bioRxiv · 10.1101/2024.01.29.577696
Disease resistance of Brassica juncea to Sclerotinia sclerotiorum is established through the induction of indole glucosinolate biosynthesis
Abstract
Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum, is the main disease threat to oilseeds in Brassiceae, causing significant yield losses and reduction in oil content and quality. The studies on S. sclerotiorum require a great focus and extensive research on B. juncea compared to those on B. napus and B. oleracea. Transcriptome analysis revealed a large number of defense-related genes and response processes in B. napus and B. oleracea. However, similarities and differences in the defense responses to S. sclerotiorum on B. juncea are rarely reported. In the present study, we reported a B. juncea breeding line of H83 with high S. sclerotiorum resistance, which was used for transcriptome analysis compared to L36 with low resistance. A novel regulatory network was proposed to defend against S. sclerotiorum invasion in B. juncea. Upon infection of S. sclerotiorum, a series of auxin and MAPK signaling pathways were initiated within 12 h, and then defenses were activated to restrict the development and spread of S. sclerotiorum by inducing the massive synthesis of indole glucosinolates after 24 h. Twelve hub genes involved in the network were identified by the weighted gene co-expression network (WGCNA), which are involved in plant-pathogen interaction, signaling pathway genes, indole glucosinolate biosynthesis and cell wall formation. The hub genes were further validated by qRT-PCR. The research revealed a new resistant line of H83 against S. sclerotiorum and a different regulatory network in B. juncea, which would be beneficial for the future effective breeding of Sclerotinia-resistant varieties.
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Zhang, J., Yang, X., Jiang, Y., Jin, H., Yu, K., Xiao, L., Ouyang, Q., Tian, E.. 2024-01-31. Disease resistance of Brassica juncea to Sclerotinia sclerotiorum is established through the induction of indole glucosinolate biosynthesis. https://doi.org/10.1101/2024.01.29.577696
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