli/Shigella strains representing the pathogenic and commensal diversity of the species. The distribution of 17 VFs associated to the different E. coli pathovars was superimposed on the phylogenetic tree. Three major types of VFs can be recognized: (1) VFs that arrive and are expressed in different genetic backgrounds (such as VFs associated with the pathovars of mild chronic diarrhea: enteroaggregative, enteropathogenic, and diffusely-adhering E. coli), (2) VFs that arrive in different genetic backgrounds but are preferentially found, associated with a specific pathology, in only one particular background (such as VFs associated with extraintestinal diseases), and (3) VFs that require a particular genetic background for the arrival and expression of their virulence potential (such as VFs associated with pathovars typical of severe acute diarrhea: enterohemorragic, enterotoxigenic, and enteroinvasive E. coli strains). The possibility of a single arrival of VFs by chance, followed by a vertical transmission, was ruled out by comparing the evolutionary histories of some of these VFs to the strain phylogeny. These evidences suggest that important changes in the genome of E. coli have occurred during the diversification of the species, allowing the virulence factors associated with severe acute diarrhea to arrive in the population. Thus, the E. coli genome seems to be formed by an "ancestral" and a "derived" background, each one responsible for the acquisition and expression of different virulence factors.
Mol Biol Evol 2004 Jun
PMID:A specific genetic background is required for acquisition and expression of virulence factors in Escherichia coli. 1501 51

Two electrochemical assays for detecting Staphylococcus aureus enterotoxin A and B genes were developed. The assays are based on PCR amplification with biotinylated primers, hybridization to a fluorescein-labeled probe, and detection with horseradish peroxidase-conjugated anti-fluorescein antibody using a hand-held electrochemical detector. The limit of detection (LOD) for both assays was approximately 16 copies of the sea and seb genes. The assays were evaluated in blinded studies, each with 81 samples that included genomic and cloned S. aureus DNA, and genomic DNA from Alcaligens, Bacillus, Bacteroides, Bordetella, Borkholderia, Clostridium, Comanonas, Enterobacter, Enterococcus, Escherichia, Francisella, Haemophilus, Klebsiella, Listeria, Moraxella, Neisseria, Proteus, Pseudomonas, Salmonella, Serratia, Shigella, Streptococcus, Vibrio and Yersinia species. Both assays showed 100% sensitivity. The specificity was 96% for the SEA assay and 98% for the SEB assay. These results demonstrate the feasibility of performing probe-based detection of PCR products with a low-cost, hand-held, electrochemical detection device as a viable alternative to colorimetric enzyme-linked assays of PCR products.
Mol Cell Probes 2004 Dec
PMID:Detection of Staphylococcus aureus enterotoxin A and B genes with PCR-EIA and a hand-held electrochemical sensor. 1548 76

A DNA fragment of approximately 1500 bp, harbouring the sorbitol transport gene (srlT), was amplified from the chromosomal DNA of Erwinia herbicola ATCC 21998 by PCR and cloned in Escherichia coli JM109. Degenerate oligonucleotide primers used were designed based on the conserved regions in the gene sequences within the gut operon of E. coli (Gene Bank accession no. J02708) and the srl operon of Erwinia amylovora (Gene Bank accession no. Y14603). The cloned DNA fragment was sequenced and found to contain an open reading frame of 1473 nucleotides coding for a protein of 491 amino acids, corresponding to a mass of 52410 Da. The nucleotide sequence of this ORF was highly homologous to that of the gutA gene of Escherichia coli gut operon, the srlE gene of Shigella flexrni and the sorbitol transporter gene sequence of Escherichia coli K12 (Gene Bank accession nos. J02708, AE016987 and D90892 respectively). The protein sequence showed significant homology to that of the phosphotransferase system i.e. the glucitol/sorbitol-specific IIBC components of Escherichia coli and Erwinia amylovora (P56580, O32522). The cloned DNA fragment was introduced into a pRA90 vector and the recombinant was used for developing srlT mutants of Erwinia herbicola, by homologous recombination. Mutants obtained were unable to grow on minimal medium with sorbitol. The insertion of the pRA90 vector inside the srlT gene sequence of the mutants was confirmed by DNA-DNA hybridisation.
Mol Biol Rep 2004 Sep
PMID:Cloning, sequencing and partial characterisation of sorbitol transporter (srlT) gene encoding phosphotransferase system, glucitol/sorbitol-specific IIBC components of Erwinia herbicola ATCC 21998. 1556 Mar 68

