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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #322509

Title: A SNARE-like protein and biotin are implicated in soybean cyst nematode virulence

Author
item BEKAL, SADIA - University Of Illinois
item Domier, Leslie
item GONFA, BIRUK - University Of Illinois
item LAKHSSASSI, NAOUFAL - University Of Illinois
item MEKSEM, KHALID - University Of Illinois
item LAMBERT, KRIS - University Of Illinois

Submitted to: PLOS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/15/2015
Publication Date: 12/29/2015
Citation: Bekal, S., Domier, L.L., Gonfa, B., Lakhssassi, N., Meksem, K., Lambert, K.N. 2015. A SNARE-like protein and biotin are implicated in soybean cyst nematode virulence. PLoS One. doi: 10.1371/journal.pone.0145601.

Interpretive Summary: Soybean cyst nematode (SCN), one of the most damaging pests of soybean, is estimated to cause millions of dollars in crop losses in the United States each year. Plant breeders have produced soybean lines that are highly resistant to many SCN populations. However, some SCN populations can infect and reproduce on SCN-resistant soybean varieties. Such nematode populations are referred to as virulent and the mechanisms they use to evade or suppress host plant defenses are not well understood. Here, we used a genetic strategy to identify regions on SCN chromosomes associated with the ability of virulent nematodes to overcome the most widely used soybean genes for SCN resistance. One of the chromosomal regions contained a gene predicted to express a bacterial-like protein that we showed was excreted into host plants during infection. The nematode protein interacted with the product of one of the soybean SCN resistance genes, and the numbers of the SCN gene were reduced in virulent SCN populations. Collectively, our data suggest that virulent nematode populations overcome SCN resistance by reducing the number of copies of the gene encoding a bacterial-like protein that directly interacts with the product of a soybean resistance gene. This data will be useful to scientist who are interested in developing new SCN resistant soybean varieties and understanding the mechanisms of pathogenesis by plant parasitic nematodes.

Technical Abstract: Some phytoparasitic nematodes have the ability to infect and reproduce on plants that are normally considered resistant to nematode infection. Such nematodes are referred to as virulent and the mechanisms they use to evade or suppress host plant defenses are not well understood. Here, we report the use of a genetic strategy, allelic imbalance analysis, to associate single nucleotide polymorphisms (SNPs) with nematode virulence on the most common source of resistance used to control Heterodera glycines, the soybean cyst nematode (SCN). To accomplish this analysis, a custom SCN SNP array was developed and used to genotype SCN F3-derived populations growing on resistant and susceptible soybean plants. Three SNPs reproducibly showed SNP allele imbalances between nematodes grown on resistant and susceptible plants. Two candidate SCN virulence genes that were tightly linked to the SNPs were identified. One SCN gene encoded a biotin synthase (HgBioB) and the other encoded a bacterial-like protein containing a putative SNARE domain (HgSLP-1). The two genes mapped to two different linkage groups. Both genes contained sequence polymorphisms between avirulent and virulent nematodes. In addition, the HgSLP-1 gene was reduced in copy number in virulent nematode populations. The gene encoding HgSLP-1 appeared to produce multiple forms of the protein via intron retention and alternative splicing, but was also part of a gene family. HgSLP-1 encodes an esophageal-gland protein that is secreted by the nematode during plant parasitism. In bacterial co-expression experiments, HgSLP-1 co-purified with the Rhg1-SNAP protein, suggesting this nematode protein binds to this SCN resistance protein. Collectively our data suggest that multiple SCN genes are involved in SCN virulence and that HgSLP-1 may function as an avirulence protein and its absence may be used to evade detection of host defenses.