Disease resistance through impairment of α-SNAP–NSF interaction and vesicular trafficking by soybean
            <i>Rhg1</i>

Bayless, Adam M.; Smith, John L.; Song, Junqi; McMinn, Patrick H.; Teillet, Alice; August, Benjamin K.; Bent, Andrew F.

doi:10.1073/pnas.1610150113

Cited by 72 publications

(167 citation statements)

References 55 publications

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“…It has been reported that the interaction of two or more alleles (epistasis) plays a major role in an organism's resistance to diseases and pests (Bayless et al ., ; Meksem et al ., ; Nagel, ). The rhg1 GmSNAP18 protein interacts with NSF (N‐ethylmaleimide–sensitive factor) protein and disturbs vesicle trafficking (Bayless et al ., , ). We discovered that soybean germplasm provided a wide range of SCN resistance controlled by natural variants (SNP and CNV) at both the rhg1 and Rhg4 loci.…”

Section: Discussionmentioning

confidence: 98%

Whole‐genome re‐sequencing reveals the impact of the interaction of copy number variants of the rhg1 and Rhg4 genes on broad‐based resistance to soybean cyst nematode

Patil

Lakhssassi

Wan

et al. 2019

Plant Biotechnology Journal

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Summary Soybean cyst nematode ( SCN ) is the most devastating plant‐parasitic nematode. Most commercial soybean varieties with SCN resistance are derived from PI 88788. Resistance derived from PI 88788 is breaking down due to narrow genetic background and SCN population shift. PI 88788 requires mainly the rhg1‐b locus, while ‘Peking’ requires rhg1‐a and Rhg4 for SCN resistance. In the present study, whole genome re‐sequencing of 106 soybean lines was used to define the Rhg haplotypes and investigate their responses to the SCN HG ‐Types. The analysis showed a comprehensive profile of SNP s and copy number variations ( CNV ) at these loci. CNV of rhg1 (Gm SNAP 18) only contributed towards resistance in lines derived from PI 88788 and ‘Cloud’. At least 5.6 copies of the PI 88788‐type rhg1 were required to confer SCN resistance, regardless of the Rhg4 ( Gm SHMT 08 ) haplotype. However, when the Gm SNAP 18 copies dropped below 5.6, a ‘Peking’‐type Gm SHMT 08 haplotype was required to ensure SCN resistance. This points to a novel mechanism of epistasis between Gm SNAP 18 and Gm SHMT 08 involving minimum requirements for copy number. The presence of more Rhg4 copies confers resistance to multiple SCN races. Moreover, transcript abundance of the Gm SHMT 08 in root tissue correlates with more copies of the Rhg4 locus, reinforcing SCN resistance. Finally, haplotype analysis of the Gm SHMT 08 and Gm SNAP 18 promoters inferred additional levels of the resistance mechanism. This is the first report revealing the genetic basis of broad‐based resistance to SCN and providing new insight into epistasis, haplotype‐compatibility, CNV , promoter variation and its impact on broad‐based disease resistance in plants.

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Section: Discussionmentioning

confidence: 98%

Whole‐genome re‐sequencing reveals the impact of the interaction of copy number variants of the rhg1 and Rhg4 genes on broad‐based resistance to soybean cyst nematode

Patil

Lakhssassi

Wan

et al. 2019

Plant Biotechnology Journal

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“…A recent report suggests that the rhg1 a-SNAP confers resistance by cytotoxic effects of the large-scale accumulation of the aberrant a-SNAP protein at the nematode feeding sites, which disrupts SNARE complexes and vesicle trafficking (Bayless et al, 2016). How GmSHMT08 conditions this process is not clear.…”

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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“…However, the molecular mechanisms of how SNAP proteins mediate SCN resistance remain unclear. Recently, it has been described that elevated expression of resistance-type Rhg1 α-SNAP negatively affected the abundance of SNARE-recycling 20 S complexes, disrupting vesicle trafficking, and induced elevated abundance of NSF causing cytotoxicity27. However, expression of other loci encoding a canonical wild-type α-SNAPs counteracted the cytotoxicity of resistance-type Rhg1 α-SNAP27.…”

mentioning

confidence: 99%

“…Recently, it has been described that elevated expression of resistance-type Rhg1 α-SNAP negatively affected the abundance of SNARE-recycling 20 S complexes, disrupting vesicle trafficking, and induced elevated abundance of NSF causing cytotoxicity27. However, expression of other loci encoding a canonical wild-type α-SNAPs counteracted the cytotoxicity of resistance-type Rhg1 α-SNAP27. Furthermore, a SCN gene encoding a bacterial-like protein containing a putative SNARE domain (HgSLP-1), an esophageal-gland protein that is secreted by the nematode during plant parasitism, has been suggested to physically interact with the Rhg1 α-SNAP in SCN resistance28.…”

mentioning

confidence: 99%

Characterization of the Soluble NSF Attachment Protein gene family identifies two members involved in additive resistance to a plant pathogen

Lakhssassi

Liu

Bekal

et al. 2017

Sci Rep

113

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Proteins with Tetratricopeptide-repeat (TPR) domains are encoded by large gene families and distributed in all plant lineages. In this study, the Soluble NSF-Attachment Protein (SNAP) subfamily of TPR containing proteins is characterized. In soybean, five members constitute the SNAP gene family: GmSNAP18, GmSNAP11, GmSNAP14, GmSNAP02, and GmSNAP09. Recently, GmSNAP18 has been reported to mediate resistance to soybean cyst nematode (SCN). Using a population of recombinant inbred lines from resistant and susceptible parents, the divergence of the SNAP gene family is analysed over time. Phylogenetic analysis of SNAP genes from 22 diverse plant species showed that SNAPs were distributed in six monophyletic clades corresponding to the major plant lineages. Conservation of the four TPR motifs in all species, including ancestral lineages, supports the hypothesis that SNAPs were duplicated and derived from a common ancestor and unique gene still present in chlorophytic algae. Syntenic analysis of regions harbouring GmSNAP genes in soybean reveals that this family expanded from segmental and tandem duplications following a tetraploidization event. qRT-PCR analysis of GmSNAPs indicates a co-regulation following SCN infection. Finally, genetic analysis demonstrates that GmSNAP11 contributes to an additive resistance to SCN. Thus, GmSNAP11 is identified as a novel minor gene conferring resistance to SCN.

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Disease resistance through impairment of α-SNAP–NSF interaction and vesicular trafficking by soybean Rhg1

Cited by 72 publications

References 55 publications

Whole‐genome re‐sequencing reveals the impact of the interaction of copy number variants of the rhg1 and Rhg4 genes on broad‐based resistance to soybean cyst nematode

Whole‐genome re‐sequencing reveals the impact of the interaction of copy number variants of the rhg1 and Rhg4 genes on broad‐based resistance to soybean cyst nematode

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

Characterization of the Soluble NSF Attachment Protein gene family identifies two members involved in additive resistance to a plant pathogen

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