scholarly journals Dynamic cell wall modifications in brassicas during clubroot disease

2020 ◽  
Author(s):  
Julia Badstöber ◽  
Stefan Ciaghi ◽  
Sigrid Neuhauser
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Plasmodiophora Brassicae ◽  
Characteristic Root ◽  
Biotic Interactions ◽  
Microbial Pathogens ◽  
Cell Wall Degrading Enzymes ◽  
Cell Wall Modification ◽  
Clubroot Disease ◽  
Host Cell Wall

AbstractBiotic interactions of plants and microbial pathogens can cause drastic changes in cell wall composition in response to developmental reprogramming caused as consequence of an infection. Clubroot disease, caused by the biotrophic plant pathogen Plasmodiophora brassicae (Phytomyxea, Rhizaria), is the economically most important disease of Brassica crops worldwide. The disease is best known by the characteristic hypertrophied roots (root galls, clubroots). Amongst a series of physiological changes of the host tissue, the formation of the characteristic root galls leads to cell wall modification and reorganization. Cell wall chemistry and the hosts genetic repertoire are discussed to play a role in the resilience of plants against clubroot disease. Plant cells infected with P. brassicae are markedly enlarged, and look very differently from uninfected, healthy cells. Here we systematically review cell wall related processes that lead to the typical clubroot phenotype and provide novel insights how P. brassicae uses these modifications to benefit its own development. An infection with P. brassicae impacts on nearly all cell wall related processes, but all alterations are meaningful for successful growth and development of P. brassicae. Processes related to cell wall stability and rigidity (e.g. cellulose, pectin or lignin synthesis) are down-regulated, while cell wall degrading enzymes or processes that increase the flexibility of the host cell wall (e.g. expansin) are up-regulated. The here presented findings indicate that P. brassicae weakens the structural stability of its host cell while it increases its elasticity, which in consequence allows P. brassicae to grow bigger and ultimately to develop more resting spores. Consequently, the understanding of the modification of the host cell wall is important for the formation of the characteristic root galls but also to better understand clubroot disease.

scholarly journals Comparative Transcriptomic Analysis of Race 1 and Race 4 of Fusarium oxysporum f. sp. cubense Induced with Different Carbon Sources

2017 ◽  
Vol 7 (7) ◽  
pp. 2125-2138 ◽  
Author(s):  
Shiwen Qin ◽  
Chunyan Ji ◽  
Yunfeng Li ◽  
Zhenzhong Wang
Keyword(s):  
Gene Expression ◽  
Cell Wall ◽  
Fusarium Oxysporum ◽  
Host Cell ◽  
Expression Profiles ◽  
Cell Wall Polysaccharide ◽  
Host Cell Wall ◽  
Race 1 ◽  
Race 4 ◽  
Banana Cultivar

Abstract The fungal pathogen Fusarium oxysporum f. sp. cubense causes Fusarium wilt, one of the most destructive diseases in banana and plantain cultivars. Pathogenic race 1 attacks the “Gros Michel” banana cultivar, and race 4 is pathogenic to the Cavendish banana cultivar and those cultivars that are susceptible to Foc1. To understand the divergence in gene expression modules between the two races during degradation of the host cell wall, we performed RNA sequencing to compare the genome-wide transcriptional profiles of the two races grown in media containing banana cell wall, pectin, or glucose as the sole carbon source. Overall, the gene expression profiles of Foc1 and Foc4 in response to host cell wall or pectin appeared remarkably different. When grown with host cell wall, a much larger number of genes showed altered levels of expression in Foc4 in comparison with Foc1, including genes encoding carbohydrate-active enzymes (CAZymes) and other virulence-related genes. Additionally, the levels of gene expression were higher in Foc4 than in Foc1 when grown with host cell wall or pectin. Furthermore, a great majority of genes were differentially expressed in a variety-specific manner when induced by host cell wall or pectin. More specific CAZymes and other pathogenesis-related genes were expressed in Foc4 than in Foc1 when grown with host cell wall. The first transcriptome profiles obtained for Foc during degradation of the host cell wall may provide new insights into the mechanism of banana cell wall polysaccharide decomposition and the genetic basis of Foc host specificity.

