Genome-wide identification of SNPs related to resistance to soybean stem canker caused by Diaporthe caulivora
摘要
Stem canker caused by Diaporthe caulivora (syn. D. phaseolorum var. caulivora) was first reported in North America in the mid-20th century and is referred to as northern stem canker. Since it was reported in Uruguay in 2013, it is considered one of the most important diseases in the crop, causing up to 24% yield losses. To date, only two single nucleotide polymorphisms (SNPs) and one resistance locus, Rdc1, have been reported in soybean, but the genomic location of Rdc1 remains unknown. To investigate the genetic basis of resistance to Diaporthe caulivora, we conducted a genome-wide association study (GWAS) using a diverse panel of 318 soybean accessions from China, the United States, Argentina, and Uruguay.
Phenotyping was conducted under controlled and field conditions. In the growth chamber, plants were inoculated using the stem wounding method, and lesion length and survival days were recorded for 12 days. Field evaluations were based on natural infection at the R5–R6 stage over two years and two sowing dates. Genotyping was performed with the BARCSoySNP6K chip and GWAS was performed using GAPIT.
ResultsFive loci were identified significantly associated with resistance: qDc11, qDc13, qDc14, qDc15, and qDc18, explaining 6.1%, 17.7%, 8.5%, 11.8%, and 7.7% of the phenotypic variance, respectively. Among these, qDc13 had the lowest p-value. The strongest candidate gene in this region is Glyma.13G092200, which encodes a TIR-NBS-LRR disease resistance protein. Its domains (NB-ARC, P-loop NTPase, ADP binding) support a functional role in resistance. Upstream (~ 240 kb), Glyma.13G094100 and Glyma.13G094200 encode PR-1 proteins, while the neighboring Glyma.13G093300 encodes a glutamate receptor, suggesting the presence of a local defense-related gene cluster.
ConclusionsA polygenic, quantitative genetic architecture of Diaporthe caulivora resistance was found and characterized. Several candidate genes associated with disease response were identified. Future research should aim to fine-map these loci to confirm their functional relevance and enable their integration into resistance breeding strategies.