Identification of appressorial and mycelial cell wall proteins and a survey of the membrane proteome of Phytophthora infestans

Gordonia jacobaea was isolated and characterized in the Department of Microbiology, University of Santiago de Compostela, in 2000. Here we present the draft genome sequence of this species, which will improve our understanding of the diversity and the relation of the cell wall proteins of G. jacobaea with other mycolata.

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Proteomic Analysis ofPhytophthora infestansReveals the Importance of Cell Wall Proteins in Pathogenicity

Molecular & Cellular Proteomics ◽

10.1074/mcp.m116.065656 ◽

2017 ◽

Vol 16 (11) ◽

pp. 1958-1971 ◽

Cited By ~ 10

Author(s):

Svante Resjö ◽

Maja Brus ◽

Ashfaq Ali ◽

Harold J. G. Meijer ◽

Marianne Sandin ◽

...

Keyword(s):

Cell Wall ◽

Proteomic Analysis ◽

Cell Wall Proteins

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A proposed nomenclature for cell wall proteins of Clostridium difficile

Journal of Medical Microbiology ◽

10.1099/jmm.0.028472-0 ◽

2011 ◽

Vol 60 (8) ◽

pp. 1225-1228 ◽

Cited By ~ 38

Author(s):

Robert P. Fagan ◽

Claire Janoir ◽

Anne Collignon ◽

Paola Mastrantonio ◽

Ian R. Poxton ◽

...

Keyword(s):

Cell Wall ◽

Clostridium Difficile ◽

Cell Wall Proteins

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Homologous Recombination in Clostridioides difficile Mediates Diversification of Cell Surface Features and Transport Systems

mSphere ◽

10.1128/msphere.00799-20 ◽

2020 ◽

Vol 5 (6) ◽

Author(s):

Hannah D. Steinberg ◽

Evan S. Snitkin

Keyword(s):

Cell Wall ◽

Homologous Recombination ◽

Sugar Transport ◽

The United States ◽

Strain Typing ◽

Cell Wall Proteins ◽

Genetic Loci ◽

Content Type ◽

Clostridioides Difficile ◽

Host Pathogen

ABSTRACT Illness caused by the pathogen Clostridioides difficile is widespread and can range in severity from mild diarrhea to sepsis and death. Strains of C. difficile isolated from human infections exhibit great genetic diversity, leading to the hypothesis that the genetic background of the infecting strain at least partially determines a patient’s clinical course. However, although certain strains of C. difficile have been suggested to be associated with increased severity, strain typing alone has proved insufficient to explain infection severity. The limited explanatory power of strain typing has been hypothesized to be due to genetic variation within strain types, as well as genetic elements shared between strain types. Homologous recombination is an evolutionary mechanism that can result in large genetic differences between two otherwise clonal isolates, and also lead to convergent genotypes in distantly related strains. More than 400 C. difficile genomes were analyzed here to assess the effect of homologous recombination within and between C. difficile clades. Almost three-quarters of single nucleotide variants in the C. difficile phylogeny are predicted to be due to homologous recombination events. Furthermore, recombination events were enriched in genes previously reported to be important to virulence and host-pathogen interactions, such as flagella, cell wall proteins, and sugar transport and metabolism. Thus, by exploring the landscape of homologous recombination in C. difficile, we identified genetic loci whose elevated rates of recombination mediated diversification, making them strong candidates for being mediators of host-pathogen interaction in diverse strains of C. difficile. IMPORTANCE Infections with C. difficile result in up to half a million illnesses and tens of thousands of deaths annually in the United States. The severity of C. difficile illness is dependent on both host and bacterial factors. Studying the evolutionary history of C. difficile pathogens is important for understanding the variation in pathogenicity of these bacteria. This study examines the extent and targets of homologous recombination, a mechanism by which distant strains of bacteria can share genetic material, in hundreds of C. difficile strains and identifies hot spots of realized recombination events. The results of this analysis reveal the importance of homologous recombination in the diversification of genetic loci in C. difficile that are significant in its pathogenicity and host interactions, such as flagellar construction, cell wall proteins, and sugar transport and metabolism.

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Slipped strand mispairing in the gene encoding sialidase NanH3 in Gardnerella spp

10.1101/2020.09.16.300947 ◽

2020 ◽

Author(s):

Shakya P. Kurukulasuriya ◽

Mo H. Patterson ◽

Janet E. Hill

Keyword(s):

Cell Wall ◽

Biofilm Formation ◽

Gene Sequence ◽

Phase Variation ◽

Cell Wall Proteins ◽

Vaginal Microbiome ◽

Gene Encoding ◽

Reading Frame ◽

Sialidase Activity ◽

Mucosal Surfaces

AbstractCell wall proteins with sialidase activity are involved in carbohydrate assimilation, adhesion to mucosal surfaces, and biofilm formation. Gardnerella spp. inhabit the human vaginal microbiome and encode up to three sialidase enzymes, two of which are suspected to be cell wall associated. Here we demonstrate that the gene encoding extracellular sialidase NanH3 is found almost exclusively in G. piotii and closely related Gardnerella genome sp. 3, and its presence correlates with sialidase positive phenotype in a collection of 112 Gardnerella isolates. The nanH3 gene sequence includes a homopolymeric repeat of cytosines that varies in length within cell populations, indicating that this gene is subject to slipped-strand mispairing, a mechanisms of phase variation in bacteria. Variation in the length of the homopolymer sequence results in encoding of either the full length sialidase protein or truncated peptides lacking the sialidase domain due to introduction of reading-frame shifts and premature stop codons. Phase variation in NanH3 may be involved in immune evasion or modulation of adhesion to host epithelial cells, and formation of biofilms characteristic of the vaginal dysbiosis known as bacterial vaginosis.

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A family of cell wall transglutaminases is essential for appressorium development and pathogenicity in Phytophthora infestans

10.1101/2021.11.23.469665 ◽

2021 ◽

Author(s):

Maja Brus-Szkalej ◽

Christian B. Andersen ◽

Ramesh R. Vetukuri ◽

Laura J. Grenville-Briggs Didymus

Keyword(s):

Cell Wall ◽

Phytophthora Infestans ◽

Sequence Similarity ◽

Turgor Pressure ◽

Intermediate Phenotype ◽

Entire Family ◽

Drug Concentrations ◽

Lower Drug ◽

Chemical Inhibition ◽

Eukaryotic Organisms

Transglutaminases (TGases) are enzymes highly conserved among prokaryotic and eukaryotic organisms, where their role is to catalyse protein cross-linking. One of the putative TGases of Phytophthora infestans has previously been shown to be localised to the cell wall. Based on sequence similarity we were able to identify six more genes annotated as putative TGases and show that these seven genes group together in phylogenetic analysis. All of the seven proteins are predicted to contain transmembrane helices and both a TGase domain and a MANSC domain, the latter of which was previously shown to play a role in protein stability. Chemical inhibition of transglutaminase activity and silencing of the entire family of the putative cell wall TGases are both lethal to P. infestans indicating the importance of these proteins in cell wall formation and stability. The intermediate phenotype obtained with lower drug concentrations and less efficient silencing displays a number of deformations to germ tubes and appressoria. Both chemically treated and silenced lines show lower pathogenicity than the wild type in leaf infection assays. Finally, we show that appressoria of P. infestans possess the ability to build up turgor pressure and that this ability is decreased by chemical inhibition of TGases.

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