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Gma-miR398c/d negatively regulates soybean resistance to Soybean mosaic virus by targeting SOD family genes
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DOI:10.1016/j.cj.2025.07.003.png)
Abstract
En 中文
Soybean mosaic virus (SMV) poses a substantial threat to the yield and quality of soybean (Glycine max (L.) Merr.), leading to significant economic losses in soybean production. However, the mining of SMV-resistance loci and the exploration of the underlying disease resistance mechanisms remain relatively limited. MicroRNAs (miRNAs) are a class of post-transcriptional regulators that play a pivotal role in modulating plant growth, development and responding to various stresses. In this study, we demonstrated the function of the “miR398c/d-GmCSDs” module between soybean resistant and susceptible varieties, focusing on its differential regulatory roles in SMV infection. Specifically, SMV infection downregulated gma-miR398c/d expression in the resistant variety (Qihuang 1, QH), while upregulated them in the susceptible variety (Nannong 1138-2, NN). Transient expression assay in N. benthamiana confirmed that gma-miR398c/d can target six superoxide dismutase (SOD) family genes, which responded to SMV infection in both varieties. Stable overexpression of Gma-MIR398c/d in soybean or inhibition of the corresponding target genes’ expression via Bean pod mottle virus (BPMV)-induced gene silencing (VIGS) led to reduced H2O2 content and thereby promoted SMV infection. Conversely, plants overexpressing the target genes exhibited the opposite phenotypes. The functions of gma-miR398c/d and their target genes were further validated in N. benthamiana through transient co-expression with SMV infectious clone (pSC7-GFP), indicating that gma-miR398c/d negatively regulated soybean resistance to SMV, while the target genes positively contributed to disease resistance. Collectively, our findings provide novel insights into the regulatory mechanisms underlying soybean resistance to SMV.
Keywords:
Soybean
Soybean mosaic virus
MiR398
Target gene
Reactive oxygen species
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