Two Decades of Molecular Marker‐Assisted Breeding for Resistance to Soybean Sudden Death Syndrome

Lightfoot, David A.

doi:10.2135/cropsci2014.10.0721

Cited by 18 publications

(22 citation statements)

References 133 publications

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“…Soybean sudden death syndrome (SDS), which is caused by a soilborne fungus F. virguliforme , is responsible for annual losses around US$190 million [ 18 ]. Breeding for SDS resistance is difficult because the interaction between F. virguliforme and soybean is quantitative [ 19 ]. Instead, it has been suggested that transgenic approaches may be suitable to manage SDS, and transgenic soybeans expressing exogenous toxin-specific antibody has been shown to reduce SDS foliar symptoms [ 18 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Genomic characterization of plant cell wall degrading enzymes and in silico analysis of xylanses and polygalacturonases of Fusarium virguliforme

et al. 2016

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BackgroundPlant cell wall degrading enzymes (PCWDEs) are a subset of carbohydrate-active enzymes (CAZy) produced by plant pathogens to degrade plant cell walls. To counteract PCWDEs, plants release PCWDEs inhibitor proteins (PIPs) to reduce their impact. Several transgenic plants expressing exogenous PIPs that interact with fungal glycoside hydrolase (GH)11-type xylanases or GH28-type polygalacturonase (PG) have been shown to enhance disease resistance. However, many plant pathogenic Fusarium species were reported to escape PIPs inhibition. Fusarium virguliforme is a soilborne pathogen that causes soybean sudden death syndrome (SDS). Although the genome of F. virguliforme was sequenced, there were limited studies focused on the PCWDEs of F. virguliforme. Our goal was to understand the genomic CAZy structure of F. viguliforme, and determine if exogenous PIPs could be theoretically used in soybean to enhance resistance against F. virguliforme.ResultsF. virguliforme produces diverse CAZy to degrade cellulose and pectin, similar to other necrotorphic and hemibiotrophic plant pathogenic fungi. However, some common CAZy of plant pathogenic fungi that catalyze hemicellulose, such as GH29, GH30, GH44, GH54, GH62, and GH67, were deficient in F. virguliforme. While the absence of these CAZy families might be complemented by other hemicellulases, F. virguliforme contained unique families including GH131, polysaccharide lyase (PL) 9, PL20, and PL22 that were not reported in other plant pathogenic fungi or oomycetes. Sequence analysis revealed two GH11 xylanases of F. virguliforme, FvXyn11A and FvXyn11B, have conserved residues that allow xylanase inhibitor protein I (XIP-I) binding. Structural modeling suggested that FvXyn11A and FvXyn11B could be blocked by XIP-I that serves as good candidate for developing transgenic soybeans. In contrast, one GH28 PG, FvPG2, contains an amino acid substitution that is potentially incompatible with the bean polygalacturonase-inhibitor protein II (PvPGIP2).ConclusionsIdentification and annotation of CAZy provided advanced understanding of genomic composition of PCWDEs in F. virguliforme. Sequence and structural analyses of FvXyn11A and FvXyn11B suggested both xylanases were conserved in residues that allow XIP-I inhibition, and expression of both xylanases were detected during soybean roots infection. We postulate that a transgenic soybean expressing wheat XIP-I may be useful for developing root rot resistance to F. virguliforme.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-016-0761-0) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Genomic characterization of plant cell wall degrading enzymes and in silico analysis of xylanses and polygalacturonases of Fusarium virguliforme

et al. 2016

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“…These include dip inoculation of sprouted seed in F. virguliforme spore suspension and planting in greenhouse mix [80,81,85], temperature-controlled water bath method [38], exposing cut stem to cell free culture filtrate [42], molecular marker-assisted breeding for resistance [60], toothpick inoculation and soil infestation methods [111], planting seeds in a mixture of 1 part inoculum with 20 part soil [64], using cones filled with steam-treated soil mix (2:1 sand: soil) and topped with 3 g of fungus infested white sorghum grains [25]. Navi and Yang (unpublished), modified greenhouse screening technique [80,81,85] to identify resistance sources in germplasm and explore efficacy tests of seed treatments with biocontrol agents (BCA) and or chemicals against SDS (Fig.…”

Section: Resistance Screening In Greenhouse Conditionsmentioning

confidence: 99%

Sudden death syndrome - a growing threat of losses in soybeans.

