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1.
Background
Sudden death syndrome (SDS) caused by the ascomycete fungus, Fusarium virguliforme, exhibits root necrosis and leaf scorch or foliar SDS. The pathogen has never been identified from the above ground diseased foliar tissues. Foliar SDS is believed to be caused by host selective toxins, including FvTox1, secreted by the fungus. This study investigated if the xylem sap of F. virguliforme-infected soybean plants contains secreted F. virguliforme-proteins, some of which could cause foliar SDS development.Results
Xylem sap samples were collected from five biological replications of F. virguliforme-infected and uninfected soybean plants under controlled conditions. We identified five F. virguliforme proteins from the xylem sap of the F. virguliforme-infected soybean plants by conducting LC-ESI-MS/MS analysis. These five proteins were also present in the excreted proteome of the pathogen in culture filtrates. One of these proteins showed high sequence identity to cerato-platanin, a phytotoxin produced by Ceratocystis fimbriata f. sp. platani to cause canker stain disease in the plane tree. Of over 500 soybean proteins identified in this study, 112 were present in at least 80% of the sap samples collected from F. virguliforme-infected and -uninfected control plants. We have identified four soybean defense proteins from the xylem sap of F. virguliforme-infected soybean plants. The data have been deposited to the ProteomeXchange with identifier PXD000873.Conclusion
This study confirms that a few F. virguliforme proteins travel through the xylem, some of which could be involved in foliar SDS development. We have identified five candidate proteinaceous toxins, one of which showed high similarity to a previously characterized phytotoxin. We have also shown the presence of four soybean defense proteins in the xylem sap of F. virguliforme-infected soybean plants. This study laid the foundation for studying the molecular basis of foliar SDS development in soybean and possible defense mechanisms that may be involved in conferring immunity against F. virguliforme and other soybean pathogens. 相似文献2.
Genome‐wide association and epistasis studies unravel the genetic architecture of sudden death syndrome resistance in soybean 下载免费PDF全文
Jiaoping Zhang Arti Singh Daren S. Mueller Asheesh K. Singh 《The Plant journal : for cell and molecular biology》2015,84(6):1124-1136
Soybean [Glycine max (L.) Merr.] is an economically important crop that is grown worldwide. Sudden death syndrome (SDS), caused by Fusarium virguliforme, is one of the top yield‐limiting diseases in soybean. However, the genetic basis of SDS resistance, especially with respect to epistatic interactions, is still unclear. To better understand the genetic architecture of soybean SDS resistance, genome‐wide association and epistasis studies were performed using a population of 214 germplasm accessions and 31 914 SNPs from the SoySNP50K Illumina Infinium BeadChip. Twelve loci and 12 SNP–SNP interactions associated with SDS resistance were identified at various time points after inoculation. These additive and epistatic loci together explained 24–52% of the phenotypic variance. Disease‐resistant, pathogenesis‐related and chitin‐ and wound‐responsive genes were identified in the proximity of peak SNPs, including stress‐induced receptor‐like kinase gene 1 (SIK1), which is pinpointed by a trait‐associated SNP and encodes a leucine‐rich repeat‐containing protein. We report that the proportion of phenotypic variance explained by identified loci may be considerably improved by taking epistatic effects into account. This study shows the necessity of considering epistatic effects in soybean SDS resistance breeding using marker‐assisted and genomic selection approaches. Based on our findings, we propose a model for soybean root defense against the SDS pathogen. Our results facilitate identification of the molecular mechanism underlying SDS resistance in soybean, and provide a genetic basis for improvement of soybean SDS resistance through breeding strategies based on additive and epistatic effects. 相似文献
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Subodh K. Srivastava Xiaoqiu Huang Hargeet K. Brar Ahmad M. Fakhoury Burton H. Bluhm Madan K. Bhattacharyya 《PloS one》2014,9(1)
Fusarium virguliforme causes sudden death syndrome (SDS) of soybean, a disease of serious concern throughout most of the soybean producing regions of the world. Despite the global importance, little is known about the pathogenesis mechanisms of F. virguliforme. Thus, we applied Next-Generation DNA Sequencing to reveal the draft F. virguliforme genome sequence and identified putative pathogenicity genes to facilitate discovering the mechanisms used by the pathogen to cause this disease.
