Ustilago maydis effector Jsi1 interacts with Topless corepressor, hijacking plant JA/ET signaling
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA595951 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10704400.fastq.gz | Fastqsanger.gz | |||
| SRR10704365.fastq.gz | Fastqsanger.gz | |||
| SRR10704366.fastq.gz | Fastqsanger.gz | |||
| SRR10704367.fastq.gz | Fastqsanger.gz | |||
| SRR10704368.fastq.gz | Fastqsanger.gz |
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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: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.
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Project description:Ustilago maydis is the causal agent of maize smut disease. During the colonization process, the fungus secretes effector proteins that 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 are 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 corepressor family Topless/Topless related (TPL/TPR). Jsi1 expression in Zea mays and Arabidopsis 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 (ET-responsive element binding-factor-associated amphiphilic repression) 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 corepressor hub.
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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.
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2023-05-09 | GSE207132 | GEO
Project description:Transcriptional corepressors of the Topless family are important regulators of plant hormone and immunity signaling. We present here the transcriptome of Arabidopsis thaliana Col-0 plants expressing GFP-tagged TPR1 (Topless-related 1). Expression of TPR1 driven by its own promoter (pTPR1:TPR1-GFP) in Arabidopsis results in EDS1-dependent defense activation and dwarfed growth affected by the plant immune regulator EDS1 but not by accumulation of salicylic acid. We used total RNA sequencing to characterize the transcriptional status of TPR1-GFP expressing lines in Col, eds1-2 and sid2-1 mutant backgrounds.
2021-06-29 | GSE154652 | GEO
Project description:Genome-wide chromatin binding of transcriptional corepressor Topless-related 1 in Arabidopsis
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Project description:Plant Topless-related 1 (TPR1), belonging to a family of transcriptional corepressors found across eukaryotes, contributes to immunity signaling in Arabidopsis thaliana and wild tobacco. We used chromatin immunoprecipitation and sequencing (ChIP-seq) of Arabidopsis TPR1-GFP expressing transgenic lines to characterize genome-wide TPR1-chromatin associations.
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Project description:The corepressor of Topless-related 1 (TPR1): Transcript analysis of TPR1-GFP lines
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Project description:Plants integrate endogenous and environmental signals to regulate growth and developmental programs by the use different hormonal pathways. Perception of Pathogen/Microbial Associated Molecular Patterns (PAMPs/MAMPs) from invading microorganisms triggers a series of defense reactions known as Pathogen Triggered Immunity (PTI) that inhibit growth promoting signaling pathways such as auxin signaling. On the contrary, pathogens manipulate growth signaling and metabolism to promote disease susceptibility, but how this hormone acts on immunity is not fully understood. Ustilago maydis is a fungal pathogen of maize. Infected plants show formation of galls, masses of undifferentiated tissue, and upregulation of auxin signaling. Here we show that a secreted protein from U. maydis, the effector Naked1 (Nkd1), translocates into the host nucleus where it interacts with members of the Topless/Topless related family of transcriptional co-repressors. Nkd1 binds to TPL/TPRs through its native EAR motif and prevents recruitment of transcriptional repressors involved in hormonal signaling, leading to the de-repression of jasmonic acid and auxin responsive genes. We show that up-regulation of auxin signaling leads to inhibition of PAMP-triggered ROS burst, one of the earliest PTI responses, and increased susceptibility to pathogens. Thus, establishing a clear mechanism for auxin-induced pathogen susceptibility. Using engineered variants of Nkd1, with altered affinity/specificity to TPL/TPRs, we show that increased EAR-mediated binding triggers typical salicylic acid mediated defense reactions, leading to pathogen resistance.
2021-06-01 | GSE141597 | GEO