scholarly journals A functionally conserved Zn2Cys6binuclear cluster transcription factor class regulates necrotrophic effector gene expression and host-specific virulence of two major Pleosporales fungal pathogens of wheat

2017 ◽  
Vol 18 (3) ◽  
pp. 420-434 ◽  
Author(s):  
Kasia Rybak ◽  
Pao Theen See ◽  
Huyen T. T. Phan ◽  
Robert A. Syme ◽  
Caroline S. Moffat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Fungal Pathogens ◽  
Effector Gene ◽  
Necrotrophic Effector ◽  
Specific Virulence

scholarly journals Expression of the ToxA and PtrPf2 genes of the phytopathogenic fungus Pyrenophora tritici-repentis at the beginning of the infection process

2019 ◽  
Author(s):  
Nina V. Mironenko ◽  
Alexandra S. Orina ◽  
Nadezhda M. Kovalenko
Keyword(s):  
Transcription Factor ◽  
Wheat Variety ◽  
Infection Process ◽  
Phytopathogenic Fungus ◽  
In Planta ◽  
Effector Gene ◽  
Pyrenophora Tritici Repentis ◽  
Wheat Leaves ◽  
Necrotrophic Effector

This study shows that the necrotrophic effector gene ToxA is differentially expressed in isolates of P. tritici-repentis fungus at different time periods after inoculation of the wheat variety Glenlea which has the gene Tsn1 controlling sensitivity to the necrosis inducing toxin Ptr ToxA. Two P. tritici-repentis isolates with different ability to cause necrosis on the leaves of Glenlea variety (nec + and nec-) and with different expression level of ToxA and gene of factor transcription PtrPf2 in vitro were used for analysis. Isolates of P. tritici-repentis are characterized by the differential expression of ToxA in planta. The expression of the ToxA gene in P. tritici-repentis ToxA+ isolates significantly increased when infected the wheat leaves compared to ToxA expression results obtained in vitro. The levels of ToxA expression in both isolates differed significantly after 24, 48 and 96 hours after inoculation, however, the dynamics of the trait change over time were similar. However, the highest ToxA expression in the virulent (nec+) isolate in contrast with the avirulent (nec-) isolate was observed at a point of 48 hours. Whereas the expression of regulating transcription factor PtrPf2 in planta differed imperceptibly from expression in vitro throughout the observation period. Obviously, the role of the fungal transcription factor in regulating the effector gene expression weakens in planta, and other mechanisms regulating the expression of pathogen genes at the biotrophic stage of the disease develop.

scholarly journals Novel Antifungal Drug Discovery Based on Targeting Pathways Regulating the Fungus-Conserved Upc2 Transcription Factor

2013 ◽  
Vol 58 (1) ◽  
pp. 258-266 ◽  
Author(s):  
Christina Gallo-Ebert ◽  
Melissa Donigan ◽  
Ilana L. Stroke ◽  
Robert N. Swanson ◽  
Melissa T. Manners ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Dna Binding ◽  
Fungal Pathogens ◽  
Direct Interaction ◽  
Antifungal Drugs ◽  
Sterol Biosynthesis ◽  
Content Type ◽  
Stressed Cells

ABSTRACTInfections byCandida albicansand related fungal pathogens pose a serious health problem for immunocompromised patients. Azole drugs, the most common agents used to combat infections, target the sterol biosynthetic pathway. Adaptation to azole therapy develops as drug-stressed cells compensate by upregulating several genes in the pathway, a process mediated in part by the Upc2 transcription factor. We have implemented a cell-based high-throughput screen to identify small-molecule inhibitors of Upc2-dependent induction of sterol gene expression in response to azole drug treatment. The assay is designed to identify not only Upc2 DNA binding inhibitors but also compounds impeding the activation of gene expression by Upc2. An AlphaScreen assay was developed to determine whether the compounds identified interact directly with Upc2 and inhibit DNA binding. Three compounds identified by the cell-based assay inhibited Upc2 protein level andUPC2-LacZgene expression in response to a block in sterol biosynthesis. The compounds were growth inhibitory and attenuated antifungal-induced sterol gene expressionin vivo. They did so by reducing the level of Upc2 protein and Upc2 DNA binding in the presence of drug. The mechanism by which the compounds restrict Upc2 DNA binding is not through a direct interaction, as demonstrated by a lack of DNA binding inhibitory activity using the AlphaScreen assay. Rather, they likely inhibit a novel pathway activating Upc2 in response to a block in sterol biosynthesis. We suggest that the compounds identified represent potential precursors for the synthesis of novel antifungal drugs.

scholarly journals A specific fungal transcription factor controls effector gene expression and orchestrates the establishment of the necrotrophic pathogen lifestyle on wheat

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Darcy A. B. Jones ◽  
Evan John ◽  
Kasia Rybak ◽  
Huyen T. T. Phan ◽  
Karam B. Singh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Wall ◽  
Transcription Factor ◽  
Plant Cell ◽  
Plant Cell Wall ◽  
Cell Wall Degradation ◽  
Necrotrophic Pathogen ◽  
Effector Gene ◽  
Plant Cell Wall Degradation