Methodology/Principal Findings
We have generated the draft genome sequence of F. virguliforme by conducting whole-genome shotgun sequencing on a 454 GS-FLX Titanium sequencer. Initially, single-end reads of a 400-bp shotgun library were assembled using the PCAP program. Paired end sequences from 3 and 20 Kb DNA fragments and approximately 100 Kb inserts of 1,400 BAC clones were used to generate the assembled genome. The assembled genome sequence was 51 Mb. The N50 scaffold number was 11 with an N50 Scaffold length of 1,263 Kb. The AUGUSTUS gene prediction program predicted 14,845 putative genes, which were annotated with Pfam and GO databases. Gene distributions were uniform in all but one of the major scaffolds. Phylogenic analyses revealed that F. virguliforme was closely related to the pea pathogen, Nectria haematococca. Of the 14,845 F. virguliforme genes, 11,043 were conserved among five Fusarium species: F. virguliforme, F. graminearum, F. verticillioides, F. oxysporum and N. haematococca; and 1,332 F. virguliforme-specific genes, which may include pathogenicity genes. Additionally, searches for candidate F. virguliforme pathogenicity genes using gene sequences of the pathogen-host interaction database identified 358 genes.Conclusions
The F. virguliforme genome sequence and putative pathogenicity genes presented here will facilitate identification of pathogenicity mechanisms involved in SDS development. Together, these resources will expedite our efforts towards discovering pathogenicity mechanisms in F. virguliforme. This will ultimately lead to improvement of SDS resistance in soybean. 相似文献5.
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Unravelling early events in the Taphrina deformans–Prunus persica interaction: an insight into the differential responses in resistant and susceptible genotypes 下载免费PDF全文
Camila Goldy Nery Rivero Gabriela L. Müller Gabriel H. Valentini Alisdair R. Fernie María F. Drincovich María V. Lara 《Plant, cell & environment》2017,40(8):1456-1473
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Soybean is one of the most important crops grown across the globe. In the United States, approximately 15% of the soybean yield is suppressed due to various pathogen and pests attack. Sudden death syndrome (SDS) is an emerging fungal disease caused by Fusarium virguliforme. Although growing SDS resistant soybean cultivars has been the main method of controlling this disease, SDS resistance is partial and controlled by a large number of quantitative trait loci (QTL). A proteinacious toxin, FvTox1, produced by the pathogen, causes foliar SDS. Earlier, we demonstrated that expression of an anti-FvTox1 single chain variable fragment antibody resulted in reduced foliar SDS development in transgenic soybean plants. Here, we investigated if synthetic FvTox1-interacting peptides, displayed on M13 phage particles, can be identified for enhancing foliar SDS resistance in soybean. We screened three phage-display peptide libraries and discovered four classes of M13 phage clones displaying FvTox1-interacting peptides. In vitro pull-down assays and in vivo interaction assays in yeast were conducted to confirm the interaction of FvTox1 with these four synthetic peptides and their fusion-combinations. One of these peptides was able to partially neutralize the toxic effect of FvTox1 in vitro. Possible application of the synthetic peptides in engineering SDS resistance soybean cultivars is discussed. 相似文献
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Mapping and confirmation of a new sudden death syndrome resistance QTL on linkage group D2 from the soybean genotypes PI 567374 and ‘Ripley’ 总被引:1,自引:0,他引:1
Austeclinio L. de Farias Neto Rizwan Hashmi Michael Schmidt Shawn R. Carlson Glen L. Hartman Shuxian Li Randall L. Nelson Brian W. Diers 《Molecular breeding : new strategies in plant improvement》2007,20(1):53-62
The use of resistant cultivars is the most effective method for controlling sudden death syndrome (SDS), caused by Fusarium solani f. sp. glycines (FSG) (syn. Fusarium virguliforme Akoi, O’Donnell, Homma and Lattanzi), in soybean [Glycine max (L.) Merr.]. Previous research has led to the identification of soybean genotypes with partial resistance to SDS and quantitative
trait loci (QTL) controlling this resistance. The objective of our study was to map QTL conferring SDS resistance in populations
developed from the crosses Ripley × Spencer (R×S-1) and PI 567374 × Omaha (P×O-1). Both Ripley and PI 567374 have partial
resistance to SDS and Spencer and Omaha are susceptible. The R×S-1 population was evaluated for SDS resistance in three field
environments and the P×O-1 population was greenhouse evaluated. Three SDS resistance QTL were mapped in the R×S-1 population
and two in the P×O-1 population. One resistance QTL was mapped to the same location on linkage group (LG) D2 in both backgrounds.
