scholarly journals How the Necrotrophic Fungus Alternaria brassicicola Kills Plant Cells Remains an Enigma

2015 ◽  
Vol 14 (4) ◽  
pp. 335-344 ◽  
Author(s):  
Yangrae Cho
Keyword(s):  
Cell Wall ◽  
Plant Pathogens ◽  
Host Cells ◽  
Alternaria Brassicicola ◽  
Full Genome Sequencing ◽  
Cell Wall Degrading Enzymes ◽  
Content Type ◽  
Pathogenicity Factors ◽  
Degrading Enzymes ◽  
Host Specific Toxins

ABSTRACTAlternariaspecies are mainly saprophytic fungi, but some are plant pathogens. Seven pathotypes ofAlternaria alternatause secondary metabolites of host-specific toxins as pathogenicity factors. These toxins kill host cells prior to colonization. Genes associated with toxin synthesis reside on conditionally dispensable chromosomes, supporting the notion that pathogenicity might have been acquired several times byA. alternata.Alternaria brassicicola, however, seems to employ a different mechanism. Evidence on the use of host-specific toxins as pathogenicity factors remains tenuous, even after a diligent search aided by full-genome sequencing and efficient reverse-genetics approaches. Similarly, no individual genes encoding lipases or cell wall-degrading enzymes have been identified as strong virulence factors, although these enzymes have been considered important for fungal pathogenesis. This review describes our current understanding of toxins, lipases, and cell wall-degrading enzymes and their roles in the pathogenesis ofA. brassicicolacompared to those of other pathogenic fungi. It also describes a set of genes that affect pathogenesis inA. brassicicola. They are involved in various cellular functions that are likely important in most organisms and probably indirectly associated with pathogenesis. Deletion or disruption of these genes results in weakly virulent strains that appear to be sensitive to the defense mechanisms of host plants. Finally, this review discusses the implications of a recent discovery of three important transcription factors associated with pathogenesis and the putative downstream genes that they regulate.

The Biocontrol Mechanism of Trichoderma asperellum Resistance Plant Pathogenic Fungi

2013 ◽  
Vol 726-731 ◽  
pp. 4525-4528
Author(s):  
Ping Yang ◽  
Qian Xu
Keyword(s):  
Cell Wall ◽  
Plant Pathogens ◽  
Control Plant ◽  
Hydrolytic Enzymes ◽  
Pathogenic Fungi ◽  
Dry Weight ◽  
Plant Pathogenic Fungi ◽  
Cell Wall Degrading Enzymes ◽  
Antifungal Metabolites ◽  
Degrading Enzymes

T. asperellum is an important biocontrol fungus owing to their ability to antagonize plant pathogenic fungi. The biocontrol effects of T. asperellum were played by secreting many kinds of hydrolytic enzymes and antibiotics. T. asperellum producing more cell wall degrading enzymes when meeting plant pathogens. Moreover, the growth of the plant pathogens was inhibited by T. asperellum secondary metabolites. The yield of antibiotic 6-PP was 1.32 mg 6-PP/g mycelial dry weight. T. asperellum control plant pathogens through secreting cell wall degrading enzymes and producing antifungal metabolites.

scholarly journals The snf1 Gene of Ustilago maydis Acts as a Dual Regulator of Cell Wall Degrading Enzymes

2010 ◽  
Vol 100 (12) ◽  
pp. 1364-1372 ◽  
Author(s):  
Marina Nadal ◽  
Maria D. Garcia-Pedrajas ◽  
Scott E. Gold
Keyword(s):  
Cell Wall ◽  
Growth Medium ◽  
Plant Pathogens ◽  
Ustilago Maydis ◽  
Fungal Genome ◽  
Wild Type ◽  
Cell Wall Degrading Enzymes ◽  
Relative Expression ◽  
Degrading Enzymes ◽  
In The Wild

