QTL, additive and epistatic effects for SCN resistance in PI 437654

Wu, Xiaolei; Blake, Sean M.; Sleper, D. A.; Shannon, J. Grover; Cregan, Perry B.; Nguyen, Henry T.

doi:10.1007/s00122-009-0965-x

Cited by 117 publications

(165 citation statements)

References 56 publications

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“…However, we discovered the near identity of PI 437654 Rhg1 copy number and sequence to other, less broadly resistant Rhg1 low-copy soybean lines. Although Rhg1 makes one of the strongest contributions to PI 437654-derived resistance (Webb, 2012), the present finding reemphasizes the importance of identifying and cloning additional SCN resistance quantitative trait loci from PI 437654 (Wu et al, 2009). …”

Section: Discussionmentioning

confidence: 61%

Distinct Copy Number, Coding Sequence, and Locus Methylation Patterns UnderlieRhg1-Mediated Soybean Resistance to Soybean Cyst Nematode

Cook¹,

Bayless²,

et al. 2014

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Copy number variation of kilobase-scale genomic DNA segments, beyond presence/absence polymorphisms, can be an important driver of adaptive traits. Resistance to Heterodera glycines (Rhg1) is a widely utilized quantitative trait locus that makes the strongest known contribution to resistance against soybean cyst nematode (SCN), Heterodera glycines, the most damaging pathogen of soybean (Glycine max). Rhg1 was recently discovered to be a complex locus at which resistance-conferring haplotypes carry up to 10 tandem repeat copies of a 31-kb DNA segment, and three disparate genes present on each repeat contribute to SCN resistance. Here, we use whole-genome sequencing, fiber-FISH (fluorescence in situ hybridization), and other methods to discover the genetic variation at Rhg1 across 41 diverse soybean accessions. Based on copy number variation, transcript abundance, nucleic acid polymorphisms, and differentially methylated DNA regions, we find that SCN resistance is associated with multicopy Rhg1 haplotypes that form two distinct groups. The tested high-copy-number Rhg1 accessions, including plant introduction (PI) 88788, contain a flexible number of copies (seven to 10) of the 31-kb Rhg1 repeat. The identified low-copy-number Rhg1 group, including PI 548402 (Peking) and PI 437654, contains three copies of the Rhg1 repeat and a newly identified allele of Glyma18g02590 (a predicted α-SNAP [α-soluble N-ethylmaleimide–sensitive factor attachment protein]). There is strong evidence for a shared origin of the two resistance-conferring multicopy Rhg1 groups and subsequent independent evolution. Differentially methylated DNA regions also were identified within Rhg1 that correlate with SCN resistance. These data provide insights into copy number variation of multigene segments, using as the example a disease resistance trait of high economic importance.

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Section: Discussionmentioning

confidence: 61%

Distinct Copy Number, Coding Sequence, and Locus Methylation Patterns UnderlieRhg1-Mediated Soybean Resistance to Soybean Cyst Nematode

Cook¹,

Bayless²,

et al. 2014

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“…Yu et al (2016) showed that rhg1-a alone may confer some level of resistance in crosses using PI 437654, a PI with a similar copy number (three copies) to that in cv Forrest. PI 437654 has a similar epistatic relationship between rhg1 and Rhg4 in conferring resistance to SCN (Wu et al, 2009). Unlike cv Forrest, PI 437654 is resistant to multiple SCN HG types, and although its resistance is poorly understood, it likely involves other unknown loci in addition to rhg1 and Rhg4.…”

Section: Discussionmentioning

confidence: 99%

Systematic Mutagenesis of Serine Hydroxymethyltransferase Reveals an Essential Role in Nematode Resistance

et al. 2017

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Rhg4 is a major genetic locus that contributes to soybean cyst nematode (SCN) resistance in the Peking-type resistance of soybean (Glycine max), which also requires the rhg1 gene. By map-based cloning and functional genomic approaches, we previously showed that the Rhg4 gene encodes a predicted cytosolic serine hydroxymethyltransferase (GmSHMT08); however, the novel gain of function of GmSHMT08 in SCN resistance remains to be characterized. Using a forward genetic screen, we identified an allelic series of GmSHMT08 mutants that shed new light on the mechanistic aspects of GmSHMT08-mediated resistance. The new mutants provide compelling genetic evidence that Peking-type rhg1 resistance in cv Forrest is fully dependent on the GmSHMT08 gene and demonstrates that this resistance is mechanistically different from the PI 88788-type of resistance that only requires rhg1. We also demonstrated that rhg1-a from cv Forrest, although required, does not exert selection pressure on the nematode to shift from HG type 7, which further validates the bigenic nature of this resistance. Mapping of the identified mutations onto the SHMT structural model uncovered key residues for structural stability, ligand binding, enzyme activity, and protein interactions, suggesting that GmSHMT08 has additional functions aside from its main enzymatic role in SCN resistance. Lastly, we demonstrate the functionality of the GmSHMT08 SCN resistance gene in a transgenic soybean plant.

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“…In contrast to the mapping of only two QTL from PI 88788, many resistance QTL have been mapped from PI 437654 (Webb et al, 1995;Wu et al, 2009). This may explain why PI 437654 is resistant to more HG (Heterodera glycines Ichinohe) types than PI 88788 (Anand et al, 1988;Diers et al, 1997;Niblack et al, 2002).…”

mentioning

confidence: 99%

Stacking Resistance Alleles from Wild and Domestic Soybean Sources Improves Soybean Cyst Nematode Resistance

et al. 2011

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The soybean cyst nematode (SCN; Heterodera glycines Ichinohe) is the most economically important soybean [Glycine max (L.) Merr.] pathogen in the United States. Field SCN populations are adapting to the narrowly based SCN resistance currently deployed in soybean cultivars. The objective of our research was to measure the effects of combinations of SCN resistance genes or quantitative trait loci (QTL) from the wild soybean (Glycine soja Siebold & Zucc.) PI 468916 and the domesticated soybean accessions PI 88788 and PI 437654. Two populations were developed to test the combinations of QTL and genes. Both populations segregated for the G. soja resistance QTL cqSCN‐006 and cqSCN‐007. Population 1 also segregated for resistance from PI 88788 and Population 2 segregated for resistance from PI 437654. The populations were tested for resistance to three SCN isolates in a greenhouse and with single nucleotide polymorphism (SNP) and simple sequence repeat (SSR) markers. In both populations, the two G. soja resistance alleles significantly increased SCN resistance compared with the alternative alleles. The SCN resistance alleles rhg1 and Rhg4 from PI 437654 and rhg1‐b from PI 88788 also significantly increased resistance compared with the alternative alleles. The two G. soja QTL alleles significantly enhanced the resistance derived from PI 88788. These results show that SCN resistance can be increased through stacking genes and QTL from multiple resistance sources.

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QTL, additive and epistatic effects for SCN resistance in PI 437654

Cited by 117 publications

References 56 publications

Distinct Copy Number, Coding Sequence, and Locus Methylation Patterns UnderlieRhg1-Mediated Soybean Resistance to Soybean Cyst Nematode

Distinct Copy Number, Coding Sequence, and Locus Methylation Patterns UnderlieRhg1-Mediated Soybean Resistance to Soybean Cyst Nematode

Systematic Mutagenesis of Serine Hydroxymethyltransferase Reveals an Essential Role in Nematode Resistance

Stacking Resistance Alleles from Wild and Domestic Soybean Sources Improves Soybean Cyst Nematode Resistance

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