This QTL was then tested in a population of F2 plants developed through one backcross (BC1F2) in the PI 567374 source and in a population of F8 plants derived from a heterozygous F5 plant in the Ripley source. The LG D2 QTL was also significant in confirmation populations in both resistant backgrounds.
Since none of the SDS resistance QTL identified in the R×S-1 or P×O-1 populations mapped to previously reported SDS resistance
regions, these new QTL should be useful sources of SDS resistance for soybean breeders. 相似文献
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Responsiveness of different citrus genotypes to the Xanthomonas citri ssp. citri‐derived pathogen‐associated molecular pattern (PAMP) flg22 correlates with resistance to citrus canker 下载免费PDF全文
Qingchun Shi Vicente J. Febres Jeffrey B. Jones Gloria A. Moore 《Molecular Plant Pathology》2015,16(5):507-520
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Yu‐Hua Fu Jin‐Ju Wei Yong‐Bao Pan Xiang Zhou Er‐Qi He Rong Liu Hui Huang Jia‐Ju Lu Fan‐Zhi Liu 《Journal of Phytopathology》2019,167(11-12):633-644
Ratoon stunting disease (RSD) caused by bacterium Leifsoniaxyli subsp. xyli (Lxx) is a devastating disease of sugarcane over a large part of the world. Genetic improvement for RSD‐resistant varieties is considered the most effective method to control the disease. However, genetic improvement of sugarcane is hindered by the limited information about the molecular mechanisms underlying Lxx pathogenicity and defence responses in sugarcane. In this study, genome‐wide gene expression profiling was used to compare RSD‐resistant (CP72‐2086) and RSD‐susceptible (GT11) genotypes at different infection time points in order to identify the candidate regulators for RSD resistance. A total of 14,494 differentially expressed genes (DEGs) were identified, indicating that dramatic changes had occurred in gene expression upon Lxx infection, especially in the susceptible genotype. Enrichment analysis showed that a large number of genes related to plant hormone signal transduction, phenylalanine metabolism, phenylpropanoid biosynthesis and starch and sucrose metabolism was responsible for sugarcane response to Lxx infection. Plant hormone signalling pathway genes were significantly differentially expressed at the early infection stage between the two genotypes. The resistant genotype chose the jasmonic acid‐ and ethylene‐dependent host‐defence pathways to resist Lxx infection, whereas the susceptible genotype preferred the salicylic acid‐dependent host‐defence pathways. These findings help unravel the molecular mechanisms of sugarcane plant–Lxx interactions and may pave the way for sugarcane breeding for disease resistance. 相似文献
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Two thiadiazole compounds promote rice defence against Xanthomonas oryzae pv. oryzae by suppressing the bacterium's production of extracellular polysaccharides 下载免费PDF全文
Xiaoyu Liang Xiaoyue Yu Wenxia Dong Shijian Guo Shu Xu Jianxin Wang Mingguo Zhou 《Molecular Plant Pathology》2015,16(8):882-892
Thiazole, isothiazole, thiadiazole, and their derivatives are used to control various human, animal and plant diseases. In addition to having direct anti‐microbial and anti‐fungal properties, these compounds are thought to induce host defences, but the mechanism of defence induction remains poorly understood. This article reports that the thiadiazoles of zinc thiazole and bismerthiazol induce H2O2 accumulation, up‐regulation of defence‐related genes, callose deposition and hypersensitive response‐like cell death in rice leaves infected with Xanthomonas oryaze pv. oryzae (Xoo) strain ZJ173, but not in non‐infected leaves. These defence responses in Xoo‐infected leaves were suppressed by the exogenous application of catalase, which reduces H2O2 accumulation. The application of extracellular polysaccharides (EPSs) extracted from strain ZJ173 significantly compromised rice defence against ZJ173 with or without thiadiazole treatment. The EPS‐deficient Xoo mutant ?gumH triggered a stronger defence than its parent strain ZJ173. The thiadiazole treatments reduced EPS production by strain ZJ173, but not by the thiadiazole‐resistant strain 2‐1‐1, which is thiadiazole resistant in vivo, but not in vitro; moreover, enhanced defence was not detected in thiadiazole‐treated rice inoculated with 2‐1‐1. Based on these data, we infer that zinc thiazole and bismerthiazol promote rice defence against Xoo by inhibiting the production of bacterial EPS. 相似文献
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An (E,E)‐α‐farnesene synthase gene of soybean has a role in defence against nematodes and is involved in synthesizing insect‐induced volatiles 下载免费PDF全文
