scholarly journals Marchantia polymorpha model reveals conserved infection mechanisms in the vascular wilt fungal pathogen Fusarium oxysporum

2021 ◽  
Author(s):  
Amey Redkar ◽  
Selena Gimenez Ibanez ◽  
Mugdha Sabale ◽  
Bernd Zechmann ◽  
Roberto Solano ◽  
...  
2021 ◽  
Author(s):  
Amey Redkar ◽  
Selena Gimenez Ibanez ◽  
Mugdha Sabale ◽  
Bernd Zechmann ◽  
Roberto Solano ◽  
...  

The non-vascular plant Marchantia polymorpha has emerged as a valuable model for studying evolutionarily conserved microbial infection strategies and plant immune responses. However, only a handful of fungal pathogens of Marchantia have been described so far. Here we establish a new pathosystem using the root-infecting vascular wilt fungus Fusarium oxysporum. On angiosperms, this fungus exhibits exquisite adaptation to the plant vascular niche and host-specific pathogenicity, both of which are conferred by lineage-specific effectors secreted during growth in the xylem. We show that F. oxysporum isolates with different lifestyles - pathogenic or endophytic - are able to infect this non-vascular liverwort causing tissue maceration and plant cell killing. Similar to bacterial pathogens, F. oxysporum induces a PAMP-triggered immune response in M. polymorpha. Analysis of isogenic fungal mutants established that infection of Marchantia requires conserved fungal pathogenicity mechanisms such as mitogen activated protein kinases, transcriptional regulators and cell wall remodeling enzymes. Remarkably, lineage-specific virulence effectors are dispensable for infection, most likely due to the absence of xylem tissue in this non-vascular plant. The F. oxysporum - M. polymorpha system provides new insights into the mechanism and evolution of pathogenic and endophytic fungus-plant interactions.


1999 ◽  
Vol 79 (3) ◽  
pp. 351-356 ◽  
Author(s):  
B. C. Venuto ◽  
R. R. Smith ◽  
C. R. Grau

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


PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e95543 ◽  
Author(s):  
Lijia Guo ◽  
Lijuan Han ◽  
Laying Yang ◽  
Huicai Zeng ◽  
Dingding Fan ◽  
...  

2018 ◽  
Vol 64 (5) ◽  
pp. 349-357 ◽  
Author(s):  
Xingrong Hou ◽  
Bang An ◽  
Qiannan Wang ◽  
Yunfeng Guo ◽  
Hongli Luo ◽  
...  

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.


PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0250064
Author(s):  
Hui Zhou ◽  
Yueqiang Xu ◽  
Frank Ebel ◽  
Cheng Jin

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.


Author(s):  
Paula Andrea Castillo-Sanmiguel ◽  
Laura Rocío Cortés-Sánchez ◽  
Jovanna Acero-Godoy

<p>Tomato plants (<em>Solanum lycopersicum</em>) are susceptible to the infection by diverse pathogens that cause devastating diseases such as vascular wilt, which causes great losses at the production level. The fungus <em>Fusarium oxysporum</em> f. sp. <em>lycopersici</em> (<em>Fol</em>) is one of the etiologic agents of this disease and its control lies in the use of synthetic chemicals which generate a negative impact in both health and the environment; thus, it is necessary to implement biological control as a healthier and more efficient alternative. The fungus <em>Trichoderma</em> spp. is a favorable option to be employed as a biocontroller against this pathogen thanks to its antagonist mechanisms, determined by metabolic and genetic characteristics. On the one hand, for <em>Fol</em> it is indispensable the activation of signaling routes such as MAPK Fmk1, MAPK Mpk1 y HOG, while <em>Trichoderma</em> spp. uses effectors involved in the interaction with the plant such as proteins, enzymes and secondary metabolites that also strengthen its immune response against infection, determined by both Pathogen Associated Molecular Patterns (PAMP) and effectors. Therefore, this article makes a review about the mentioned characteristics and suggests a greater application of tools and molecular markers for the management of this disease.</p>


Author(s):  
D. Brayford

Abstract A description is provided for Fusarium oxysporum f. sp. elaeidis. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Elaeis guineensis (Oil palm). May also infect E. oleifera, E. madagascariensis and E. melanococca. DISEASE: Vascular wilt. GEOGRAPHICAL DISTRIBUTION: West and central Africa: Cameroon, Congo, Ivory Coast, Nigeria, Zaire. Possibly Colombia. TRANSMISSION: Contaminated soil or plant material. Potentially by means of seed (52, 4182).


Author(s):  
D. Brayford

Abstract A description is provided for Fusarium oxysporum f. sp. melonis. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Cucumis melo (Muskmelon, Cantaloupe). DISEASE: Vascular wilt. GEOGRAPHICAL DISTRIBUTION: IMI Distribution Map 496. Africa: Morocco, Zimbabwe. Asia: India, Iraq, Iran, Israel, Japan, Korea, Lebanon, Philippines, Saudi Arabia, Thailand, USSR. Australasia: Australia. Europe: Belgium, France, Germany, Great Britain, Greece, Netherlands, Turkey. America: Canada, USA. TRANSMISSION: The fungus is soil borne and may be tramsmitted by seed.


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