Transcriptome of two maize lines seedlings show resistance and susceptible to corn smut during infection of Ustilago maydis
Ontology highlight
ABSTRACT:
ORGANISM(S): Zea mays
PROVIDER: GSE172071 | GEO | 2021/04/15
REPOSITORIES: GEO
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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: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 | PXD010583 | Pride
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
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 | PXD010582 | Pride
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 | PXD010584 | Pride
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:Sporisorium reilianum f. sp. zeae is an important biotrophic pathogen that causes head smut disease in maize. Head smut is not obvious until the tassels and ears emerge. S. reilianum has a very long life cycle that spans almost the entire developmental program of maize after the pathogen successfully invades the root. The aim of this study was to understand at a molecular level how this pathogen interacts with the host during its long life cycle, and how this interaction differs between susceptible and resistant varieties of maize after hyphal invasion. We investigated transcriptional changes in the resistant maize line Mo17 at four developmental stages using a maize 70mer-oligonucleotide microarray. We found that there was a lengthy compatible relationship between the pathogen and host until the early 8th-leaf stage. The resistance in Mo17 relied on the assignment of auxins and regulation of flavonoids in the early floral primordium during the early floral transition stage. We propose a model describing the putative mechanism of head smut resistance in Mo17 during floral transition. In the model, the synergistic regulations among auxins, flavonoids, and hyphal growth play a key role in maintaining compatibility with S. reilianum in the resistant maize line
2013-01-29 | GSE41916 | 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. Experiment Overall Design: In three independent experiments plants were infected with the solopathogenic U. maydis strain SG200. Samples from infected leaves were taken at 12 and 24 hours post infection, as well as 2, 4 and 8 days post infection. Samples from uninfected control plants were taken at the same time points.
2008-04-07 | E-GEOD-10023 | biostudies-arrayexpress
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:Sporisorium reilianum f. sp. zeae is an important biotrophic pathogen that causes head smut disease in maize. Head smut is not obvious until the tassels and ears emerge. S. reilianum has a very long life cycle that spans almost the entire developmental program of maize after the pathogen successfully invades the root. The aim of this study was to understand at a molecular level how this pathogen interacts with the host during its long life cycle, and how this interaction differs between susceptible and resistant varieties of maize after hyphal invasion. We investigated transcriptional changes in the resistant maize line Mo17 at four developmental stages using a maize 70mer-oligonucleotide microarray. We found that there was a lengthy compatible relationship between the pathogen and host until the early 8th-leaf stage. The resistance in Mo17 relied on the assignment of auxins and regulation of flavonoids in the early floral primordium during the early floral transition stage. We propose a model describing the putative mechanism of head smut resistance in Mo17 during floral transition. In the model, the synergistic regulations among auxins, flavonoids, and hyphal growth play a key role in maintaining compatibility with S. reilianum in the resistant maize line After inoculation using the hyphae of S. reilianum, the shoot apexes of inoculated Mo17 (resistant maize line) that contained hyphae but displayed normal morphology were collected for RNA extraction at at four vegetative stages; the 2nd-, 4th-, 6th-, and 8th-leaf stages. RNA samples from mock-inoculated and inocultated Mo17 were hybridized to the 46K maize 70-mer oligonucleotide microarray. Hybridization was performed in three biological replicates with Cy5/Cy3 dye swap as technical replicates.
2013-01-29 | E-GEOD-41916 | biostudies-arrayexpress