A combination of organic acids and glucose prime a late stage of fungal biotrophy
Ontology highlight
ABSTRACT:
ORGANISM(S): Ustilago maydis 521
PROVIDER: GSE194157 | GEO | 2022/12/31
REPOSITORIES: GEO
Similar Datasets
Project description:The basidiomycete Ustilago maydis is the causal agent of corn smut disease and induces tumor formation during biotrophic growth in its host plant maize. The Usilago maydis genome harbors a homolog to the GATA transcription factors Nit2 and AreA that act as global regulators of nitrogen catabolite repression in filamentous model fungi Neurospora crassa and Aspergillus nidulans, respectively. We aimed at resolving the role of the Ustilago maydis Nit2 homolog for the utilization of complex nitrogen sources and pathogenicity.
2012-01-01 | GSE28916 | GEO
Project description:The biotrophic fungal pathogen Ustilago maydis cause common smut in maize, and lead to gall formation on all aerial organs, especially on maize kernel thus reduce yield. The interaction of U. maydis with maize is a well-established model to study the interaction between maize and biotrophic pathogen. U. maydis infection could activate host immune responses including: ROS accumulation, protease activation, salicylic acid signaling. U. maydis employ several strategies to overcome maize immune response, thus initial the biotrophic interaction with host. It has been suggested that genetic factors of maize host affected the disease severity of U. maydis infection, here we investigated the transcriptome profile of resistance and susceptible maize lines upon U. maydis infection, thus propose candidate maize genes involved in the defense response in maize to corn smut cause by U. maydis.
2021-04-15 | GSE172071 | GEO
Project description:The basidiomycete fungus Ustilago maydis causes smut disease in maize and has become an important model for elucidating the strategies used for host colonization by biotrophic fungi. In this study, we performed an in-depth transcriptional profiling of the plant-associated development of a cross between U. maydis FB1 and FB2 wildtype strains. The analysis of eight different stages, including the development on the leaf surface, early colonization, tumor induction and spore maturation, offers an unprecedented view of the changes in the fungal transcriptome associated with the passage through the entirely biotrophic life cycle. In our analysis, we focus on fungal metabolism, nutritional strategies, secreted effectors and regulatory networks. Secreted proteins were enriched in three distinct expression modules corresponding to the plant surface, establishment of biotrophy and tumor formation, respectively. These modules are likely the key determinants for U. maydis virulence. With respect to nutrient utilization, we observed that expression of several nutrient transporters was tied to these virulence modules rather than being controlled by nutrient availability. We show that oligopeptide transporters likely involved in nitrogen supply during infection are important virulence determinants. By measuring the intramodular connectivity of transcription factors, we identified potential drivers for the virulence modules. While known components of the b-cascade served as inducers for the plant surface and biotrophy module, we identified a set of yet uncharacterized transcription factors as likely responsible for expression of the tumor module. We demonstrate a crucial role in effector gene expression and tumor formation for one of these transcription factors.
2018-01-11 | GSE103876 | GEO
Project description:Ustilago maydis is a plant-pathogenic fungus that establishes a biotrophic relationship with its host Zea mays. The biotrophic interaction is initiated upon host penetration, and involves expansion of the host plasma membrane around hyphae, which is thought to facilitate the exchange of nutrients and virulence factors. Transcriptional regulators involved in the establishment of an infectious dikaryon and penetration into the host have been identified, however, regulators involved in the post-penetration stages remained to be elucidated. In the study we report the identification of an Ustilago maydis forkhead transcription factor, Fox1, which is exclusively expressed during biotrophic development. Deletion of fox1 results in reduced virulence and impaired tumour development in planta. Microarray analyses of Δfox1-infected plant tissue identified Fox1 as a transcriptional activator, involved in the expression of secreted effectors required for virulence.
2010-12-31 | GSE19591 | GEO
Project description:• Ustilago maydis (U. maydis) is the causal agent of maize smut disease. During the colonization process, the fungus secretes effector proteins which suppress immune responses and redirect the host metabolism in favor of the pathogen. As effectors play a critical role during plant colonization, their identification and functional characterization is essential to understanding biotrophy and disease. • Using biochemical, molecular, and transcriptomic techniques, we performed a functional characterization of the U. maydis effector Jasmonate/Ethylene signaling inducer 1 (Jsi1). • Jsi1 interacts with several members of the plant co‐repressor family Topless/Topless related (TPL/TPR). Jsi1 expression in Zea mays (Z. mays) and Arabidopsis thaliana (A. thaliana) leads to transcriptional induction of the ethylene response factor (ERF) branch of the jasmonate/ethylene (JA/ET) signaling pathway. In A. thaliana, activation of the ERF‐branch leads to biotrophic susceptibility. Jsi1 likely activates the ERF‐branch via an EAR motif, which resembles EAR motifs from plant ERF transcription factors, that interacts with TPL/TPR proteins. • EAR motif‐containing effector candidates were identified from different fungal species including Magnaporthe oryzae, Sporisorium scitamineum, and Sporisorium reilianum. Interaction between plant TPL proteins and these effector candidates from biotrophic and hemibiotrophic fungi indicates the convergent evolution of effectors modulating the TPL/TPR co‐repressor hub.
