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Integrating Genetics and Genomics to Advance Soybean Research



Reference Report for LBC20180521.1
Title:Loci and candidate genes conferring resistance to soybean cyst nematode HG type 2.5.7
Authors:Xue Zhao, Weili Teng, Yinghui Li, Dongyuan Liu, Guanglu Cao, Dongmei Li, Lijuan Qiu, Hongkun Zheng, Yingpeng Han, Wenbin Li, Zixiang Wen, Ruijuan Tan, Jiazheng Yuan, Carmille Bales, Wenyan Du, Shichen Zhang, Martin I Chilvers, Cathy Schmidt, Qijian Song, Perry B Cregan, Dechun Wang
Source:BMC Genomics 2017, 18:462
Abstract:Soybean (Glycine max L. Merr.) cyst nematode (SCN, Heterodera glycines I,) is a major pest of soybean worldwide. The most effective strategy to control this pest involves the use of resistant cultivars. The aim of the present study was to investigate the genome-wide genetic architecture of resistance to SCN HG Type 2.5.7 (race 1) in landrace and elite cultivated soybeans.
A total of 200 diverse soybean accessions were screened for resistance to SCN HG Type 2.5.7 and genotyped through sequencing using the Specific Locus Amplified Fragment Sequencing (SLAF-seq) approach with a 6.14-fold average sequencing depth. A total of 33,194 SNPs were identified with minor allele frequencies (MAF) over 4%, covering 97% of all the genotypes. Genome-wide association mapping (GWAS) revealed thirteen SNPs associated with resistance to SCN HG Type 2.5.7. These SNPs were distributed on five chromosomes (Chr), including Chr7, 8, 14, 15 and 18. Four SNPs were novel resistance loci and nine SNPs were located near known QTL. A total of 30 genes were identified as candidate genes underlying SCN resistance.
A total of sixteen novel soybean accessions were identified with significant resistance to HG Type 2.5. 7. The beneficial alleles and candidate genes identified by GWAS might be valuable for improving marker-assisted breeding efficiency and exploring the molecular mechanisms underlying SCN resistance.
Title:Genome-wide association mapping of quantitative resistance to sudden death syndrome in soybean
Authors:Xue Zhao, Weili Teng, Yinghui Li, Dongyuan Liu, Guanglu Cao, Dongmei Li, Lijuan Qiu, Hongkun Zheng, Yingpeng Han, Wenbin Li, Zixiang Wen, Ruijuan Tan, Jiazheng Yuan, Carmille Bales, Wenyan Du, Shichen Zhang, Martin I Chilvers, Cathy Schmidt, Qijian Song, Perry B Cregan, Dechun Wang
Source:BMC Genomics 2014, 15:809
Abstract:Sudden death syndrome (SDS) is a serious threat to soybean production that can be managed with host plant resistance. To dissect the genetic architecture of quantitative resistance to the disease in soybean, two independent association panels of elite soybean cultivars, consisting of 392 and 300 unique accessions, respectively, were evaluated for SDS resistance in multiple environments and years. The two association panels were genotyped with 52,041 and 5,361 single nucleotide polymorphisms (SNPs), respectively. Genome-wide association mapping was carried out using a mixed linear model that accounted for population structure and cryptic relatedness.
A total of 20 loci underlying SDS resistance were identified in the two independent studies, including 7 loci localized in previously mapped QTL intervals and 13 novel loci. One strong peak of association on chromosome 18, associated with all disease assessment criteria across the two panels, spanned a physical region of 1.2 Mb around a previously cloned SDS resistance gene (GmRLK18-1) in locus Rfs2. An additional variant independently associated with SDS resistance was also found in this genomic region. Other peaks were within, or close to, sequences annotated as homologous to genes previously shown to be involved in plant disease resistance. The identified loci explained an average of 54.5% of the phenotypic variance measured by different disease assessment criteria.
This study identified multiple novel loci and refined the map locations of known loci related to SDS resistance. These insights into the genetic basis of SDS resistance can now be used to further enhance durable resistance to SDS in soybean. Additionally, the associations identified here provide a basis for further efforts to pinpoint causal variants and to clarify how the implicated genes affect SDS resistance in soybean.






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