scholarly journals Host–Pathogen Interaction in Fusarium oxysporum Infections: Where Do We Stand?

2018 ◽  
Vol 31 (9) ◽  
pp. 889-898 ◽  
Author(s):  
Amjad M. Husaini ◽  
Aafreen Sakina ◽  
Souliha R. Cambay

Fusarium oxysporum, a ubiquitous soilborne pathogen, causes devastating vascular wilt in more than 100 plant species and ranks 5th among the top 10 fungal plant pathogens. It has emerged as a human pathogen, too, causing infections in immune-compromised patients. Therefore, it is important to gain insight into the molecular processes involved in the pathogenesis of this transkingdom pathogen. A complex network comprising interconnected and overlapping signal pathways—mitogen-activated protein kinase signaling pathways, Ras proteins, G-protein signaling components and their downstream pathways, components of the velvet (LaeA/VeA/VelB) complex, and cAMP pathways—is involved in perceiving the host. This network regulates the expression of various pathogenicity genes. However, plants have evolved an elaborate protection system to combat this attack. They, too, possess intricate mechanisms at the molecular level which, once triggered by pathogen attack, transduce signals to activate defense response. This review focuses on understanding and presenting a wholistic picture of the molecular mechanisms of F. oxysporum–host interactions in plant immunity.

2020 ◽  
Vol 33 (7) ◽  
pp. 902-910
Author(s):  
Zhan-Bin Sun ◽  
Qi Wang ◽  
Man-Hong Sun ◽  
Shi-Dong Li

Clonostachys chloroleuca is a mycoparasite used for biocontrol of numerous fungal plant pathogens. Sequencing of the transcriptome of C. chloroleuca following mycoparasitization of the sclerotia of Sclerotinia sclerotiorum revealed significant upregulation of a mitogen-activated protein kinase (MAPK)-encoding gene, crmapk. Although MAPKs are known to regulate fungal growth and development, the function of crmapk in C. chloroleuca mycoparasitism is unclear. In this study, we investigated the role of crmapk in C. chloroleuca mycoparasitism through gene knockout and complementation. Deletion of crmapk had no influence on the C. chloroleuca morphological characteristics but could significantly reduce the mycoparasitic ability to sclerotia and biocontrol capacity to soybean Sclerotinia stem rot; crmapk complementation restored these abilities. Transcriptome analysis between Δcrmapk and the wild-type strain revealed numerous genes were significantly down-regulated after crmapk deletion, including cytochrome P450, transporters, and cell wall–degrading enzymes (CWDEs). Our findings indicate that crmapk influences C. chloroleuca mycoparasitism by regulation of genes controlling the activity of CWDEs or antibiotic production. This study provides a basis for further studies of the molecular mechanism of C. chloroleuca mycoparasitism.


2009 ◽  
Vol 22 (7) ◽  
pp. 830-839 ◽  
Author(s):  
Nicolas Rispail ◽  
Antonio Di Pietro

A conserved mitogen-activated protein kinase (MAPK) cascade homologous to the yeast Fus3/Kss1 mating/filamentation pathway regulates virulence in fungal plant pathogens. In the soilborne fungus Fusarium oxysporum, the MAPK Fmk1 is required for infection and development of vascular wilt disease on tomato plants. Knockout mutants lacking Fmk1 are deficient in multiple virulence-related functions, including root adhesion and penetration, invasive growth, secretion of pectinolytic enzymes, and vegetative hyphal fusion. The transcription factors mediating these different outputs downstream of the MAPK cascade are currently unknown. In this study, we have analyzed the role of ste12 which encodes an orthologue of the yeast homeodomain transcription factor Ste12p. F. oxysporum mutants lacking the ste12 gene were impaired in invasive growth on tomato and apple fruit tissue and in penetration of cellophane membranes. However, ste12 was not required for adhesion to tomato roots, secretion of pectinolytic enzymes, and vegetative hyphal fusion, suggesting that these Fmk1-dependent functions are mediated by other downstream MAPK targets. The Δste12 strains displayed dramatically reduced virulence on tomato plants, similar to the Δfmk1 mutant. These results indicate that invasive growth is the major virulence function controlled by the Fmk1 MAPK cascade and depends critically on the transcription factor Ste12.


