Galactofuranose (Galf)-containing sugar chain contributes to the hyphal growth, conidiation and virulence of F. oxysporum f.sp. cucumerinum

The ascomycete fungus Fusarium oxysporum f.sp. cucumerinum causes vascular wilt diseases in cucumber. However, few genes related to morphogenesis and pathogenicity of this fungal pathogen have been functionally characterized. BLASTp searches of the Aspergillus fumigatus UgmA and galatofuranosyltransferases (Galf-transferases) sequences in the F. oxysporum genome identified two genes encoding putative UDP-galactopyranose mutase (UGM), ugmA and ugmB, and six genes encoding putative Galf-transferase homologs. In this study, the single and double mutants of the ugmA, ugmB and gfsB were obtained. The roles of UGMs and GfsB were investigated by analyzing the phenotypes of the mutants. Our results showed that deletion of the ugmA gene led to a reduced production of galactofuranose-containing sugar chains, reduced growth and impaired conidiation of F. oxysporum f.sp. cucumerinum. Most importantly, the ugmA deletion mutant lost the pathogenicity in cucumber plantlets. Although deletion of the ugmB gene did not cause any visible phenotype, deletion of both ugmA and ugmB genes caused more severe phenotypes as compared with the ΔugmA, suggesting that UgmA and UgmB are redundant and they can both contribute to synthesis of UDP-Galf. Furthermore, the ΔgfsB exhibited an attenuated virulence although no other phenotype was observed. Our results demonstrate that the galactofuranose (Galf) synthesis contributes to the cell wall integrity, germination, hyphal growth, conidiation and virulence in Fusarium oxysporum f.sp. cucumerinum and an ideal target for the development of new anti-Fusarium agents.

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SGE1 is involved in conidiation and pathogenicity of Fusarium oxysporum f.sp. cubense

Canadian Journal of Microbiology ◽

10.1139/cjm-2017-0638 ◽

2018 ◽

Vol 64 (5) ◽

pp. 349-357 ◽

Cited By ~ 4

Author(s):

Xingrong Hou ◽

Bang An ◽

Qiannan Wang ◽

Yunfeng Guo ◽

Hongli Luo ◽

...

Keyword(s):

Fusarium Oxysporum ◽

Vegetative Growth ◽

Fungal Pathogen ◽

Deletion Mutant ◽

Vascular Wilt ◽

Proteomics Analysis ◽

Musa Spp ◽

Race 4

The ascomycete fungus Fusarium oxysporum f.sp. cubense race 4 (Foc TR4) causes vascular wilt diseases in banana (Musa spp.). In the present study, the role of SGE1 in regulating growth, conidiation, and pathogenicity of Foc TR4 was investigated. Deletion of SGE1 did not influence vegetative growth but impaired the conidiation of Foc TR4. Besides, the SGE1 deletion mutant basically lost pathogenicity on banana plantlets. Observation under the microscope indicated that the penetration and colonization processes were severely impaired in the SGE1 deletion mutant. Proteomics analysis suggested that SGE1 regulated the production of a series of proteins of Foc TR4. Taken together, our results suggest that SGE1 plays an important role in regulating conidiation and pathogenicity in fungal pathogen Foc TR4.

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The Transcription Factor Con7-1 Is a Master Regulator of Morphogenesis and Virulence in Fusarium oxysporum

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-07-14-0205-r ◽

2015 ◽

Vol 28 (1) ◽

pp. 55-68 ◽

Cited By ~ 16

Author(s):

Carmen Ruiz-Roldán ◽

Yolanda Pareja-Jaime ◽

José Antonio González-Reyes ◽

M. Isabel G. Roncero

Keyword(s):

