scholarly journals Comparison of the Genome Sequence of the Poultry Pathogen Bordetella avium with Those of B. bronchiseptica, B. pertussis, and B. parapertussis Reveals Extensive Diversity in Surface Structures Associated with Host Interaction

2006 ◽  
Vol 188 (16) ◽  
pp. 6002-6015 ◽  
Author(s):  
Mohammed Sebaihia ◽  
Andrew Preston ◽  
Duncan J. Maskell ◽  
Holly Kuzmiak ◽  
Terry D. Connell ◽  
...  
Keyword(s):  
Genome Sequence ◽  
Outer Membrane Proteins ◽  
Phase Variation ◽  
Regulatory System ◽  
Secreted Proteins ◽  
Type I ◽  
Host Interaction ◽  
Bordetella Avium ◽  
Evolutionary Relatedness ◽  
Large Genes

ABSTRACT Bordetella avium is a pathogen of poultry and is phylogenetically distinct from Bordetella bronchiseptica, Bordetella pertussis, and Bordetella parapertussis, which are other species in the Bordetella genus that infect mammals. In order to understand the evolutionary relatedness of Bordetella species and further the understanding of pathogenesis, we obtained the complete genome sequence of B. avium strain 197N, a pathogenic strain that has been extensively studied. With 3,732,255 base pairs of DNA and 3,417 predicted coding sequences, it has the smallest genome and gene complement of the sequenced bordetellae. In this study, the presence or absence of previously reported virulence factors from B. avium was confirmed, and the genetic bases for growth characteristics were elucidated. Over 1,100 genes present in B. avium but not in B. bronchiseptica were identified, and most were predicted to encode surface or secreted proteins that are likely to define an organism adapted to the avian rather than the mammalian respiratory tracts. These include genes coding for the synthesis of a polysaccharide capsule, hemagglutinins, a type I secretion system adjacent to two very large genes for secreted proteins, and unique genes for both lipopolysaccharide and fimbrial biogenesis. Three apparently complete prophages are also present. The BvgAS virulence regulatory system appears to have polymorphisms at a poly(C) tract that is involved in phase variation in other bordetellae. A number of putative iron-regulated outer membrane proteins were predicted from the sequence, and this regulation was confirmed experimentally for five of these.

scholarly journals CpxRA Influences Xenorhabdus nematophila Colonization Initiation and Outgrowth in Steinernema carpocapsae Nematodes through Regulation of the nil Locus

2009 ◽  
Vol 75 (12) ◽  
pp. 4007-4014 ◽  
Author(s):  
Erin E. Herbert Tran ◽  
Aaron W. Andersen ◽  
Heidi Goodrich-Blair
Keyword(s):  
Regulatory System ◽  
Negative Regulator ◽  
Type I ◽  
Bacterial Cells ◽  
Xenorhabdus Nematophila ◽  
Wild Type ◽  
Host Interactions ◽  
Host Interaction ◽  
Two Stages ◽  
Mutualistic Association

ABSTRACT The gammaproteobacterium Xenorhabdus nematophila mutualistically colonizes an intestinal region of a soil-dwelling nematode and is a blood pathogen of insects. The X. nematophila CpxRA two-component regulatory system is necessary for both of these host interactions (E. Herbert et al., Appl. Environ. Microbiol. 73:7826-7836, 2007). Mutualistic association of X. nematophila with its nematode host consists of two stages: initiation, where a small number of bacterial cells establish themselves in the colonization site, and outgrowth, where these cells grow to fill the space. In this study, we show that the Cpx system is necessary for both of these stages. X. nematophila ΔcpxR1 colonized fewer nematodes than its wild-type parent and did not achieve as high a density as did the wild type within a portion of the colonized nematodes. To test whether the ΔcpxR1 host interaction phenotypes are due to its overexpression of mrxA, encoding the type I pilin subunit protein, we assessed the colonization phenotype of a ΔcpxR1 ΔmrxA1 double mutant. This mutant displayed the same colonization defect as ΔcpxR1, indicating that CpxR negative regulation of mrxA does not play a detectable role in X. nematophila-host interactions. CpxR positively regulates expression of nilA, nilB, and nilC genes necessary for nematode colonization. Here we show that the nematode colonization defect of the ΔcpxR1 mutant is rescued by elevating nil gene expression through mutation of nilR, a negative regulator of nilA, nilB, and nilC. These data suggest that the nematode colonization defect previously observed in ΔcpxR1 is caused, at least in part, by altered regulation of nilA, nilB, and nilC.