Navi¹,

Yang²

2016

CABI Reviews

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Sudden death syndrome (SDS) caused by Fusarium virguliforme is one of the major yield-limiting soil borne diseases of soybean (Glycine max). The SDS has been reported from 21 U.S. states and is known to occur in Africa, North America, and South America. In the U.S. the losses due to SDS was estimated at $3.06 billion for a period from 1988 to 2010. Since 1983, several management approaches have been investigated to reduce SDS and yet, continued efforts are necessary to develop long term disease management programs and to sustain disease below economic threshold levels. Integrating available control measures is an option, but adaptability and real-world assessments are equally important. Support of several funding agencies to better understand the disease in identifying suitable control measures to reduce yield losses in commercial cultivations has been indispensable in accomplishing these goals. In spite of sustained efforts, SDS continued to spread within the U.S. and reported in seven other countries since its first report in 1971.Comprehensive reviews have previously been published on this disease by Roy et al. [98], Leandro et al. [58], and Hartman et al. [32]. In this review, updated information on geographic distribution and economic significance of SDS, epidemiology, factors affecting SDS, and management options for SDS including screening techniques have been compiled. Also, discussed significant gaps in use of plant, fungi and bacteria based biocontrol agents in addressing management of SDS.Keywords: Soybean sudden death syndrome, SDS, Fusarium virguliforme, biocontrol, global reports, yield losses due to SDS, epidemiological factors, greenhouse and field screening. ______________________________________________________________________________This is a manuscript of an article from CAB Reviews 11 (2016): 039, doi: 10.1079/PAVSNNR201611039. Navi, S. S.; Yang, X. B. 2016. Sudden death syndrome -a growing threat of losses in soybeans. CAB International, Wallingford, UK. Aoki et al., and F. virguliforme,90] is an economically significant soil-borne disease, and a risk to many soybean production areas worldwide. The disease was first observed by H.J. Walters in Arkansas, United States in 1971[100], but it was only in 1983 that the disease was named as sudden death syndrome (SDS) of unknown etiology [40]. As of this review, the disease has been reported in three continents, North America (Canada and United States), South America (Argentina, Bolivia, Brazil, Paraguay, and Uruguay), and Africa (South Africa), and within the United States 21 states (Fig. 1) Whether the pathogens causing SDS have been introduced in to new regions or if they have been present in the soil in production fields of these countries for some time without being detected is unknown. After the SDS was detected in Iowa [150], Scherm and Yang [114] developed a risk assessment model to determine potential geographic range of development of this disease, which was considered a southern disease by then, in North America. They predi...

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“…Losses to SCN have been reduced by almost half since 1990, but it still remains a major problem in soybean (Lightfoot, 2015). SCN causes plant and root stunting and leaf chlorosis.…”

Section: Introductionmentioning

confidence: 99%

“…Sudden death syndrome (SDS) has been shown to be a facultative hemibiotrophic fungus (Li, 2009;Roy, 1997) that causes yield loss in soybean. The amount of loss has doubled every decade in the US, since 1990 (Wrather, 2001;Lightfoot, 2015). SDS, as a syndrome, is disease complex of both a root rot and a leaf scorch.…”

Section: Introductionmentioning

confidence: 99%

Annotation of Cultivar Variations at the Multigeneic Rhg1/Rfs2 Locus:

Hemmati

Geisler²,

Meksem³

et al. 2017

AJB

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Soybean (Glycine max (L.) Merr.) suffers yield loss due to root infection from soil infestation by Heterodera glycine I. (soybean cyst nematode SCN) and Fusarium virguliforme (Aoki; sudden death syndrome (SDS)). The major locus for SCN and SDS resistance has previously been identified as Rhg1/Rfs2 (chr18; LG G) (site reference). The objective of this experiment was to compare the Sanger DNA sequence of a resistant cultivar ('Forrest') and two susceptible cultivars ('Williams 82' and 'Asgrow A3244'). Sequences were downloaded from GenBank for Williams 82, Phytzome for A3244 and a newly sequenced BAC-B73P06 (82,157 bp) encompassing the Rfs2/Rhg1 locus. Using the resistant cultivars, 800 single nucleotide polymorphisms (SNPs) and 57 indels were identified. In contrast, the susceptible cultivars had just 12 SNPs and no indels between them. Polymorphisms were clustered within 59 kbp, divided into three sections. There were 5 predicted recombination breakpoints. The third and fourth breakpoints were located before gene 3 and after gene 5 (Glyma18g02680; the RLK at Rhg1/Rfs2) which were therefore inferred to be derived from Peking, within the Rhg1/Rfs2 region. Comparisons of SNPs identified in Illumina sequences from 31 semi-domesticated genomes showed 80% of the total SNPs in Forrest were found among the genomes. Annotation and gene prediction showed the BAC gene prediction encoded 9-10 genes. There were 31 SNPs within exons and 137 among introns. Just 11 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.SNPs caused amino acid changes. There were 5 SNPs in cis regulatory elements (CREs) and 14 in promoters. Polymorphisms indicated the regions that were introgressed from Peking had defined limits. Proteins across the region were highly conserved compared to non-coding regions, suggesting purifying selection occurred.

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Two Decades of Molecular Marker‐Assisted Breeding for Resistance to Soybean Sudden Death Syndrome

Cited by 18 publications

References 133 publications

Genomic characterization of plant cell wall degrading enzymes and in silico analysis of xylanses and polygalacturonases of Fusarium virguliforme

Genomic characterization of plant cell wall degrading enzymes and in silico analysis of xylanses and polygalacturonases of Fusarium virguliforme

Sudden death syndrome - a growing threat of losses in soybeans.

Annotation of Cultivar Variations at the Multigeneic Rhg1/Rfs2 Locus:

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