Cell Wall ◽

Fusarium Oxysporum ◽

Gene Expression Analysis ◽

Wall Structure ◽

Targeted Deletion ◽

Signal Perception ◽

Cell Wall Biogenesis ◽

Primary And Secondary Metabolism ◽

Genes Encoding

Previous studies have demonstrated the essential role of morphogenetic regulation in Fusarium oxysporum pathogenesis, including processes such as cell-wall biogenesis, cell division, and differentiation of infection-like structures. We identified three F. oxysporum genes encoding predicted transcription factors showing significant identities to Magnaporthe oryzae Con7p, Con7-1, plus two identical copies of Con7-2. Targeted deletion of con7-1 produced nonpathogenic mutants with altered morphogenesis, including defects in cell wall structure, polar growth, hyphal branching, and conidiation. By contrast, simultaneous inactivation of both con7-2 copies caused no detectable defects in the resulting mutants. Comparative microarray-based gene expression analysis indicated that Con7-1 modulates the expression of a large number of genes involved in different biological functions, including host–pathogen interactions, morphogenesis and development, signal perception and transduction, transcriptional regulation, and primary and secondary metabolism. Taken together, our results point to Con7-1 as general regulator of morphogenesis and virulence in F. oxysporum.

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Selection for resistance to Fusarium wilt in red clover

Canadian Journal of Plant Science ◽

10.4141/p98-005 ◽

1999 ◽

Vol 79 (3) ◽

pp. 351-356 ◽

Cited By ~ 2

Author(s):

B. C. Venuto ◽

R. R. Smith ◽

C. R. Grau

Keyword(s):

Fusarium Oxysporum ◽

Fungal Pathogen ◽

Trifolium Pratense ◽

Red Clover ◽

Severity Index ◽

Research Station ◽

Vascular Wilt ◽

Trifolium Pratense L ◽

Selection For ◽

Overall Resistance

In Wisconsin, Fusarium oxysporum, Schlect., a pathogen causing vascular wilt, is the most prevalent fungal pathogen recovered from diseased red clover (Trifolium pratense L.) plants. This study was conducted to determine the mode of inheritance for red clover resistance to this pathogen and to develop resistant germplasm. Virulent isolates of this pathogen, collected from red clover plants at the Ashland Research Station, Ashland, Wisconsin, were used to screen three populations, the red clover cultivars Arlington and Marathon and the C11 germplasm, for resistant plants. Plants were inoculated with the pathogen and evaluated for reaction, using a disease-severity index (DSI) score from 1 to 5 (1 = no reaction, 5 = plant dead). Selected plants from each cycle were intercrossed to produce subsequent generations. After two and three cycles of selection, the developed populations were simultaneously evaluated for gain from selection. The gain from selection for resistance in these populations (cycle 0 minus cycle 2) ranged from 0.31 to 0.48, 0.12 to 0.75, and 0.13 to 0.83 DSI units, respectively, for Arlington, Marathon, and C11. Estimated narrow-sense heritabilities, based on cycle-1 and cycle-2 progeny, were, respectively, 0.20 and 0.37 for Arlington, 0.15 and 0.13 for Marathon, and 0.06 and 0.17 for C11. These results indicate that resistance is a quantitative trait controlled by many loci, each contributing some portion to overall resistance in the host. Key words: Red clover, Trifolium pratense L., Fusarium oxysporum, vascular wilt, resistance

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Role of Transcription Factor CaNdt80p in Cell Separation, Hyphal Growth, and Virulence in Candida albicans

Eukaryotic Cell ◽

10.1128/ec.00325-09 ◽

2010 ◽

Vol 9 (4) ◽

pp. 634-644 ◽

Cited By ~ 47

Author(s):

Adnane Sellam ◽

Christopher Askew ◽

Elias Epp ◽

Faiza Tebbji ◽

Alaka Mullick ◽

...

Keyword(s):

