|Matsye, P -|
|Lawrence, G -|
|Youssef, Reham -|
|Kim, Kyung-Hwan -|
|Klink, V -|
Submitted to: Plant Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 17, 2012
Publication Date: June 12, 2012
Citation: Matsye, P.D., Lawrence, G.W., Youssef, R., Kim, K., Matthews, B.F., Klink, V.P. 2012. Functional analysis of a naturally occurring mutant of an alpha soluble NSF attachment protein gene residing within the RHG1 locus. Plant Molecular Biology. 79:1-25. Interpretive Summary: Soybean is one of the top five agricultural products in the United States with an estimated production of 3.36 billion bushels in 2009. The soybean cyst nematode (SCN) is the major pathogen of soybean in the United States. One section of the soybean genome, called rhg1, gives partial resistance to the soybean cyst nematode (SCN). We identified a small, but important, difference in how a gene in this region is expressed in resistant soybean as compared to susceptible soybean. When the DNA sequence found in resistant soybean is transferred into susceptible soybean, the soybean provides an increase in resistance to SCN. This is now a "candidate gene" for further testing to help develop soybean with broad resistance to SCN.
Technical Abstract: rhg1, defined within a 67 kb region of DNA on chromosome 18, is a major quantitative trait locus (QTL) in Glycine max (soybean) providing defense to the soybean cyst nematode (Heterodera glycines). Transcriptional mapping experiments identified an alpha soluble NSF attachment protein (alpha-SNAP) within the rhg1 locus being expressed specifically during defense. Sequencing the alpha-SNAP cDNA from the resistant G. max[Peking/PI 548402] revealed it has an additional 17 nucleotides of sequence containing an in-frame premature stop codon caused by a G-A transition that does not exist in the susceptible alpha-SNAP from G. max[Williams 82/PI 518671]. Sequencing genomic DNA confirmed that both G. max[Williams 82/PI 518671] and G. max[Peking/PI 548402] have the 17 nt stretch of polynucleotide sequence. Thus, the added mRNA sequence was due to altered splicing. A G-T transversion at genomic position 2,882 in alpha-SNAP[Peking/PI 548402] that is upstream from the premature stop codon, eliminated the function of an intron splice site. The altered alpha-SNAP[Peking/PI 548402] allele was also found in the resistant genotype G. max[PI 437654], but not other G. max genotypes that exhibit resistance to H. glycines. Expression of the alpha-SNAP[Peking/PI 548402] allele in the susceptible genotype G. max[Williams 82/PI 518671] resulted in an altered capability of H. glycines to infect G. max. The results suggest a role of the vesicular transport machinery in regulating the interaction between G. max by H. glycines.