Many fungal plant pathogens are known to produce extracellular enzymes that degrade cell wall elements required for host penetration and infection. Due to gene redundancy, single gene deletions generally do not address the importance of these enzymes in pathogenicity. Cell wall degrading enzymes (CWDEs) in fungi are often subject to carbon catabolite repression at the transcriptional level such that, when glucose is available, CWDE-encoding genes, along with many other genes, are repressed. In Saccharomyces cerevisiae, one of the main players controlling this process is SNF1, which encodes a protein kinase. In this yeast, Snf1p is required to release glucose repression when this sugar is depleted from the growth medium. We have employed a reverse genetic approach to explore the role of the SNF1 ortholog as a potential regulator of CWDE gene expression in Ustilago maydis. We identified U. maydis snf1 and deleted it from the fungal genome. Consistent with our hypothesis, the relative expression of an endoglucanase and a pectinase was higher in the wild type than in the Δsnf1 mutant strain when glucose was depleted from the growth medium. However, when cells were grown in derepressive conditions, the relative expression of two xylanase genes was unexpectedly higher in the Δsnf1 strain than in the wild type, indicating that, in this case, snf1 negatively regulated the expression of these genes. Additionally, we found that, contrary to several other fungal species, U. maydis Snf1 was not required for utilization of alternative carbon sources. Also, unlike in ascomycete plant pathogens, deletion of snf1 did not profoundly affect virulence in U. maydis.

scholarly journals The Trk Potassium Transporter Is Required for RsmB-Mediated Activation of Virulence in the Phytopathogen Pectobacterium wasabiae

2015 ◽  
Vol 198 (2) ◽  
pp. 248-255 ◽  
Author(s):  
Rita S. Valente ◽  
Karina B. Xavier
Keyword(s):  
Cell Wall ◽  
Environmental Factor ◽  
Plant Cell ◽  
Plant Pathogen ◽  
Plant Cell Wall ◽  
Cell Wall Degrading Enzymes ◽  
Content Type ◽  
Regulatory Pathways ◽  
Potassium Transporter ◽  
Degrading Enzymes

ABSTRACTPectobacterium wasabiae(previously known asErwinia carotovora) is an important plant pathogen that regulates the production of plant cell wall-degrading enzymes through anN-acyl homoserine lactone-based quorum sensing system and through the GacS/GacA two-component system (also known as ExpS/ExpA). At high cell density, activation of GacS/GacA induces the expression of RsmB, a noncoding RNA that is essential for the activation of virulence in this bacterium. A genetic screen to identify regulators of RsmB revealed that mutants defective in components of a putative Trk potassium transporter (trkHandtrkA) had decreasedrsmBexpression. Further analysis of these mutants showed that changes in potassium concentration influencedrsmBexpression and consequent tissue damage in potato tubers and that this regulation required an intact Trk system. Regulation ofrsmBexpression by potassium via the Trk system occurred even in the absence of the GacS/GacA system, demonstrating that these systems act independently and are both required for full activation of RsmB and for the downstream induction of virulence in potato infection assays. Overall, our results identified potassium as an essential environmental factor regulating the Rsm system, and the consequent induction of virulence, in the plant pathogenP. wasabiae.IMPORTANCECrop losses from bacterial diseases caused by pectolytic bacteria are a major problem in agriculture. By studying the regulatory pathways involved in controlling the expression of plant cell wall-degrading enzymes inPectobacterium wasabiae, we showed that the Trk potassium transport system plays an important role in the regulation of these pathways. The data presented further identify potassium as an important environmental factor in the regulation of virulence in this plant pathogen. We showed that a reduction in virulence can be achieved by increasing the extracellular concentration of potassium. Therefore, this work highlights how elucidation of the mechanisms involved in regulating virulence can lead to the identification of environmental factors that can influence the outcome of infection.

The Contribution of Cell Wall Degrading Enzymes to Pathogenesis of Fungal Plant Pathogens

2002 ◽  
pp. 341-358 ◽  
Author(s):  
Arjen ten Have ◽  
Klaus B. Tenberge ◽  
Jacques A. E. Benen ◽  
Paul Tudzynski ◽  
Jaap Visser ◽  
...  
Keyword(s):  
Cell Wall ◽  
Plant Pathogens ◽  
Cell Wall Degrading Enzymes ◽  
Degrading Enzymes ◽  
Fungal Plant Pathogens

scholarly journals The role of l-arabinose metabolism for Escherichia coli O157:H7 in edible plants