Cell Wall ◽

Transcription Factor ◽

Candida Albicans ◽

Cell Separation ◽

Hyphal Growth ◽

Functional Domain ◽

Transcription Factor Family ◽

Content Type ◽

Genes Encoding

ABSTRACT The NDT80/PhoG transcription factor family includes ScNdt80p, a key modulator of the progression of meiotic division in Saccharomyces cerevisiae. In Candida albicans, a member of this family, CaNdt80p, modulates azole sensitivity by controlling the expression of ergosterol biosynthesis genes. We previously demonstrated that CaNdt80p promoter targets, in addition to ERG genes, were significantly enriched in genes related to hyphal growth. Here, we report that CaNdt80p is indeed required for hyphal growth in response to different filament-inducing cues and for the proper expression of genes characterizing the filamentous transcriptional program. These include noteworthy genes encoding cell wall components, such as HWP1, ECE1, RBT4, and ALS3. We also show that CaNdt80p is essential for the completion of cell separation through the direct transcriptional regulation of genes encoding the chitinase Cht3p and the cell wall glucosidase Sun41p. Consistent with their hyphal defect, ndt80 mutants are avirulent in a mouse model of systemic candidiasis. Interestingly, based on functional-domain organization, CaNdt80p seems to be a unique regulator characterizing fungi from the CTG clade within the subphylum Saccharomycotina. Therefore, this study revealed a new role of the novel member of the fungal NDT80 transcription factor family as a regulator of cell separation, hyphal growth, and virulence.

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Differential Effects of Inhibiting Chitin and 1,3-β-d-Glucan Synthesis in Ras and Calcineurin Mutants of Aspergillus fumigatus

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01154-08 ◽

2008 ◽

Vol 53 (2) ◽

pp. 476-482 ◽

Cited By ~ 92

Author(s):

Jarrod R. Fortwendel ◽

Praveen Rao Juvvadi ◽

Nadthanan Pinchai ◽

B. Zachary Perfect ◽

J. Andrew Alspaugh ◽

...

Keyword(s):

Cell Wall ◽

Aspergillus Fumigatus ◽

Hyphal Growth ◽

Invasive Disease ◽

Growth Defect ◽

Compensatory Response ◽

Ras Protein ◽

Genes Encoding ◽

Glucan Synthesis ◽

Calcineurin Pathway

ABSTRACT Aspergillus fumigatus must be able to properly form hyphae and maintain cell wall integrity in order to establish invasive disease. Ras proteins and calcineurin each have been implicated as having roles in these processes. Here, we further delineate the roles of calcineurin and Ras activity in cell wall biosynthesis and hyphal morphology using genetic and pharmacologic tools. Strains deleted for three genes encoding proteins of these pathways, rasA (the Ras protein), cnaA (calcineurin), or crzA (the zinc finger transcription factor downstream of calcineurin), all displayed decreased cell wall 1,3-β-d-glucan content. Echinocandin treatment further decreased the levels of 1,3-β-d-glucan for all strains tested yet also partially corrected the hyphal growth defect of the ΔrasA strain. The inhibition of glucan synthesis caused an increase in chitin content for wild-type, dominant-active rasA, and ΔrasA strains. However, this important compensatory response was diminished in the calcineurin pathway mutants (ΔcnaA and ΔcrzA). Taken together, our data suggest that the Ras and calcineurin pathways act in parallel to regulate cell wall formation and hyphal growth. Additionally, the calcineurin pathway elements cnaA and crzA play a major role in proper chitin and glucan incorporation into the A. fumigatus cell wall.

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Cell wall-degrading enzymes of vascular wilt fungi. II. Properties and modes of action of polysaccharidases of Verticillium albo-atrum and Fusarium oxysporum f. sp. lycopersici

Physiological Plant Pathology ◽

10.1016/0048-4059(78)90079-6 ◽

1978 ◽

Vol 13 (1) ◽

pp. 101-134 ◽

Cited By ~ 60

Author(s):

R.M. Cooper ◽

B. Rankin ◽

R.K.S. Wood

Keyword(s):

Cell Wall ◽

Fusarium Oxysporum ◽

Vascular Wilt ◽

Cell Wall Degrading Enzymes ◽

Modes Of Action ◽

Degrading Enzymes ◽

Verticillium Albo Atrum

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Impaired Colonization and Infection of Tomato Roots by the Δfrp1 Mutant of Fusarium oxysporum Correlates with Reduced CWDE Gene Expression

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-22-5-0507 ◽

2009 ◽

Vol 22 (5) ◽

pp. 507-518 ◽

Cited By ~ 26

Author(s):

Wilfried Jonkers ◽

Christopher D. Andrade Rodrigues ◽

Martijn Rep

Keyword(s):