Jingyu Lin Dan Wang Xinlu Chen Tobias G. Köllner Mitra Mazarei Hong Guo Vincent R. Pantalone Prakash Arelli Charles Neal Stewart Jr Ningning Wang Feng Chen 《Plant biotechnology journal》2017,15(4):510-519
Plant terpene synthase genes (TPSs) have roles in diverse biological processes. Here, we report the functional characterization of one member of the soybean TPS gene family, which was designated GmAFS. Recombinant GmAFS produced in Escherichia coli catalysed the formation of a sesquiterpene (E,E)‐α‐farnesene. GmAFS is closely related to (E,E)‐α‐farnesene synthase gene from apple, both phylogenetically and structurally. GmAFS was further investigated for its biological role in defence against nematodes and insects. Soybean cyst nematode (SCN) is the most important pathogen of soybean. The expression of GmAFS in a SCN‐resistant soybean was significantly induced by SCN infection compared with the control, whereas its expression in a SCN‐susceptible soybean was not changed by SCN infection. Transgenic hairy roots overexpressing GmAFS under the control of the CaMV 35S promoter were generated in an SCN‐susceptible soybean line. The transgenic lines showed significantly higher resistance to SCN, which indicates that GmAFS contributes to the resistance of soybean to SCN. In soybean leaves, the expression of GmAFS was found to be induced by Tetranychus urticae (two‐spotted spider mites). Exogenous application of methyl jasmonate to soybean plants also induced the expression of GmAFS in leaves. Using headspace collection combined with gas chromatography–mass spectrometry analysis, soybean plants that were infested with T. urticae were shown to emit a mixture of volatiles with (E,E)‐α‐farnesene as one of the most abundant constituents. In summary, this study showed that GmAFS has defence roles in both below‐ground and above‐ground organs of soybean against nematodes and insects, respectively. 相似文献
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Bernarda Calla Laureen Blahut‐Beatty Lisa Koziol Daina H. Simmonds Steven J. Clough 《Molecular Plant Pathology》2014,15(6):576-588
Sclerotinia sclerotiorum is a serious pathogen of numerous crops around the world. The major virulence factor of this pathogen is oxalic acid (OA). Mutants that cannot produce OA do not cause disease, and plants that express enzymes that degrade OA, such as oxalate oxidase (OxO), are very resistant to S. sclerotiorum. To examine the effect of OA on plants, we infiltrated soybean leaves with 5 mm OA and examined the gene expression changes at 2 h post‐infiltration. By comparing the gene expression levels between leaves of a transgenic soybean carrying an OxO gene (OxO) and its parent AC Colibri (AC) infiltrated with OA (pH 2.4) or water (pH 2.4 or 5.5), we were able to compare the effects of OA dependent or independent of its pH. Gene expression by microarray analysis identified 2390 genes that showed changes in expression, as determined using an overall F‐test P‐value cut‐off of 0.001. The additional requirement that at least one pairwise t‐test false discovery rate (FDR)‐corrected P value should be less than 0.001 reduced the list of the most highly significant differentially expressed genes to 1054. Independent of pH, OA altered the expression levels of 78 genes, with ferritin showing the strongest induction by OA. The combination of OA plus its low pH caused 1045 genes (99% of all significant genes) to be differentially expressed, with many of the up‐regulated genes being related to basal defence, such as genes of the phenylpropanoid pathway and various cytochrome P450s. RNA‐seq was also conducted on four samples: OxO and AC genotypes infiltrated with either OA pH 2.4 or water pH 2.4. The RNA‐seq analysis also identified ferritin paralogues as being strongly induced by OA. As the expression of ferritin, a gene that encodes for an iron storage protein, is induced by free iron, these results suggest that S. sclerotiorum benefits from the ability of OA to free iron from plant proteins, as this induces host cell death, and also allows the uptake and assimilation of the iron for its own metabolic needs. 相似文献
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M. Alagar S. Suresh D. Saravanakumar R. Samiyappan 《Journal of Applied Entomology》2010,134(2):123-131