2020-11-30 | GSE142128 | GEO
Project description:The fungal pathogen Ustilago maydis establishes a biotrophic relationship with its host plant maize. Hallmarks of the disease are large plant tumors in which fungal proliferation occurs. Plants have developed various defense pathways to cope with pathogens. We used microarrays to detail the global programme of gene expression during the infection process of Ustilago maydis in its host plant to get insights into the defense programs and the metabolic reprogramming needed to supply the fungus with nutrients. Keywords: time course
2008-03-01 | GSE10023 | GEO
Project description:Ustilago maydis is a biotrophic fungus that causes tumor formation on all aerial parts of maize. U. maydis secretes effector proteins during penetration and colonization to successfully overcome the plant immune response and reprogram host physiology to promote infection. In this study, we functionally characterized the U. maydis effector protein Topless (TPL) interacting protein 6 (Tip6). We found that Tip6 interacts with the N-terminus of ZmTPL2 through its two EAR (Ethylene-responsive element binding factor-associated amphiphilic repression) motifs. We show that the EAR motifs are essential for the virulence function of Tip6 and critical for altering the nuclear distribution pattern of ZmTPL2. We propose that Tip6 mimics the recruitment of ZmTPL2 by plant repressor proteins, thus disrupting host transcriptional regulation. We show that a large group of AP2/ERF B1 subfamily transcription factors are misregulated in the presence of Tip6. Our study suggests a regulatory mechanism where the U. maydis effector Tip6 utilizes repressive domains to recruit the corepressor ZmTPL2 to disrupt the transcriptional networks of the host plant.
2023-11-09 | PXD042605 | Pride
Project description:Ustilago maydis is a biotrophic fungus that causes tumor formation on all aerial parts of maize. U. maydis secretes effector proteins during penetration and colonization to successfully overcome the plant immune response and reprogram host physiology to promote infection. In this study, we functionally characterized the U. maydis effector protein Topless (TPL) interacting protein 6 (Tip6). We found that Tip6 interacts with the N-terminus of RELK2 through its two Ethylene-responsive element binding factor-associated amphiphilic repression (EAR) motifs. We show that the EAR motifs are essential for the virulence function of Tip6 and critical for altering the nuclear distribution pattern of RELK2. We propose that Tip6 mimics the recruitment of RELK2 by plant repressor proteins, thus disrupting host transcriptional regulation. We show that a large group of AP2/ERF B1 subfamily transcription factors are misregulated in the presence of Tip6. Our study suggests a regulatory mechanism where the U. maydis effector Tip6 utilizes repressive domains to recruit the corepressor RELK2 to disrupt the transcriptional networks of the host plant.
2023-11-09 | GSE234067 | GEO
Project description:Ustilago maydis is a plant-pathogenic fungus that establishes a biotrophic relationship with its host Zea mays. The biotrophic interaction is initiated upon host penetration, and involves expansion of the host plasma membrane around hyphae, which is thought to facilitate the exchange of nutrients and virulence factors. Transcriptional regulators involved in the establishment of an infectious dikaryon and penetration into the host have been identified, however, regulators involved in the post-penetration stages remained to be elucidated. In the study we report the identification of an Ustilago maydis forkhead transcription factor, Fox1, which is exclusively expressed during biotrophic development. Deletion of fox1 results in reduced virulence and impaired tumour development in planta. Δfox1 hyphae induce plant defences including the overproduction and accumulation of H2O2 in and around infected cells. This oxidative burst acts as an intercellular signal, which elicits a specific host defence response phenotypically represented by the encasement of proliferating hyphae in extensions of the plant cell wall. Maize microarrays experiments were performed to identify genes involved in the observed plant defence responses on leaf tissue infected with U. maydis strain SG200∆fox1 4 dpi.
2010-12-31 | GSE19559 | GEO
Project description:Ustilago maydis is a biotrophic fungus causing corn smut disease in maize. To downregulate immune responses and promote host colonization, U. maydis secretes a set of effector proteins into the plant apoplast. An effector essential for U. maydis virulence is Pit2, an inhibitor of papain-like cysteine proteases (PLCPs). Pit2 virulence function relies on a 14 amino acids motif (PID14). While sequence of the Pit2 effector is highly diverse amongst related pathogen species, the PID14 motif is highly conserved. Interestingly, synthetic PID14 peptides act more efficiently as PLCP inhibitors than the full-length Pit2 effector. In line with this finding, mass spectrometry showed processing of Pit2 by maize PLCPs, which releases an inhibitory core motif of the PID14. Mutational analysis demonstrated that two residues of the released inhibitor peptide are essential for Pit2 function and, consequently, for U. maydis virulence. Based on these findings, we propose a model, in which the Pit2 effector functions as a decoy: Pit2 represents a favorable substrate for apoplastic PLCPs, which are central hubs of the maize immune system. Processing of Pit2 releases the inhibitor peptide, which in turn efficiently blocks PLCPs to modulate host immunity.
2019-02-25 | PXD010596 | Pride