ArticleMolecular plant pathology2014
A short motif in the N-terminal part of the coat protein is a host-specific determinant of systemic infectivity for two potyviruses.
Article in Molecular plant pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 14 citations in OpenAlex.
- Variability and population structure of watermelon mosaic virus in zucchini crops in Poland.The Journal of general virology · 2026Article
- Genetic Diversity and Phylogenetic Analysis of Watermelon Mosaic Virus in Türkiye: Insights into Emerging and Classic Populations.Current microbiology · 2025Article
- Article
- A pathogenicity determinant maps to the N-terminal coat protein region of the Pepino mosaic virus genome.Molecular plant pathology · 2015Article
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3 authors at 1 institution in 1 country.
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Abstract
Although the biological variability of Watermelon mosaic virus is limited, isolates from the three main molecular groups differ in their ability to infect systemically Chenopodium quinoa. Mutations were introduced in a motif of three or five amino acids located in the N-terminal part of the coat protein, and differing in isolates from group 1 (motif: lysine-glutamic acid-alanine (Lys-Glu-Ala) or KEA, systemic on C. quinoa), group 2 (Lys-Glu-Thr or KET, not systemic on C. quinoa) and group 3 (KEKET, not systemic on C. quinoa). Mutagenesis of KEKET in an isolate from group 3 to KEA or KEKEA was sufficient to make the virus systemic on C. quinoa, whereas mutagenesis to KET had no effect. Introduction of a KEA motif in Zucchini yellow mosaic virus coat protein also resulted in systemic infection on C. quinoa. These mutations had no obvious effect on the disorder profile or potential post-translational modifications of the coat protein as determined in silico.
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