QTL mapping and epistatic interaction analysis of field resistance to sudden death syndrome (Fusarium virguliforme) in soybean

Tan, Ruijuan; Serven, Bradley; Collins, Paul J.; Zhang, Zhongnan; Zhang, Wen; Boyse, John F.; Gu, Cuihua; Chilvers, Martin I.; Diers, Brian W.; Wang, Dechun

doi:10.1007/s00122-018-3110-x

Cited by 15 publications

(11 citation statements)

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“…This resistance to SDS foliar chlorosis was also observed in a soybean variety GD2422 (Fig. 1B), which was a parent used in generating a recombinant inbred line (RIL) population with another parent,LD01-5907, which displayed susceptibility to SDS foliar chlorosis (Tan et al, 2018). These soybean RILs therefore became useful materials to test our hypothesis that SDS foliar chlorosis is controlled by a soybean S locus.…”

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confidence: 63%

“…In our study, soybean varieties carrying STAY-GREEN alleles with a loss-of-susceptibility mechanism (d1d1d2d2 genotype) exhibited interveinal necrosis, and the leaves became dehydrated and fragile in response to the phytotoxin treatment. Moreover, the parent GD2422 (d1d1d2d2 genotype) was more susceptible in SDS field trials than another parent, LD01-5907 (Tan et al, 2018), and phytotoxins decreased photosynthesis efficiency in GD2422 faster than in LD01-5907 ( Fig. 3B).…”

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confidence: 95%

“…4). It is worth noting that soybean STAY-GREEN genes were rarely detected in previous SDS resistance mapping studies (Chang et al, 2018), even when the same RIL population was screened in the fields (Tan et al, 2018). Although the environment and other factors may play an important role in field screening, a possible reason could be the method and precision in phenotyping.…”

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confidence: 97%

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Characterization of Soybean STAY-GREEN Genes in Susceptibility to Foliar Chlorosis of Sudden Death Syndrome

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Fusarium virguliforme causes sudden death syndrome (SDS) of soybean (Glycine max) in the United States. This fungal pathogen inhabits soil and produces multiple phytotoxins, which are translocated from infected roots to leaves, causing SDS foliar chlorosis and necrosis (Hartman et al., 2015). Because SDS foliar symptoms are solely induced by phytotoxins, it represents a unique pathosystem to study plant-phytotoxin interactions (Chang et al., 2016). SDS foliar symptoms typically appear near flowering through late reproductive growth stages, with chlorotic spots that gradually develop into interveinal chlorosis and necrosis (Fig. 1A). The sudden appearance of SDS foliar symptoms not only explains the origin of the disease name, but also reflects the difficulty of early detection in managing this disease. Yield reductions caused by SDS have been documented at 5% to15%, and the economic loss was estimated up to $669 million U.S. dollars in a single year (Navi and Yang, 2016). Seed treatments have been used

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Characterization of Soybean STAY-GREEN Genes in Susceptibility to Foliar Chlorosis of Sudden Death Syndrome

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“…Other evidence of SDS and SCN pleiotropy includes studies by Tan et al. (2018). This study mapped SDS resistance and found an epistatic resistance mechanism in regions overlapping with the rhg1 and Rhg4 alleles.…”

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Genetic mapping of host resistance to soybean sudden death syndrome

et al. 2022

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Soybean sudden death syndrome (SDS) is a disease caused by a soil‐borne fungus, Fusarium virguliforme. Many genetic studies have attempted to identify genes responsible for the quantitative host resistance to SDS. Three recombinant inbred line (RIL) populations were evaluated for foliar SDS resistance at a naturally infested field site in Decatur, MI, during the 2014 and 2015 growing seasons. Lines were evaluated for disease severity (DS) on a 1–9 scale, disease incidence (DI) as an estimate of the percentage of plants with symptoms per plot, and disease index (DX) as a metric which integrates DS and DI. Phenotypic data was spatially adjusted to account for uneven pathogen distribution in the naturally infested field. A subset of RILs from each population were genotyped with the SoySNP6K Illumina Infinium BeadChip. Linkage maps unique to each population were constructed using JoinMap ver. 2. Composite interval mapping was performed using WinQTLCartographer ver. 2.5. Three quantitative trait loci (QTL) were identified across 2 yr and/or multiple populations. One QTL on Chromosome 10 appeared to be colocalized with the E2 maturity locus. Another QTL identified was on Chromosome 18, in a region which has been demonstrated to provide soybean cyst nematode (SCN) and SDS resistance in many studies (rhg1/Rfs2).

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“…Epistasis, interaction between one pair of loci located in the same or different chromosomes, as an important genetic basis of complex traits [18]. Some studies had shown that epistasis signi cantly affected the expression of genes and genetic variation underlying soybean [17,[19][20][21][22][23][24]. Hou et al(2014) [20] mapped oil content QTLs using simple repeat sequence (SSR) markers derived from Charleston and Dongnong594, which detected 4 pairs oil epistatic effect QTLs, and Qi et al (2017) [12] identi ed epistatic interactions for seed oil content under multi-environments based on a high-density single-nucleotide polymorphisms (SNP) using the same population.…”

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Identification of additive and epistatic effects QTLs for seed oil content in soybean based on an integrating map of two RIL populations

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Liu²,

Wang³

et al. 2020

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Background Soybean seed oil has been widely used in human consumption and industrial production. Results In order to identify the additive and epistatic effects QTLs and QTLs by environments interactions (AE and AAE) for seed oil content in soybean, an eight-environment conjoint analysis based on two populations RIL3613 and RIL6013 with an integrating map was conducted. An new high-density integrated genetic map containing 2212 SNP markers and covering 5718.01 cM with an average distance of 2.61 cM were constructed by the combination of two linkage maps of two associated recombinant inbred line (A-RIL) populations. A total of 64 additive effect and additive × environment interaction (AE) QTL were identified on 19 chromosomes by both ICIM and IM methods, and the proportion of phenotypic variations explained (PVE) range of QTL related to oil content was 1.29–10.75%, of which 19 QTLs had overlapping marker intervals, and qOil-5-1 was identified simultaneously in both RIL populations. Compared with previous SSR positioning results, it is found 8 SNP sites within the QTL physical interval located in the SSR sites. Among them, 4 QTLs were new found. Twelve pairs of epistatic QTLs (additive × additive, AA) and QTL interactions with environments (AAE) for oil content were identified by the ICIM method, of which 3 QTLs were new found, and 2 additive effect QTLs, qOil-9-2 and qOil-15-1, linked to the other two QTLs to produce epistatic effects. A total of 5 potential candidate genes were identified based on genetic ontology and annotated information showing the relationship with seed oil content and/or fatty acid biosynthesis and metabolism. Conclusion These QTLs with different effects provide the good basis for molecular-assisted breeding of soybean oil content-related traits and further fine mapping of related genes.

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QTL mapping and epistatic interaction analysis of field resistance to sudden death syndrome (Fusarium virguliforme) in soybean

Cited by 15 publications

References 46 publications

Characterization of Soybean STAY-GREEN Genes in Susceptibility to Foliar Chlorosis of Sudden Death Syndrome

Characterization of Soybean STAY-GREEN Genes in Susceptibility to Foliar Chlorosis of Sudden Death Syndrome

Genetic mapping of host resistance to soybean sudden death syndrome

Identification of additive and epistatic effects QTLs for seed oil content in soybean based on an integrating map of two RIL populations

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