Affiliation:
1. Key Laboratory of Plant Functional Genomics of the Ministry of Education, Yangzhou University , Yangzhou 225009 , China
2. Jiangsu Key Laboratory of Crop Genomics and Molecular Breeding, Yangzhou University , Yangzhou 225009 , China
Abstract
Abstract
Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum, is among the most devastating diseases in Brassica napus worldwide. Conventional breeding for SSR resistance in Brassica species is challenging due to the limited availability of resistant germplasm. Therefore, genetic engineering is an attractive approach for developing SSR-resistant Brassica crops. Compared with the constitutive promoter, an S. sclerotiorum-inducible promoter would avoid ectopic expression of defense genes that may cause plant growth deficits. In this study, we generated a S. sclerotiorum-inducible promoter. pBnGH17D7, from the promoter of B. napus glycosyl hydrolase 17 gene (pBnGH17). Specifically, 5'-deletion and promoter activity analyses in transgenic Arabidopsis thaliana plants defined a 189 bp region of pBnGH17 which was indispensable for S. sclerotiorum-induced response. Compared with pBnGH17, pBnGH17D7 showed a similar response upon S. sclerotiorum infection, but lower activity in plant tissues in the absence of S. sclerotiorum infection. Moreover, we revealed that the transcription factor BnTGA7 directly binds to the TGACG motif in pBnGH17D7 to activate BnGH17. Ultimately, pBnGH17D7 was exploited for engineering Sclerotinia-resistant B. napus via host-induced gene silencing. It induces high expression of siRNAs against the S. sclerotiorum pathogenic factor gene specifically during infection, leading to increased resistance.
Funder
National Natural Science Foundation of China
Jiangsu Agricultural Science and Technology Innovation Fund
Project of Special Funding for Crop Science Discipline Development
Priority Academic Program Development of Jiangsu Higher Education Institutions, the Postgraduate Research & Practice Innovation Program of Jiangsu Province
Publisher
Oxford University Press (OUP)
Cited by
3 articles.
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