Six rice genotypes showing susceptible and resistant reactions to brown planthopper (BPH), Nilaparvata lugens were studied for feeding‐induced changes in defence enzymes and pathogenesis‐related (PR) proteins. The high resistant genotypes PTB 33, ADT 45 and ASD 7 and moderately resistant genotypes CO 43 and KAU 1661 recorded the greater expression of defence enzymes peroxidase, polyphenol oxidase, phenylalanine ammonia lyase, total phenol and β‐1,3 glucanase in response to N. lugens feeding at 1 day after infestation (DAI) compared with susceptible genotype TN1. The greater activity of chitinase was observed in resistant cultivars at 3 DAI and the activity was sustained for more than 1 week compared with susceptible TN1. In conclusion, the current study revealed that these defence enzymes and PR proteins might attribute to the resistance mechanisms in rice plants against BPH infestation. 相似文献
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Mateusz Dyda Iwona Wsek Mirosaw Tyrka Maria Wdzony Magdalena Szechyska‐Hebda 《Physiologia plantarum》2019,165(4):711-727
Microdochium nivale is a fungal pathogen that causes yield losses of cereals during winter. Cold hardening under light conditions induces genotype‐dependent resistance of a plant to infection. We aim to show how photosystem II (PSII) regulation contributes to plant resistance. Using mapping population of triticale doubled haploid lines, three M. nivale strains and different infection assays, we demonstrate that plants that maintain a higher maximum quantum efficiency of PSII show less leaf damage upon infection. The fungus can establish necrotrophic or biotrophic interactions with susceptible or resistant genotypes, respectively. It is suggested that local inhibition of photosynthesis during the infection of sensitive genotypes is not balanced by a supply of energy from the tissue surrounding the infected cells as efficiently as in resistant genotypes. Thus, defence is limited, which in turn results in extensive necrotic damage. Quantitative trait loci regions, involved in the control of both PSII functioning and resistance, were located on chromosomes 4 and 6, similar to a wide range of PSII‐ and resistance‐related genes. A meta‐analysis of microarray experiments showed that the expression of genes involved in the repair and de novo assembly of PSII was maintained at a stable level. However, to establish a favourable energy balance for defence, genes encoding PSII proteins resistant to oxidative degradation were downregulated to compensate for the upregulation of defence‐related pathways. Finally, we demonstrate that the structural and functional integrity of the plant is a factor required to meet the energy demand of infected cells, photosynthesis‐dependent systemic signalling and defence responses. 相似文献
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Overexpression of a soybean salicylic acid methyltransferase gene confers resistance to soybean cyst nematode 总被引:1,自引:0,他引:1
Jingyu Lin Mitra Mazarei Nan Zhao Junwei J. Zhu Xiaofeng Zhuang Wusheng Liu Vincent R. Pantalone Prakash R. Arelli Charles N. Stewart Jr Feng Chen 《Plant biotechnology journal》2013,11(9):1135-1145
Salicylic acid plays a critical role in activating plant defence responses after pathogen attack. Salicylic acid methyltransferase (SAMT) modulates the level of salicylic acid by converting salicylic acid to methyl salicylate. Here, we report that a SAMT gene from soybean (GmSAMT1) plays a role in soybean defence against soybean cyst nematode (Heterodera glycines Ichinohe, SCN). GmSAMT1 was identified as a candidate SCN defence‐related gene in our previous analysis of soybean defence against SCN using GeneChip microarray experiments. The current study started with the isolation of the full‐length cDNAs of GmSAMT1 from a SCN‐resistant soybean line and from a SCN‐susceptible soybean line. The two cDNAs encode proteins of identical sequences. The GmSAMT1 cDNA was expressed in Escherichia coli. Using in vitro enzyme assays, E. coli‐expressed GmSAMT1 was confirmed to function as salicylic acid methyltransferase. The apparent Km value of GmSAMT1 for salicylic acid was approximately 46 μm . To determine the role of GmSAMT1 in soybean defence against SCN, transgenic hairy roots overexpressing GmSAMT1 were produced and tested for SCN resistance. Overexpression of GmSAMT1 in SCN‐susceptible backgrounds significantly reduced the development of SCN, indicating that overexpression of GmSAMT1 in the transgenic hairy root system could confer resistance to SCN. Overexpression of GmSAMT1 in transgenic hairy roots was also found to affect the expression of selected genes involved in salicylic acid biosynthesis and salicylic acid signal transduction. 相似文献
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Hao-Xun Chang Mitchell G. Roth Dechun Wang Silvia R. Cianzio David A. Lightfoot Glen L. Hartman Martin I. Chilvers 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2018,131(4):757-773