Abstract The fungus Parastagonospora nodorum infects wheat through the use of necrotrophic effector (NE) proteins that cause host-specific tissue necrosis. The Zn2Cys6 transcription factor PnPf2 positively regulates NE gene expression and is required for virulence on wheat. Little is known about other downstream targets of PnPf2. We compared the transcriptomes of the P. nodorum wildtype and a strain deleted in PnPf2 (pf2-69) during in vitro growth and host infection to further elucidate targets of PnPf2 signalling. Gene ontology enrichment analysis of the differentially expressed (DE) genes revealed that genes associated with plant cell wall degradation and proteolysis were enriched in down-regulated DE gene sets in pf2-69 compared to SN15. In contrast, genes associated with redox control, nutrient and ion transport were up-regulated in the mutant. Further analysis of the DE gene set revealed that PnPf2 positively regulates twelve genes that encode effector-like proteins. Two of these genes encode proteins with homology to previously characterised effectors in other fungal phytopathogens. In addition to modulating effector gene expression, PnPf2 may play a broader role in the establishment of a necrotrophic lifestyle by orchestrating the expression of genes associated with plant cell wall degradation and nutrient assimilation.

scholarly journals The APSES transcription factor LmStuA is required for sporulation, pathogenic development and effector gene expression inLeptosphaeria maculans

2015 ◽  
Vol 16 (9) ◽  
pp. 1000-1005 ◽  
Author(s):  
Jessica L. Soyer ◽  
Audrey Hamiot ◽  
Bénédicte Ollivier ◽  
Marie-Hélène Balesdent ◽  
Thierry Rouxel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Effector Gene

scholarly journals Mechanisms Underlying the Delayed Activation of the Cap1 Transcription Factor in Candida albicans following Combinatorial Oxidative and Cationic Stress Important for Phagocytic Potency

mBio ◽  
2016 ◽  
Vol 7 (2) ◽  
Author(s):  
Iaroslava Kos ◽  
Miranda J. Patterson ◽  
Sadri Znaidi ◽  
Despoina Kaloriti ◽  
Alessandra da Silva Dantas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Candida Albicans ◽  
Stress Responses ◽  
Nuclear Export ◽  
Fungal Pathogens ◽  
Target Genes ◽  
Nacl Stress ◽  
Nuclear Accumulation ◽  
Simultaneous Exposure

ABSTRACT Following phagocytosis, microbes are exposed to an array of antimicrobial weapons that include reactive oxygen species (ROS) and cationic fluxes. This is significant as combinations of oxidative and cationic stresses are much more potent than the corresponding single stresses, triggering the synergistic killing of the fungal pathogen Candida albicans by “stress pathway interference.” Previously we demonstrated that combinatorial oxidative plus cationic stress triggers a dramatic increase in intracellular ROS levels compared to oxidative stress alone. Here we show that activation of Cap1, the major regulator of antioxidant gene expression in C. albicans , is significantly delayed in response to combinatorial stress treatments and to high levels of H 2 O 2 . Cap1 is normally oxidized in response to H 2 O 2 ; this masks the nuclear export sequence, resulting in the rapid nuclear accumulation of Cap1 and the induction of Cap1-dependent genes. Here we demonstrate that following exposure of cells to combinatorial stress or to high levels of H 2 O 2 , Cap1 becomes trapped in a partially oxidized form, Cap1 OX-1 . Notably, Cap1-dependent gene expression is not induced when Cap1 is in this partially oxidized form. However, while Cap1 OX-1 readily accumulates in the nucleus and binds to target genes following high-H 2 O 2 stress, the nuclear accumulation of Cap1 OX-1 following combinatorial H 2 O 2 and NaCl stress is delayed due to a cationic stress-enhanced interaction with the Crm1 nuclear export factor. These findings define novel mechanisms that delay activation of the Cap1 transcription factor, thus preventing the rapid activation of the stress responses vital for the survival of C. albicans within the host. IMPORTANCE Combinatorial stress-mediated synergistic killing represents a new unchartered area in the field of stress signaling. This phenomenon contrasts starkly with “stress cross-protection,” where exposure to one stress protects against subsequent exposure to a different stress. Previously we demonstrated that the pathogen Candida albicans is acutely sensitive to combinations of cationic and oxidative stresses, because the induction of H 2 O 2 -responsive genes is blocked in the presence of cationic stress. We reveal that this is due to novel mechanisms that delay activation of the Cap1 AP-1-like transcription factor, the major regulator of the H 2 O 2 -induced regulon. Cap1 becomes trapped in a partially oxidized form following simultaneous exposure to oxidative and cationic stresses. In addition, cationic stress promotes the interaction of Cap1 with the Crm1 nuclear export factor, thus inhibiting its nuclear accumulation. These mechanisms probably explain the potency of neutrophils, which employ multiple stresses to kill fungal pathogens.

scholarly journals Transcripts and tumors: regulatory and metabolic programming during biotrophic phytopathogenesis

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1812 ◽  
Author(s):  
Lara Schmitz ◽  
Sean McCotter ◽  
Matthias Kretschmer ◽  
James W. Kronstad ◽  
Kai Heimel
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Life Cycle ◽  
Fungal Pathogens ◽  
Ustilago Maydis ◽  
Life Cycles ◽  
Tumor Formation ◽  
Transcriptome Data ◽  
Host Environment ◽  
Key Features

Biotrophic fungal pathogens of plants must sense and adapt to the host environment to complete their life cycles. Recent transcriptome studies of the infection of maize by the biotrophic pathogen Ustilago maydis are providing molecular insights into an ordered program of changes in gene expression and the deployment of effectors as well as key features of nutrient acquisition. In particular, the transcriptome data provide a deeper appreciation of the complexity of the transcription factor network that controls the biotrophic program of invasion, proliferation, and sporulation. Additionally, transcriptome analysis during tumor formation, a key late stage in the life cycle, revealed features of the remodeling of host and pathogen metabolism that may support the formation of tremendous numbers of spores. Transcriptome studies are also appearing for other smut species during interactions with their hosts, thereby providing opportunities for comparative approaches to understand biotrophic adaptation.

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