Journal
PLANT SCIENCE
Volume 256, Issue -, Pages 208-216Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.plantsci.2016.12.014
Keywords
Benzylisoquinoline alkaloids; Phytophthora infestans; Quantitative resistance; Solanum tuberosum; Transcription factors; Transcriptional regulation
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Funding
- Natural Sciences and Engineering Council of Canada (NSERC)
- International Development Research Center (IDRC), Canada
- Department of Foreign Affairs, Trade and Development Canada (DFATD)
- Indian Council of Agriculture Research (ICAR), New Delhi, India
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The resistance to late blight is either qualitative or quantitative in nature. Quantitative resistance is durable, but challenging due to polygenic inheritance. In the present study, the diploid potato genotypes resistant and susceptible to late blight, were profiled for metabolites. Tissue specific metabolite analysis of benzylisoquinoline alkaloids (BIAs) in response to pathogen infection revealed increased accumulation of morphinone, codeine-6-glucuronide and morphine-3-glucuronides. These BIAs are antimicrobial compounds and possibly involved in cell wall reinforcement, especially through cross-linking cell wall pectins. Quantitative reverse transcription-PCR studies revealed higher expressions of TyDC, NCS, COR-2 and StWRICYS transcription factor genes, in resistant genotypes than in susceptible genotype, following pathogen inoculation. A luciferase transient expression assay confirmed the binding of the StWRIN8 TF to promoters of downstream genes, elucidating a direct regulatory role on BIAs biosynthetic genes. Sequence analysis of StWRKY8 in potato genotypes revealed polymorphism in the WRKY DNA binding domain in the susceptible genotype, which is important for the regulatory function of this gene. A complementation assay of StWRKYS in Arabidopsis wrky33 mutant background was associated with decreased fungal biomass. In conclusion, StWRICY8 regulates the biosynthesis of BIAS that are both antimicrobial and reinforce cell walls to contain the pathogen to initial infection. (C) 2017 Elsevier B.V. All rights reserved.
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