scholarly journals Extracellular Polysaccharides from Xanthomonas axonopodis pv. manihotis Interact with Cassava Cell Walls During Pathogenesis

1997 ◽  
Vol 10 (7) ◽  
pp. 803-811 ◽  
Author(s):  
B. Boher ◽  
M. Nicole ◽  
M. Potin ◽  
J. P. Geiger
Keyword(s):  
Cell Wall ◽  
Monoclonal Antibodies ◽  
Host Cell ◽  
Cell Walls ◽  
Plant Cell Wall ◽  
Infection Process ◽  
Extracellular Polysaccharides ◽  
Xanthomonas Axonopodis ◽  
Cassava Leaves ◽  
Host Cell Wall

The location of lipopolysaccharides produced by Xanthomonas axonopodis pv. manihotis during pathogenesis on cassava (Manihot esculenta) was determined by fluorescence and electron microscopy immunolabeling with monoclonal antibodies. During the early stages of infection, pathogen lipopolysaccharides were detected on the outer surface of the bacterial envelope and in areas of the plant middle lamellae in the vicinity of the pathogen. Later in the infection process, lipopolysaccharide-specific antibodies bound to areas where the plant cell wall was heavily degraded. Lipopolysaccharides were not detected in the fibrillar matrix filling intercellular spaces of infected cassava leaves. Monoclonal antibodies specific for the exopolysaccharide xanthan side chain labeled the bacteria, the fibrillar matrix, and portions of the host cell wall. The association of Xanthomonas lipopolysaccharides with host cell walls during plant infection is consistent with a role of these bacterial extracellular polysaccharides in the infection process.

Ultrastructure of compatible and incompatible reactions of sunflower to Plasmopara halstedii

1979 ◽  
Vol 57 (4) ◽  
pp. 315-323 ◽  
Author(s):  
Glenn Wehtje ◽  
Larry J. Littlefield ◽  
David E. Zimmer
Keyword(s):  
Cell Wall ◽  
Plasma Membrane ◽  
Host Cell ◽  
Epidermal Cell ◽  
Cortical Cell ◽  
Hypersensitive Reaction ◽  
Host Cells ◽  
Plasmopara Halstedii ◽  
Host Cell Wall ◽  
Host Plasma Membrane

Penetration of sunflower, Heliantluis animus, root epidermal cells by zoospores of Plasmopara halstedii is preceded by formation of a papilla on the inner surface of the host cell wall that invaginates the host plasma membrane. Localized degradation and penetration of the host cell wall by the pathogen follow. The invading fungus forms an allantoid primary infection vesicle in the penetrated epidermal cell. The host plasma membrane invaginates around the infection vesicle but its continuity is difficult to follow. Upon exit from the epidermal cell the fungus may grow intercellularly, producing terminal haustorial branches which extend into adjacent host cells. The fungus may grow through one or two cortical cell is after growing from the epidermal cell before it becomes intercellular. Host plasma membrane is not penetrated by haustoria. Intercellular hyphae grow toward the apex of the plant and ramify the seedling tissue. Resistance in an immune cultivar is hypersensitive and is triggered upon contact of the host cell with the encysting zoospore before the host cell wall is penetrated. Degeneration of zoospore cytoplasm accompanies the hypersensitive reaction of the host. Zoospores were often parasitized by bacteria and did not germinate unless penicillin and streptomycin were added to the inoculum suspension.

