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      Improved prediction of fungal effector proteins from secretomes with EffectorP 2.0 : Prediction of fungal effectors with EffectorP 2.0

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          Abstract

          <p id="d5415808e260">Plant‐pathogenic fungi secrete effector proteins to facilitate infection. We describe extensive improvements to EffectorP, the first machine learning classifier for fungal effector prediction. EffectorP 2.0 is now trained on a larger set of effectors and utilizes a different approach based on an ensemble of classifiers trained on different subsets of negative data, offering different views on classification. EffectorP 2.0 achieves an accuracy of 89%, compared with 82% for EffectorP 1.0 and 59.8% for a small size classifier. Important features for effector prediction appear to be protein size, protein net charge as well as the amino acids serine and cysteine. EffectorP 2.0 decreases the number of predicted effectors in secretomes of fungal plant symbionts and saprophytes by 40% when compared with EffectorP 1.0. However, EffectorP 1.0 retains value, and combining EffectorP 1.0 and 2.0 results in a stringent classifier with a low false positive rate of 9%. EffectorP 2.0 predicts significant enrichments of effectors in 12 of 13 sets of infection‐induced proteins from diverse fungal pathogens, whereas a small cysteine‐rich classifier detects enrichment in only seven of 13. EffectorP 2.0 will fast track the prioritization of high‐confidence effector candidates for functional validation and aid in improving our understanding of effector biology. EffectorP 2.0 is available at <a data-untrusted="" href="http://effectorp.csiro.au" id="d5415808e262" target="xrefwindow">http://effectorp.csiro.au</a>. </p>

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          Most cited references48

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          Insights from the genome of the biotrophic fungal plant pathogen Ustilago maydis.

          Ustilago maydis is a ubiquitous pathogen of maize and a well-established model organism for the study of plant-microbe interactions. This basidiomycete fungus does not use aggressive virulence strategies to kill its host. U. maydis belongs to the group of biotrophic parasites (the smuts) that depend on living tissue for proliferation and development. Here we report the genome sequence for a member of this economically important group of biotrophic fungi. The 20.5-million-base U. maydis genome assembly contains 6,902 predicted protein-encoding genes and lacks pathogenicity signatures found in the genomes of aggressive pathogenic fungi, for example a battery of cell-wall-degrading enzymes. However, we detected unexpected genomic features responsible for the pathogenicity of this organism. Specifically, we found 12 clusters of genes encoding small secreted proteins with unknown function. A significant fraction of these genes exists in small gene families. Expression analysis showed that most of the genes contained in these clusters are regulated together and induced in infected tissue. Deletion of individual clusters altered the virulence of U. maydis in five cases, ranging from a complete lack of symptoms to hypervirulence. Despite years of research into the mechanism of pathogenicity in U. maydis, no 'true' virulence factors had been previously identified. Thus, the discovery of the secreted protein gene clusters and the functional demonstration of their decisive role in the infection process illuminate previously unknown mechanisms of pathogenicity operating in biotrophic fungi. Genomic analysis is, similarly, likely to open up new avenues for the discovery of virulence determinants in other pathogens.
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            Genome expansion and gene loss in powdery mildew fungi reveal tradeoffs in extreme parasitism.

            Powdery mildews are phytopathogens whose growth and reproduction are entirely dependent on living plant cells. The molecular basis of this life-style, obligate biotrophy, remains unknown. We present the genome analysis of barley powdery mildew, Blumeria graminis f.sp. hordei (Blumeria), as well as a comparison with the analysis of two powdery mildews pathogenic on dicotyledonous plants. These genomes display massive retrotransposon proliferation, genome-size expansion, and gene losses. The missing genes encode enzymes of primary and secondary metabolism, carbohydrate-active enzymes, and transporters, probably reflecting their redundancy in an exclusively biotrophic life-style. Among the 248 candidate effectors of pathogenesis identified in the Blumeria genome, very few (less than 10) define a core set conserved in all three mildews, suggesting that most effectors represent species-specific adaptations.
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              Plant cell wall-degrading enzymes and their secretion in plant-pathogenic fungi.

              Approximately a tenth of all described fungal species can cause diseases in plants. A common feature of this process is the necessity to pass through the plant cell wall, an important barrier against pathogen attack. To this end, fungi possess a diverse array of secreted enzymes to depolymerize the main structural polysaccharide components of the plant cell wall, i.e., cellulose, hemicellulose, and pectin. Recent advances in genomic and systems-level studies have begun to unravel this diversity and have pinpointed cell wall-degrading enzyme (CWDE) families that are specifically present or enhanced in plant-pathogenic fungi. In this review, we discuss differences between the CWDE arsenal of plant-pathogenic and non-plant-pathogenic fungi, highlight the importance of individual enzyme families for pathogenesis, illustrate the secretory pathway that transports CWDEs out of the fungal cell, and report the transcriptional regulation of expression of CWDE genes in both saprophytic and phytopathogenic fungi.
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                Author and article information

                Journal
                Molecular Plant Pathology
                Molecular Plant Pathology
                Wiley
                14646722
                September 2018
                September 2018
                May 11 2018
                : 19
                : 9
                : 2094-2110
                Affiliations
                [1 ]Centre for Environment and Life Sciences, CSIRO Agriculture and Food; Perth, WA 6014 Australia
                [2 ]Black Mountain Laboratories, CSIRO Agriculture and Food; Canberra, ACT 2601 Australia
                [3 ]CSIRO Agriculture and Food; Queensland Bioscience Precinct; Brisbane, Qld 4067 Australia
                [4 ]Department of Environment and Agriculture, Centre for Crop and Disease Management; Curtin University; Bentley, WA 6102 Australia
                Article
                10.1111/mpp.12682
                6638006
                29569316
                d1dc37c5-adf6-4218-8b47-6bb1fef17542
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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