Developing novel soybean lines with resistance to viral diseases
Principal Investigator: Aiming Wang
Research Institution: University of Western Ontario / Agriculture and Agri-Food Canada (AAFC)
Timeline: January 2014 – December 2016
- Generate a soybean mutant population through ethyl methanesulfonate (EMS, a chemical mutagenic chemical).
- Screen for mutants resistant to soybean mosaic virus (SMV) and related soybean viruses.
- Determine the genetics and molecular mechanisms of resistance of identified mutants and introduce identified mutants to breeding programs.
- The advancement of knowledge in soybean mosaic virus (SMV)-soybean interactions may lead to soybean cultivars with improved resistance to SMV.
- The development of novel genetic resistance to SMV will allow farmers to incorporate SMV resistant soybean to their cropping rotations, reducing their yield losses to SMV and rejections of crop in the food-grade market.
- The development of new SMV resistance sources for breeding programs will allow breeders to incorporate SMV-resistance into more soybean cultivars and increase the availability of SMV-resistant commercial varieties.
Viral pathogens infect soybean wherever it is grown in the world. Viral diseases have a significant impact on yield, quality and marketability of soybeans. The incidence of a particular viral disease may vary dependent on regions and years. There are nearly 70 viral pathogens that can infect soybean; soybean mosaic virus (SMV) is the most prevalent one that impedes soybean production. The virus is seed-borne and infection is transmitted by aphids. The SMV infection results in mosaic mottling, chlorosis and roughness in leaves, mottling of the seed, and severe reductions in plant growth and seed quality. SMV not only causes severe yield losses of infected soybean plants but also increases their susceptibility to other pathogens. Moreover, SMV mottling makes seed unacceptable for many of the food-grade markets. The introduction and establishment of soybean aphids in North America in 2001 greatly increased the impact of SMV. Current genetic resistance was found to be very fragile and it can be easily overcome by SMV isolates. New durable genetic resistance is highly demanded to protect soybean production from possible catastrophic SMV outbreaks.
To develop genetic resistance to SMV, a soybean mutant population consisting of approximately 5,000 lines for screening for novel genetic resistance to SMV was generated in this project. Subsequently, large-scale screening revealed nine mutant lines that are resistant/tolerant to SMV and two lines showing hypersensitive response (HR). Five lines showed resistance/tolerance with segregation to SMV in the M4 generation. A comparative genome analysis through next generation sequencing revealed a large number of mutations in the mutant lines. Current data also suggest that SMV resistance/tolerance in the mutant lines is controlled by multiple genes.
Mutagenesis is an effective approach for the generation of novel heritable resistance/tolerance to SMV. The resistance/tolerance phenotype is apparently controlled by multiple genes. Our future work (if funding allows) is to test M5 and M6 generations until the resistance/tolerance phenotype is stabilized. Then crossing and selfing will be carried out and the resulting progeny will be assessed for SMV resistance/tolerance. These experiments will allow us to confirm that the resistance/tolerance phenotype is controlled by recessive genes and evaluate how many genes are involved.
Project Related Publications:
Chen, H., Arsovski, AA., Yu, K., Wang, A. 2016. Deep sequencing leads to the identification of eukaryotic translation initiation factor 5a as a key element in Rsv1-mediated lethal systemic hypersensitive response to soybean mosaic virus infection in soybean. Molecular Plant Pathology DOI: 10.1111/mpp.12407
Chen, H., Arsovski, AA., Yu, K., Wang, A. 2016. Genome-wide investigation using sRNA-seq, degradome-seq and transcriptome-seq reveals regulatory networks of microRNAs and their target genes in soybean during soybean mosaic virus infection. PLoS ONE 11(3): e0150582
Cheng, X., Wang, A. 2016. The potyviral silencing suppressor protein VPg mediates degradation of SGS3 via ubiquitination and autophagy pathways. Journal of Virology doi: 10.1128/JVI.01478-16
Li, Y., Cui, H., Cui, X., Wang, A. 2016. The altered photosynthetic machinery during compatible virus infection. Current Opinion in Virology 17: 19-24. (Review)
Wang, A. 2015. Dissecting the molecular network of virus-plant interactions: the complex roles of host factors. Annual Review of Phytopathology 53: 45-66. (Review)
Chen, H., Zhang, L., Yu, K., and Wang, A. 2015. Pathogenesis of soybean mosaic virus in soybean carrying Rsv1 gene is associated with miRNA and siRNA pathways, and breakdown of AGO1 homeostasis. Virology 476: 395-404.