scholarly journals Long-term persistence of crAss-like phage crAss001 is associated with phase variation in Bacteroides intestinalis

2020 ◽  
Author(s):  
Andrey N Shkoporov ◽  
Ekaterina V Khokhlova ◽  
Niamh Stephens ◽  
Cara Hueston ◽  
Samuel Seymour ◽  
...  
Keyword(s):  
Dynamic Equilibrium ◽  
Phase Variation ◽  
Carrier State ◽  
Human Gut ◽  
Rapid Phase ◽  
Host Interaction ◽  
Infected Cells ◽  
Phage Sensitivity

The crAss-like phages are ubiquitous and highly abundant members of the human gut virome that infect commensal bacteria of the order Bacteroidales. Although incapable of classical lysogeny, these viruses demonstrate unexplained long-term persistence in the human gut microbiome, dominating the virome in some individuals. Here we demonstrate that rapid phase variation of alternate capsular polysaccharides plays an important role in dynamic equilibrium between phage sensitivity and resistance in B. intestinalis cultures, allowing phage and bacteria to multiply in parallel. The data also suggests the role of concomitant phage persistence mechanisms associated with delayed lysis of infected cells, such as carrier state infection. From an ecological and evolutionary standpoint this type of phage-host interaction is consistent with the Piggyback-the-Winner model, which suggests a preference towards lysogenic or other 'benign' forms of phage infection when the host is stably present at high abundance.

scholarly journals Iron Starvation of Bordetella avium Stimulates Expression of Five Outer Membrane Proteins and Regulates a Gene Involved in Acquiring Iron from Serum

1998 ◽  
Vol 66 (8) ◽  
pp. 3597-3605 ◽  
Author(s):  
Terry D. Connell ◽  
Amy Dickenson ◽  
Andrew J. Martone ◽  
Kevin T. Militello ◽  
Melanie J. Filiatraut ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Membrane Proteins ◽  
Outer Membrane ◽  
Outer Membrane Proteins ◽  
Iron Starvation ◽  
Nutrient Source ◽  
Transposon Insertion ◽  
Bordetella Avium ◽  
Regulated Expression ◽  
Molecular Masses

ABSTRACT Iron starvation of Bordetella avium induced expression of five outer membrane proteins with apparent molecular masses of 95, 92, 91.5, 84, and 51 kDa. Iron-responsive outer membrane proteins (FeRPs) of similar sizes were detected in six of six strains ofB. avium, suggesting that the five FeRPs are common constituents of the outer membrane of most, if not all, strains ofB. avium. Iron-regulated genes of B. avium were targeted for mutagenesis with the transposon TnphoA. Two mutants with iron-responsive alkaline phosphatase activities were isolated from the transposon library. The transposon insertion did not alter the iron-regulated expression of the five FeRPs in mutant Pho-6. The mutant Pho-20 exhibited a loss in expression of the 95-kDa FeRP and the 84-kDa FeRP. Both Pho-6 and Pho-20 were able to use free iron as a nutrient source. However, Pho-20 was severely compromised in its ability to use iron present in turkey serum. The data indicated that the mutation in Pho-20 affected expression of one or more components of an uptake machinery that is involved in acquisition of iron from organic ferricomplexes.

scholarly journals Secretome Screening Reveals Fibroblast Growth Factors as Novel Inhibitors of Viral Replication

2018 ◽  
Vol 92 (16) ◽  
Author(s):  
Saskia D. van Asten ◽  
Matthijs Raaben ◽  
Benjamin Nota ◽  
Robbert M. Spaapen
Keyword(s):  
Growth Factor ◽  
Viral Replication ◽  
Viral Infection ◽  
Fibroblast Growth Factor ◽  
Oncolytic Virus ◽  
Human Cells ◽  
Secreted Proteins ◽  
Type I ◽  
Fibroblast Growth ◽  
Vesicular Stomatitis

