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An evolutionarily conserved non-synonymous SNP in a leucine-rich repeat domain determines anthracnose resistance in watermelon

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Abstract

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A non-synonymous SNP of CC–NBS–LRR was firstly mapped to confer resistance to anthracnose in watermelon. Newly proposed LRR domain harboring the SNP is evolutionary conserved in the Cucurbitaceae and Fabaceae.

Abstract

Anthracnose disease caused by Colletotrichum devastates many plants. Despite the importance of the disease, the mechanisms of resistance against it are poorly understood. Here, we identified a non-synonymous single-nucleotide polymorphism (SNP) located in a leucine-rich repeat domain as a marker for resistance to anthracnose race 1 in watermelon, using a combination of genetic analyses. We validated this SNP in segregating populations and 59 watermelon accessions using high-resolution melting assays and Sanger sequencing. We demonstrated that the resulting arginine-to-lysine substitution is particularly conserved among the Cucurbitaceae and Fabaceae. We identified a conserved motif, IxxLPxSxxxLYNLQTLxL, found in 1007 orthologues/paralogues from 89 plant species, and discovered that residue 18 of this motif could determine resistance to disease caused by external invaders. This study provides a step forward in understanding anthracnose resistance in watermelon, as well as functional and evolutionary insight into leucine-rich repeat proteins.

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Acknowledgements

This work was supported by the Golden Seed Project (213006051SBV20); the Ministry of Agriculture, Food, and Rural Affairs (MAFRA); the Ministry of Oceans and Fisheries (MOF); the Rural Development Administration (RDA); and the Korean Forest Service (KFS) of the Republic of Korea.

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Correspondence to Gung Pyo Lee.

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The datasets generated for this study are available in the NCBI SRA accession SRP150693.

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Communicated by Xiaoquan Qi.

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Jang, Y.J., Seo, M., Hersh, C.P. et al. An evolutionarily conserved non-synonymous SNP in a leucine-rich repeat domain determines anthracnose resistance in watermelon. Theor Appl Genet 132, 473–488 (2019). https://doi.org/10.1007/s00122-018-3235-y

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