Histopathology of Fusarium wilt of staghorn sumac (Rhus typhina) caused by Fusarium oxysporum f. sp. callistephi race 3. III. Host cell and tissue reactions

2006 ◽  
Vol 87 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Guillemond B. Ouellette ◽  
Mohamed Cherif ◽  
Marie Simard
Keyword(s):  
Cell Wall ◽  
Fusarium Oxysporum ◽  
Host Cell ◽  
Cross Wall ◽  
Tissue Proliferation ◽  
Host Cytoplasm ◽  
Transmission Electron ◽  
Host Cell Wall ◽  
Tissue Reactions ◽  
Rhus Typhina

Abstract Various cell reactions occurred in staghorn sumac plants inoculated with Fusarium oxysporum f. sp. callistephi. Light and transmission electron microscopy observations and results of cytochemical tests showed: 1) increased laticifers and latex production in the phloem; 2) tylosis formation; 3) host cell wall modifications, including appositions or other cell wall thickenings; and 4) unusual cross wall formation in some cells, and cell hypertrophy and hyperplasia. Tylosis walls labelled for pectin and cellulose and many displayed inner suberin-like layers. These layers were also noted in cells of the medullary sheath and in many cells with dense content and thickened walls in the barrier zones that had formed. These zones also contained fibres with newly-formed gelatinous-like layers. In the vicinity of these cells, host cell walls were frequently altered, associated with opaque matter. Many small particles present in chains also occurred in some of these cells, which contained only remnants of host cytoplasm. Light microscopy observations showed that pronounced tissue proliferation and aberrant cells occurred in the outer xylem in the infected plants. Unusual neoplasmic tissue also formed from cells surrounding the pith and medullary sheath, and it spanned directly across the pre-existing xylem tissue and burst as large mounds on the stems.

scholarly journals Plasmodiophora brassicae-Triggered Cell Enlargement and Loss of Cellular Integrity in Root Systems Are Mediated by Pectin Demethylation

2021 ◽  
Vol 12 ◽  
Author(s):  
Karolina Stefanowicz ◽  
Monika Szymanska-Chargot ◽  
William Truman ◽  
Piotr Walerowski ◽  
Marcin Olszak ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Wall ◽  
Life Cycle ◽  
Plasmodiophora Brassicae ◽  
Growth Patterns ◽  
Cellular Reprogramming ◽  
Cellular Growth ◽  
Gall Formation ◽  
Clubroot Disease ◽  
Cellular Environment

Gall formation on the belowground parts of plants infected with Plasmodiophora brassicae is the result of extensive host cellular reprogramming. The development of these structures is a consequence of increased cell proliferation followed by massive enlargement of cells colonized with the pathogen. Drastic changes in cellular growth patterns create local deformities in the roots and hypocotyl giving rise to mechanical tensions within the tissue of these organs. Host cell wall extensibility and recomposition accompany the growth of the gall and influence pathogen spread and also pathogen life cycle progression. Demethylation of pectin within the extracellular matrix may play an important role in P. brassicae-driven hypertrophy of host underground organs. Through proteomic analysis of the cell wall, we identified proteins accumulating in the galls developing on the underground parts of Arabidopsis thaliana plants infected with P. brassicae. One of the key proteins identified was the pectin methylesterase (PME18); we further characterized its expression and conducted functional and anatomic studies in the knockout mutant and used Raman spectroscopy to study the status of pectin in P. brassicae-infected galls. We found that late stages of gall formation are accompanied with increased levels of PME18. We have also shown that the massive enlargement of cells colonized with P. brassicae coincides with decreases in pectin methylation. In pme18-2 knockout mutants, P. brassicae could still induce demethylation; however, the galls in this line were smaller and cellular expansion was less pronounced. Alteration in pectin demethylation in the host resulted in changes in pathogen distribution and slowed down disease progression. To conclude, P. brassicae-driven host organ hypertrophy observed during clubroot disease is accompanied by pectin demethylation in the extracellular matrix. The pathogen hijacks endogenous host mechanisms involved in cell wall loosening to create an optimal cellular environment for completion of its life cycle and eventual release of resting spores facilitated by degradation of demethylated pectin polymers.

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