ABSTRACT Cellular antiviral programs can efficiently inhibit viral infection. These programs are often initiated through signaling cascades induced by secreted proteins, such as type I interferons, interleukin-6 (IL-6), or tumor necrosis factor alpha (TNF-α). In the present study, we generated an arrayed library of 756 human secreted proteins to perform a secretome screen focused on the discovery of novel modulators of viral entry and/or replication. The individual secreted proteins were tested for the capacity to inhibit infection by two replication-competent recombinant vesicular stomatitis viruses (VSVs) with distinct glycoproteins utilizing different entry pathways. Fibroblast growth factor 16 (FGF16) was identified and confirmed as the most prominent novel inhibitor of both VSVs and therefore of viral replication, not entry. Importantly, an antiviral interferon signature was completely absent in FGF16-treated cells. Nevertheless, the antiviral effect of FGF16 is broad, as it was evident on multiple cell types and also on infection by coxsackievirus. In addition, other members of the FGF family also inhibited viral infection. Thus, our unbiased secretome screen revealed a novel protein family capable of inducing a cellular antiviral state. This previously unappreciated role of the FGF family may have implications for the development of new antivirals and the efficacy of oncolytic virus therapy. IMPORTANCE Viruses infect human cells in order to replicate, while human cells aim to resist infection. Several cellular antiviral programs have therefore evolved to resist infection. Knowledge of these programs is essential for the design of antiviral therapeutics in the future. The induction of antiviral programs is often initiated by secreted proteins, such as interferons. We hypothesized that other secreted proteins may also promote resistance to viral infection. Thus, we tested 756 human secreted proteins for the capacity to inhibit two pseudotypes of vesicular stomatitis virus (VSV). In this secretome screen on viral infection, we identified fibroblast growth factor 16 (FGF16) as a novel antiviral against multiple VSV pseudotypes as well as coxsackievirus. Subsequent testing of other FGF family members revealed that FGF signaling generally inhibits viral infection. This finding may lead to the development of new antivirals and may also be applicable for enhancing oncolytic virus therapy.

scholarly journals Genome Sequence of Venturia oleaginea, the Causal Agent of Olive Leaf Scab

2020 ◽  
Vol 33 (9) ◽  
pp. 1095-1097
Author(s):  
Mohammed Y. Jaber ◽  
Jiandong Bao ◽  
Xiuqin Gao ◽  
Limei Zhang ◽  
Dou He ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Genome Sequence ◽  
Population Genetic ◽  
Whole Genome Sequence ◽  
Whole Genome ◽  
Olive Leaf ◽  
Spot Disease ◽  
Host Interaction ◽  
Fungal Biology

Olive leaf scab, also known as peacock spot disease, caused by Venturia oleaginea (syn. Spilocaea oleaginea and Fusicladium oleagineum) is the most widespread and economically important fungal disease attacking olive in production countries. Here, we report the first highly contiguous whole-genome sequence (46.08 Mb) of one isolate, YUN35, of V. oleaginea. The described genome sequence and annotation resource will be useful to study the fungal biology, pathogen-host interaction, characterization of genes of interest, and population genetic diversity.

scholarly journals Two Outer Membrane Proteins Are Required for Maximal Type I Secretion of the Caulobacter crescentus S-Layer Protein

2004 ◽  
Vol 186 (23) ◽  
pp. 8000-8009 ◽  
Author(s):  
Michael C. Toporowski ◽  
John F. Nomellini ◽  
Peter Awram ◽  
John Smit
Keyword(s):  
Outer Membrane ◽  
Caulobacter Crescentus ◽  
Outer Membrane Proteins ◽  
Functional System ◽  
Type I ◽  
Wild Type ◽  
Residual Level ◽  
The Individual ◽  
Multicopy Vector