Reviews on the pathogenic mechanisms of Shigella species show a lacunae in the understanding of the bacterial antioxidant defense system and its regulations. This study was done to investigate the regulation of expression of antioxidant enzymes in clinical isolates of Shigella species, under various growth conditions. The in vitro expression of superoxide dismutase in the clinical isolates of Shigella spp., is modulated by both endogenous and exogenous factors. During aerobic and iron repleted growth conditions, the expression of the MnSOD and FeSOD enzymes were higher, and an atypical SOD was also expressed. However, under anaerobic growth conditions and in plasmid-cured strains, the antioxidant enzyme activities were decreased and the atypical SOD was not expressed. Absence of the atypical form of SOD may be due to the low oxygen environment. Plasmid-encoded factors may also play a role in the expression of this SOD, which had a molecular weight of approximately 30 kDa. In the rat ileal loop ligation assay, mild lesions were observed only in the intestinal microvilli of rats injected with plasmid-cured strains of Shigella spp., suggesting that plasmid-encoded factors, including those that regulate the expression of the atypical SOD, are essential for the virulence of Shigella spp.
Mol Cell Biochem 2004 Dec
PMID:Identification of an atypical form of 30 kDa SOD--a possible virulence factor in clinical isolates of Shigella spp. 1566 90

Bacteria of Shigella spp. are responsible for shigellosis in humans. They use a type III secretion (TTS) system encoded by a 200 kb virulence plasmid to enter epithelial cells and trigger apoptosis in macrophages. This TTS system comprises a secretion apparatus, translocators and effectors that transit through this apparatus, cytoplasmic chaperones and specific transcription regulators. The TTS apparatus assembled during growth of Shigella flexneri in broth is activated upon contact with epithelial cells. Transcription of approximately 15 genes encoding effectors, including IpaH proteins, is regulated by the TTS apparatus activity and controlled by MxiE, a transcription activator of the AraC family, and IpgC, the chaperone of the translocators IpaB and IpaC. We present evidence that MxiE is produced by a frameshift between a 59-codon open reading frame (ORF) (mxiEa) containing the translation start site and a 214-codon ORF (mxiEb) encoding the DNA binding domain of the protein. The mxiEa encoded N-terminal part of MxiE is required for MxiE function. Frameshifting efficiency was approximately 30% during growth in broth and was not modulated by the activity of secretion or the coactivator IpgC. Frameshifting involves slippage of RNA polymerase during transcription of mxiE, which results in the incorporation of one additional nucleotide in the mRNA and places mxiEa and mxiEb in the same reading frame. Frameshifting might represent an additional means of controlling gene expression under specific environmental conditions.
Mol Microbiol 2005 Apr
PMID:Frameshifting by transcriptional slippage is involved in production of MxiE, the transcription activator regulated by the activity of the type III secretion apparatus in Shigella flexneri. 1577 90

A ubiquitous early step in infection of man and animals by enteric bacterial pathogens like Salmonella, Shigella and enteropathogenic Escherichia coli (EPEC) is the translocation of virulence effector proteins into mammalian cells via specialized type III secretion systems (TTSSs). Translocated effectors subvert the host cytoskeleton and stimulate signalling to promote bacterial internalization or survival. Target cell plasma membrane cholesterol is central to pathogen-host cross-talk, but the precise nature of its critical contribution remains unknown. Using in vitro cholesterol-binding assays, we demonstrate that Salmonella (SipB) and Shigella (IpaB) TTSS translocon components bind cholesterol with high affinity. Direct visualization of cell-associated fluorescently labelled SipB and parallel immunogold transmission electron microscopy revealed that cholesterol levels limit both the amount and distribution of plasma membrane-integrated translocon. Correspondingly, cholesterol depletion blocked effector translocation into cultured mammalian cells by not only the related Salmonella and Shigella TTSSs, but also the more divergent EPEC system. The data reveal that cholesterol-dependent association of the bacterial TTSS translocon with the target cell plasma membrane is essential for translocon activation and effector delivery into mammalian cells.
Mol Microbiol 2005 May
PMID:Cholesterol binding by the bacterial type III translocon is essential for virulence effector delivery into mammalian cells. 1581 15


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