Microbiology ◽  
2010 ◽  
Vol 156 (5) ◽  
pp. 1439-1447 ◽  
Author(s):  
Patrick D. Collopy ◽  
Richard C. Amey ◽  
Martin J. Sergeant ◽  
Michael P. Challen ◽  
Peter R. Mills ◽  
...  

In plant-pathogenic fungi, the pmk1 mitogen-activated protein kinase (MAPK) signalling pathway plays an essential role in regulating the development of penetration structures and the sensing of host-derived cues, but its role in other pathosystems such as fungal–fungal interactions is less clear. We report the use of a gene disruption strategy to investigate the pmk1-like MAPK, Lf pmk1 in the development of Lecanicillium fungicola (formerly Verticillium fungicola) infection on the cultivated mushroom Agaricus bisporus. Lf pmk1 was isolated using a degenerate PCR-based approach and was shown to be present in a single copy by Southern blot analysis. Quantitative RT-PCR showed the transcript to be fivefold upregulated in cap lesions compared with pure culture. Agrobacterium-mediated targeted disruption was used to delete a central portion of the Lf pmk1 gene. The resulting mutants showed normal symptom development as assessed by A. bisporus mushroom cap assays, sporulation patterns were normal and there were no apparent changes in overall growth rates. Our results indicate that, unlike the situation in fungal–plant pathogens, the pmk1-like MAPK pathway is not required for virulence in the fungal–fungal interaction between the L. fungicola pathogen and A. bisporus host. This observation may be of wider significance in other fungal–fungal and/or fungal–invertebrate interactions.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiaokang Chen ◽  
Wenbin Wang ◽  
Pingping Cai ◽  
Ziwei Wang ◽  
Tingting Li ◽  
...  

AbstractMitogen-activated protein kinase (MAPK) cascades play important roles in plant immunity. Previously, we reported that the potato StMKK1 protein negatively regulates Nicotiana benthamiana resistance to Phytophthora infestans. However, the functions of StMKK1 in potato immunity are unknown. To investigate the roles of StMKK1 in potato resistance to different pathogens, such as the potato late-blight pathogen P. infestans, the bacterial wilt pathogen Ralstonia solanacearum, and the gray-mold fungal pathogen Botrytis cinerea, we generated StMKK1 transgenic lines and investigated the response of potato transformants to destructive oomycete, bacterial, and fungal pathogens. The results showed that overexpression and silencing of StMKK1 do not alter plant growth and development. Interestingly, we found that StMKK1 negatively regulated potato resistance to the hemibiotrophic/biotrophic pathogens P. infestans and R. solanacearum, while it positively regulated potato resistance to the necrotrophic pathogen B. cinerea. Further investigation showed that overexpression of StMKK1 suppressed potato pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and salicylic acid (SA)-related responses, while silencing of StMKK1 enhanced PTI and SA-related immune responses. Taken together, our results showed that StMKK1 plays dual roles in potato defense against different plant pathogens via negative regulation of PTI and SA-related signaling pathways.