ABSTRACT Transport of RsaA, the crystalline S-layer subunit protein of Caulobacter crescentus, is mediated by a type I secretion mechanism. Two proteins have been identified that play the role of the outer membrane protein (OMP) component in the RsaA secretion machinery. The genes rsaF a and rsaF b were identified by similarity to the Escherichia coli hemolysin secretion OMP TolC by using the C. crescentus genome sequence. The rsaF a gene is located several kilobases downstream of the other transporter genes, while rsaF b is completely unlinked. An rsaF a knockout had ∼56% secretion compared to wild-type levels, while the rsaF b knockout reduced secretion levels to ∼79%. When expression of both proteins was eliminated, there was no RsaA secretion, but a residual level of ∼9% remained inside the cell, suggesting posttranslational autoregulation. Complementation with either of the individual rsaF genes by use of a multicopy vector, which resulted in 8- to 10-fold overexpression of the proteins, did not restore RsaA secretion to wild-type levels, indicating that both rsaF genes were required for full-level secretion. However, overexpression of rsaFa (with normal rsaF b levels) in concert with overexpression of rsaA resulted in a 28% increase in RsaA secretion, indicating a potential for significantly increasing expression levels of an already highly expressing type I secretion system. This is the only known example of type I secretion requiring two OMPs to assemble a fully functional system.

scholarly journals Comparative Analysis of Streptococcus pneumoniae Type I Restriction-Modification Loci: Variation in hsdS Gene Target Recognition Domains

Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 712
Author(s):  
Melissa B. Oliver ◽  
W. Edward Swords
Keyword(s):  
Streptococcus Pneumoniae ◽  
Target Recognition ◽  
Phase Variation ◽  
The Elderly ◽  
Single Amino Acid ◽  
Type I ◽  
Gene Target ◽  
Gene Orientation ◽  
Additional Level ◽  
Restriction Modification

Streptococcus pneumoniae (pneumococcus) is a respiratory commensal pathogen that causes a range of infections, particularly in young children and the elderly. Pneumococci undergo spontaneous phase variation in colony opacity phenotype, in which DNA rearrangements within the Type I restriction-modification (R-M) system specificity gene hsdS can potentially generate up to six different hsdS alleles with differential DNA methylation activity, resulting in changes in gene expression. To gain a broader perspective of this system, we performed bioinformatic analyses of Type I R-M loci from 18 published pneumococcal genomes, and one R-M locus sequenced for this study, to compare genetic content, organization, and homology. All 19 loci encoded the genes hsdR, hsdM, hsdS, and at least one hsdS pseudogene, but differed in gene order, gene orientation, and hsdS target recognition domain (TRD) content. We determined the coding sequences of 87 hsdS TRDs and excluded seven from further analysis due to the presence of premature stop codons. Comparative analyses revealed that the TRD 1.1, 1.2, and 2.1 protein sequences had single amino acid substitutions, and TRD 2.2 and 2.3 each had seven differences. The results of this study indicate that variability exists among the gene content and arrangements within Type I R-M loci may provide an additional level of divergence between pneumococcal strains, such that phase variation-mediated control of virulence factors may vary significantly between individual strains. These findings are consistent with presently available transcript profile data.

scholarly journals RNA Sensing of Mycobacterium tuberculosis and Its Impact on TB Vaccination Strategies

Vaccines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 67 ◽  
Author(s):  
Sanne Burkert ◽  
Ralf R. Schumann
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Type I Interferons ◽  
Immune Memory ◽  
Type I ◽  
Effective Prevention ◽  
Vaccination Strategies ◽  
Host Interaction ◽  
Global Threat ◽  
Antigen Presenting ◽  
The Impact

Tuberculosis (TB) is still an important global threat and although the causing organism has been discovered long ago, effective prevention strategies are lacking. Mycobacterium tuberculosis (MTB) is a unique pathogen with a complex host interaction. Understanding the immune responses upon infection with MTB is crucial for the development of new vaccination strategies and therapeutic targets for TB. Recently, it has been proposed that sensing bacterial nucleic acid in antigen-presenting cells via intracellular pattern recognition receptors (PRRs) is a central mechanism for initiating an effective host immune response. Here, we summarize key findings of the impact of mycobacterial RNA sensing for innate and adaptive host immunity after MTB infection, with emphasis on endosomal toll-like receptors (TLRs) and cytosolic sensors such as NLRP3 and RLRs, modulating T-cell differentiation through IL-12, IL-21, and type I interferons. Ultimately, these immunological pathways may impact immune memory and TB vaccine efficacy. The novel findings described here may change our current understanding of the host response to MTB and potentially impact clinical research, as well as future vaccination design. In this review, the current state of the art is summarized, and an outlook is given on how progress can be made.