Microbiology ◽  
2021 ◽  
Vol 167 (7) ◽  
Author(s):  
Louise Crozier ◽  
Jacqueline Marshall ◽  
Ashleigh Holmes ◽  
Kathryn Mary Wright ◽  
Yannick Rossez ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Wall ◽  
Type Species ◽  
Cell Wall Degrading Enzymes ◽  
Cell Wall Polysaccharides ◽  
Content Type ◽  
E Coli ◽  
Degrading Enzymes ◽  
Link Type

Arabinose is a major plant aldopentose in the form of arabinans complexed in cell wall polysaccharides or glycoproteins (AGP), but comparatively rare as a monosaccharide. l-arabinose is an important bacterial metabolite, accessed by pectolytic micro-organisms such as Pectobacterium atrosepticum via pectin and hemicellulose degrading enzymes. However, not all plant-associated microbes encode cell-wall-degrading enzymes, yet can metabolize l-arabinose, raising questions about their use of and access to the glycan in plants. Therefore, we examined l-arabinose metabolism in the food-borne pathogen Escherichia coli O157:H7 (isolate Sakai) during its colonization of plants. l-arabinose metabolism (araBA) and transport (araF) genes were activated at 18 °C in vitro by l-arabinose and expressed over prolonged periods in planta. Although deletion of araBAD did not impact the colonization ability of E. coli O157:H7 (Sakai) on spinach and lettuce plants (both associated with STEC outbreaks), araA was induced on exposure to spinach cell-wall polysaccharides. Furthermore, debranched and arabinan oligosaccharides induced ara metabolism gene expression in vitro, and stimulated modest proliferation, while immobilized pectin did not. Thus, E. coli O157:H7 (Sakai) can utilize pectin/AGP-derived l-arabinose as a metabolite. Furthermore, it differs fundamentally in ara gene organization, transport and regulation from the related pectinolytic species P. atrosepticum , reflective of distinct plant-associated lifestyles.

scholarly journals The Aspergillus fumigatuscspA Gene Encoding a Repeat-Rich Cell Wall Protein Is Important for Normal Conidial Cell Wall Architecture and Interaction with Host Cells

2010 ◽  
Vol 9 (9) ◽  
pp. 1403-1415 ◽  
Author(s):  
Emma Levdansky ◽  
Oren Kashi ◽  
Haim Sharon ◽  
Yana Shadkchan ◽  
Nir Osherov
Keyword(s):  
Cell Wall ◽  
Pathogenic Fungus ◽  
Protein A ◽  
Surface Protein ◽  
Hyphal Growth ◽  
Cell Wall Protein ◽  
Conidial Germination ◽  
Host Cells ◽  
Cell Wall Degrading Enzymes ◽  
Content Type

ABSTRACT cspA (for cell surface protein A) encodes a repeat-rich glycophosphatidylinositol (GPI)-anchored cell wall protein (CWP) in the pathogenic fungus Aspergillus fumigatus. The number of repeats in cspA varies among isolates, and this trait is used for typing closely related strains of A. fumigatus. We have previously shown that deletion of cspA is associated with rapid conidial germination and reduced adhesion of dormant conidia. Here we show that cspA can be extracted with hydrofluoric acid (HF) from the cell wall, suggesting that it is a GPI-anchored CWP. The cspA-encoded CWP is unmasked during conidial germination and is surface expressed during hyphal growth. Deletion of cspA results in weakening of the conidial cell wall, whereas its overexpression increases conidial resistance to cell wall-degrading enzymes and inhibits conidial germination. Double mutant analysis indicates that cspA functionally interacts with the cell wall protein-encoding genes ECM33 and GEL2. Deletion of cspA together with ECM33 or GEL2 results in strongly reduced conidial adhesion, increased disorganization of the conidial cell wall, and exposure of the underlying layers of chitin and β-glucan. This is correlated with increasing susceptibility of the ΔcspA, ΔECM33, and ΔcspA ΔECM33 mutants to conidial phagocytosis and killing by human macrophages and hyphal damage induced by neutrophils. However, these strains did not exhibit altered virulence in mice with infected lungs. Collectively, these results suggest a role for cspA in maintaining the strength and integrity of the cell wall.

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