2021 ◽  
Vol 7 (5) ◽  
pp. 365
Author(s):  
Dubraska Moreno-Ruiz ◽  
Linda Salzmann ◽  
Mark D. Fricker ◽  
Susanne Zeilinger ◽  
Alexander Lichius

Trichoderma atroviride is a mycoparasitic fungus used as biological control agent against fungal plant pathogens. The recognition and appropriate morphogenetic responses to prey-derived signals are essential for successful mycoparasitism. We established microcolony confrontation assays using T. atroviride strains expressing cell division cycle 42 (Cdc42) and Ras-related C3 botulinum toxin substrate 1 (Rac1) interactive binding (CRIB) reporters to analyse morphogenetic changes and the dynamic displacement of localized GTPase activity during polarized tip growth. Microscopic analyses showed that Trichoderma experiences significant polarity stress when approaching its fungal preys. The perception of prey-derived signals is integrated via the guanosine triphosphatase (GTPase) and mitogen-activated protein kinase (MAPK) signalling network, and deletion of the MAP kinases Trichoderma MAPK 1 (Tmk1) and Tmk3 affected T. atroviride tip polarization, chemotropic growth, and contact-induced morphogenesis so severely that the establishment of mycoparasitism was highly inefficient to impossible. The responses varied depending on the prey species and the interaction stage, reflecting the high selectivity of the signalling process. Our data suggest that Tmk3 affects the polarity-stress adaptation process especially during the pre-contact phase, whereas Tmk1 regulates contact-induced morphogenesis at the early-contact phase. Neither Tmk1 nor Tmk3 loss-of-function could be fully compensated within the GTPase/MAPK signalling network underscoring the crucial importance of a sensitive polarized tip growth apparatus for successful mycoparasitism.


Open Biology ◽  
2013 ◽  
Vol 3 (6) ◽  
pp. 130067 ◽  
Author(s):  
Gopal P. Sapkota

The signalling pathways downstream of the transforming growth factor beta (TGFβ) family of cytokines play critical roles in all aspects of cellular homeostasis. The phosphorylation and activation of p38 mitogen-activated protein kinase (MAPK) has been implicated in TGFβ-induced epithelial-to-mesenchymal transition and apoptosis. The precise molecular mechanisms by which TGFβ cytokines induce the phosphorylation and activation of p38 MAPK are unclear. In this study, I demonstrate that TGFβ-activated kinase 1 (TAK1/MAP3K7) does not play a role in the TGFβ-induced phosphorylation and activation of p38 MAPK in MEFs and HaCaT keratinocytes. Instead, RNAi -mediated depletion of MAP3K4 and MAP3K10 results in the inhibition of the TGFβ-induced p38 MAPK phosphorylation. Furthermore, the depletion of MAP3K10 from cells homozygously knocked-in with a catalytically inactive mutant of MAP3K4 completely abolishes the TGFβ-induced phosphorylation of p38 MAPK, implying that among MAP3Ks, MAP3K4 and MAP3K10 are sufficient for mediating the TGFβ-induced activation of p38 MAPK.


Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 735 ◽  
Author(s):  
Vaishali Aggarwal ◽  
Hardeep Tuli ◽  
Ayşegül Varol ◽  
Falak Thakral ◽  
Mukerrem Yerer ◽  
...  

Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2440
Author(s):  
Lavinia Liliana Ruta ◽  
Ileana Cornelia Farcasanu

Caffeine–a methylxanthine analogue of the purine bases adenine and guanine–is by far the most consumed neuro-stimulant, being the active principle of widely consumed beverages such as coffee, tea, hot chocolate, and cola. While the best-known action of caffeine is to prevent sleepiness by blocking the adenosine receptors, caffeine exerts a pleiotropic effect on cells, which lead to the activation or inhibition of various cell integrity pathways. The aim of this review is to present the main studies set to investigate the effects of caffeine on cells using the model eukaryotic microorganism Saccharomyces cerevisiae, highlighting the caffeine synergy with external cell stressors, such as irradiation or exposure to various chemical hazards, including cigarette smoke or chemical carcinogens. The review also focuses on the importance of caffeine-related yeast phenotypes used to resolve molecular mechanisms involved in cell signaling through conserved pathways, such as target of rapamycin (TOR) signaling, Pkc1-Mpk1 mitogen activated protein kinase (MAPK) cascade, or Ras/cAMP protein kinase A (PKA) pathway.


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