Gene Expression ◽

Amino Acids ◽

Cell Wall ◽

Fusarium Oxysporum ◽

Root Colonization ◽

Isocitrate Lyase ◽

Vascular Wilt ◽

Metabolic Defects ◽

Tomato Roots ◽

F Box Protein

The vascular wilt pathogen Fusarium oxysporum f. sp. lycopersici efficiently invades roots and colonizes vascular tissues of its host tomato. For these processes, the F-box protein Frp1 is required. The Fusarium oxysporum Δfrp1 mutant was characterized in detail to uncover the cause of its colonization defect. Using growth assays, we could attribute poor root colonization to reduced assimilation of organic acids, amino acids (except proline), or polysaccharides, singly or in combination. External root colonization by the Δfrp1 mutant is restored by the addition of 0.1% glucose or proline but infection still does not occur. This is due to the inability of the Δfrp1 mutant to penetrate the roots, as demonstrated by the lack of expression of SIX1 in the Δfrp1 strain, which is a gene exclusively expressed inside roots, and loss of cell wall–degrading enzyme (CWDE) gene expression. Many of the metabolic defects of the Δfrp1 strain can be attributed to reduced expression of the ICL1 (isocitrate lyase) gene. Strikingly, an Δicl1 mutant is still fully pathogenic and capable of external root colonization. We conclude that the inability of the Δfrp1 strain to colonize and invade roots is not primarily due to metabolic defects but can be attributed to reduced expression of several CWDE genes.

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Correction: Genome and Transcriptome Analysis of the Fungal Pathogen Fusarium oxysporum f. sp. cubense Causing Banana Vascular Wilt Disease

PLoS ONE ◽

10.1371/journal.pone.0117621 ◽

2015 ◽

Vol 10 (1) ◽

pp. e0117621 ◽

Cited By ~ 3

Author(s):

Keyword(s):

Fusarium Oxysporum ◽

Transcriptome Analysis ◽

Fungal Pathogen ◽

Wilt Disease ◽

Vascular Wilt ◽

Vascular Wilt Disease

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Production of Pyomelanin, a Second Type of Melanin, via the Tyrosine Degradation Pathway in Aspergillus fumigatus

Applied and Environmental Microbiology ◽

10.1128/aem.02077-08 ◽

2008 ◽

Vol 75 (2) ◽

pp. 493-503 ◽

Cited By ~ 116

Author(s):

Jeannette Schmaler-Ripcke ◽

Venelina Sugareva ◽

Peter Gebhardt ◽

Robert Winkler ◽

Olaf Kniemeyer ◽

...

Keyword(s):

Aspergillus Fumigatus ◽

Fungal Pathogen ◽

Deletion Mutant ◽

Proteome Analysis ◽

Degradation Pathway ◽

Homogentisic Acid ◽

Oxygen Intermediates ◽

Pigment Formation ◽

Genes Encoding ◽

Increased Sensitivity

ABSTRACT Aspergillus fumigatus is the most important airborne fungal pathogen of immunosuppressed humans. A. fumigatus is able to produce dihydroxynaphthalene melanin, which is predominantly present in the conidia. Its biosynthesis is an important virulence determinant. Here, we show that A. fumigatus is able to produce an alternative melanin, i.e., pyomelanin, by a different pathway, starting from l-tyrosine. Proteome analysis indicated that the l-tyrosine degradation enzymes are synthesized when the fungus is grown with l-tyrosine in the medium. To investigate the pathway in detail, we deleted the genes encoding essential enzymes for pigment production, homogentisate dioxygenase (hmgA) and 4-hydroxyphenylpyruvate dioxygenase (hppD). Comparative Fourier transform infrared spectroscopy of synthetic pyomelanin and pigment extracted from A. fumigatus cultures confirmed the identity of the observed pigment as pyomelanin. In the hmgA deletion strain, HmgA activity was abolished and the accumulation of homogentisic acid provoked an increased pigment formation. In contrast, homogentisic acid and pyomelanin were not observed with an hppD deletion mutant. Germlings of the hppD deletion mutant showed an increased sensitivity to reactive oxygen intermediates. The transcription of both studied genes was induced by l-tyrosine. These results confirmed the function of the deleted genes and the predicted pathway in A. fumigatus. Homogentisic acid is the major intermediate, and the l-tyrosine degradation pathway leading to pyomelanin is similar to that in humans leading to alkaptomelanin.

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