scholarly journals Genetic variation regulates the activation and specificity of Restriction-Modification systems in Neisseria gonorrhoeae

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Leonor Sánchez-Busó ◽  
Daniel Golparian ◽  
Julian Parkhill ◽  
Magnus Unemo ◽  
Simon R. Harris
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Single Molecule ◽  
Regulation Of Gene Expression ◽  
Phase Variation ◽  
Type I ◽  
Dam Methylase ◽  
Different Strains ◽  
Methylation Patterns ◽  
Restriction Modification ◽  
Restriction Modification Systems

Abstract Restriction-Modification systems (RMS) are one of the main mechanisms of defence against foreign DNA invasion and can have an important role in the regulation of gene expression. The obligate human pathogen Neisseria gonorrhoeae carries one of the highest loads of RMS in its genome; between 13 to 15 of the three main types. Previous work has described their organization in the reference genome FA1090 and has inferred the associated methylated motifs. Here, we studied the structure of RMS and target methylated motifs in 25 gonococcal strains sequenced with Single Molecule Real-Time (SMRT) technology, which provides data on DNA modification. The results showed a variable picture of active RMS in different strains, with phase variation switching the activity of Type III RMS, and both the activity and specificity of a Type I RMS. Interestingly, the Dam methylase was found in place of the NgoAXI endonuclease in two of the strains, despite being previously thought to be absent in the gonococcus. We also identified the real methylation target of NgoAXII as 5′-GCAGA-3′, different from that previously described. Results from this work give further insights into the diversity and dynamics of RMS and methylation patterns in N. gonorrhoeae.

scholarly journals Variable Lipoprotein Hemagglutinin A Gene (vlhA) Expression in VariantMycoplasmagallisepticumStrainsIn Vivo

2018 ◽  
Vol 86 (11) ◽  
Author(s):  
K. Pflaum ◽  
E. R. Tulman ◽  
J. Beaudet ◽  
J. Canter ◽  
S. J. Geary
Keyword(s):  
Gene Family ◽  
No Reduction ◽  
Phase Variation ◽  
Chronic Respiratory Disease ◽  
Etiologic Agent ◽  
Economic Losses ◽  
Wild Type ◽  
Exact Role ◽  
Content Type ◽  
Host Interaction

ABSTRACTMycoplasma gallisepticum, the primary etiologic agent of chronic respiratory disease, is a significant poultry pathogen, causing severe inflammation and leading to economic losses worldwide. Immunodominant proteins encoded by the variable lipoprotein and hemagglutinin (vlhA) gene family are thought to be important forM. gallisepticum-host interaction, pathogenesis, and immune evasion, but their exact role remains unknown. Previous work has demonstrated thatvlhAphase variation is dynamic throughout the earliest stages of infection, withvlhA3.03 being the predominantvlhAexpressed during the initial infection, and that the pattern of dominantvlhAexpression may be nonrandom and regulated by previously unrecognized mechanisms. To further investigate this gene family, we assessed thevlhAprofile of two well-characterized vaccine strains, GT5 and Mg7, avlhA3.03 mutant strain, and anM. gallisepticumpopulation expressing an alternative immunodominantvlhA. Here, we report that twoM. gallisepticumvaccine strains show differentvlhAprofiles over the first 2 days of infection compared to that of wild-type Rlow, while the population expressing an alternative immunodominantvlhAgene reverted to a profile indistinguishable from that of wild-type Rlow. Additionally, we observed a slight shift in thevlhAgene expression profile but no reduction in virulence in avlhA3.03 mutant. Taken together, these data further support the hypothesis thatM. gallisepticum vlhAgenes change in a nonstochastic temporal progression of expression and thatvlhA3.03, while preferred, is not required for virulence. Collectively, these data may be important in elucidating mechanisms of colonization and overall pathogenesis ofM. gallisepticum.

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