The core effector Cce1 is required for early infection of maize by <i>Ustilago maydis</i>

Seitner, Denise; Uhse, Simon; Gallei, Michelle; Djamei, Armin

doi:10.1111/mpp.12698

Cited by 39 publications

(31 citation statements)

References 48 publications

(83 reference statements)

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“…The core effector Cce1 contributes to early stages of infection of maize by Ustilago maydis via interfering with papillary callose deposition (Seitner et al . , 2018). Moreover, papillary callose deposition is an output of the PTI response.…”

Section: Discussionmentioning

confidence: 99%

A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase

Shang

Wang

Zhang

et al. 2020

Molecular Plant Pathology

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The ascomycete fungus Colletotrichum fructicola causes diseases on a broad range of plant species. On susceptible cultivars of apple, it induces severe early defoliation and fruit spots, named glomerella leaf spot (GLS), but the mechanisms of pathogenicity have remained elusive. Phytopathogens exhibit small secreted effectors to advance host infection by manipulating host immune reactions. We report the identification and characterization of CfEC92, an effector required for C. fructicola virulence. CfEC92 is a Colletotrichum-specific small secreted protein that suppresses BAX-triggered cell death in Nicotiana benthamiana. Accumulation of the gene transcript was barely detectable in conidia or vegetative hyphae, but was highly up-regulated in appressoria formed during early apple leaf infection. Gene deletion mutants were not affected in vegetative growth, appressorium formation, or appressoriummediated cellophane penetration. However, the mutants were significantly reduced in virulence toward apple leaves and fruits. Microscopic examination indicated that infection by the deletion mutants elicited elevated deposition of papillae at the penetration sites, and formation of infection vesicles and primary hyphae was retarded.Signal peptide activity, subcellular localization, and cell death-suppressive activity (without signal peptide) assays suggest that CfEC92 could be secreted and perform virulence functions inside plant cells. RNA sequencing and quantitative reverse transcription PCR results confirmed that the deletion mutants triggered elevated host defence reactions. Our results strongly support the interpretation that CfEC92 contributes to C. fructicola virulence as a plant immunity suppressor at the early infection phase. K E Y W O R D S apple, Colletotrichum, effector, host immune response, pathogenicity | 937 SHANG et Al. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Shang S, Wang B, Zhang S, et al. A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase. Molecular Plant Pathology. 2020;21:936-950. https://doi.

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Section: Discussionmentioning

confidence: 99%

A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase

Shang

Wang

Zhang

et al. 2020

Molecular Plant Pathology

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“…These results support the idea that Pdi1 is a disulfide-isomerase protein that might assist the folding of newly synthetized proteins in the ER via the addition of disulfide bonds, which is critical during ER stress conditions (33). Many U. maydis effector proteins harbor cysteine-rich regions suitable for the formation of disulfide bonds, which may be necessary for their acquisition of active conformations (22,62,63). Thus, Pdi1’s role in establishing disulfide bonds in proteins involved in plant infection could be a major part of how the Δ pdi1 mutation affects virulence.…”

Section: Discussionmentioning

confidence: 99%

N-glycosylation of the protein disulfide isomerase Pdi1 ensuresUstilago maydisvirulence

Marín-Menguiano

Moreno-Sánchez

Barrales

et al. 2019

Preprint

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27Fungal pathogenesis depends on accurate secretion and location of 28 virulence factors which drive host colonization. Protein glycosylation is a 29 common posttranslational modification of cell wall components and other 30 secreted factors, typically required for correct protein localization, secretion 31 and function. Thus, the absence of glycosylation is associated with animal 32 and plant pathogen avirulence. While the relevance of protein glycosylation 33 for pathogenesis has been well established, the main glycoproteins 34 responsible for the loss of virulence observed in glycosylation-defective fungi 35 have not been identified. Here, we devise a proteomics approach to identify 36 such proteins and use it to demonstrate a role for the highly conserved protein 37 disulfide isomerase Pdi1 in virulence. We show that efficient Pdi1 N-38 glycosylation, which promotes folding into the correct protein conformation, is 39 required for full pathogenic development of the corn smut fungus Ustilago 40 maydis. Remarkably, the observed virulence defects are reminiscent of those 41 seen in glycosylation-defective cells suggesting that the N-glycosylation of 42 Pdi1 is necessary for the full secretion of virulence factors. All these 43 observations, together with the fact that Pdi1 protein and RNA expression 44 levels rise upon virulence program induction, suggest that Pdi1 glycosylation 45 is a crucial event for pathogenic development in U. maydis. Our results 46 provide new insights into the role of glycosylation in fungal pathogenesis. 47 48 49 50 3 51 Author summary 52 Fungal pathogens require virulence factors to be properly secreted and 53 localized to guarantee complete infection. In common with many proteins, 54 virulence factors must be post-translationally modified by glycosylation for 55 normal localization, secretion and function. This is especially important for 56 virulence factors, which are mainly comprised of cell wall and secreted 57 proteins. Aberrant glycosylation leads to a loss of virulence in both animal and 58 plant pathogenic fungi. We have previously demonstrated that glycosylation is 59 important for virulence of the corn smut fungus, Ustilago maydis. However, 60 the glycoproteins involved and their specific roles in the infection process 61 have not yet been reported. Here, we describe a proteomic assay designed to 62 identify glycoproteins involved in plant infection. Using this method, we define 63 the role of Pdi1 protein disulfide isomerase in virulence. Interestingly, 64 abolishing Pdi1 N-glycosylation mimics pdi1 defects observed during 65 infection, suggesting that Pdi1 N-glycosylation is required for the secretion of 66 virulence factors. We hypothesize that Pdi1 N-glycosylation is crucial for 67 maintaining proper effector protein folding during the infection process, 68 especially in the harsh conditions found inside the maize plant. 69 4 70 Introduction 71 Protein glycosylation is a common eukaryotic post-translational 72 mechanism required for the correct folding, activity and sec...

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“…Mutants of the corn smut fungus Ustilago maydis were made using PCR‐based protocols combined with protoplast transformation to generate candidate effector knockout mutants (Schulz et al ., 1990; Kämper, 2004). This method is widely used and has successfully facilitated the functional characterization of U. maydis effectors, including Rsp3 and Cce1 (Ma et al ., 2018a; Seitner et al ., 2018).…”

Section: Functional Characterizationmentioning

confidence: 99%

Proteinaceous effector discovery and characterization in filamentous plant pathogens

Kanja

Hammond‐Kosack

2020

Molecular Plant Pathology

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The complicated interplay of plant–pathogen interactions occurs on multiple levels as pathogens evolve to constantly evade the immune responses of their hosts. Many economically important crops fall victim to filamentous pathogens that produce small proteins called effectors to manipulate the host and aid infection/colonization. Understanding the effector repertoires of pathogens is facilitating an increased understanding of the molecular mechanisms underlying virulence as well as guiding the development of disease control strategies. The purpose of this review is to give a chronological perspective on the evolution of the methodologies used in effector discovery from physical isolation and in silico predictions, to functional characterization of the effectors of filamentous plant pathogens and identification of their host targets.

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The core effector Cce1 is required for early infection of maize by Ustilago maydis

Cited by 39 publications

References 48 publications

A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase

A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase

N-glycosylation of the protein disulfide isomerase Pdi1 ensuresUstilago maydisvirulence

Proteinaceous effector discovery and characterization in filamentous plant pathogens

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