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cDNA Cloning of Viroid-Induced Tomato Pathogenesis-Related Protein P23 (Characterization as a Vacuolar Antifungal Factor)
Author(s) -
Ismael Rodrigo,
Pablo Vera,
Pablo Tornero,
José Hernández-Yago,
Vicente Conejero
Publication year - 1993
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.102.3.939
Subject(s) - viroid , complementary dna , biology , lycopersicon , microbiology and biotechnology , gene , rapid amplification of cdna ends , cloning (programming) , open reading frame , molecular cloning , peptide sequence , rna , biochemistry , botany , computer science , programming language
A 23-kD pathogenesis-related protein (P23) is induced in tomato (Lycopersicon esculentum Mill, cv Rutgers) plants when infected with citrus exocortis viroid. This protein is homologous to the salt-induced tomato NP24 protein (I. Rodrigo, P. Vera, R. Frank, V. Conejero [1991] Plant Mol Biol 16: 931-934). Further characterization of P23 has shown that this protein accumulates in vacuoles in association with dense inclusion bodies. In vitro assays indicated that the purified P23 protein inhibits the growth of several phytopathogenic fungi. P23-coding cDNA clones were isolated from viroid-induced and ethylene-induced libraries. Southern analysis showed that at least two genes could encode P23 or P23-related products. The accumulation of P23 protein correlated with the accumulation of its mRNA. Sequence analysis revealed significant differences in both coding and downstream untranslated regions between the cDNA sequences corresponding to the viroid-induced P23 and the salt stress-induced NP24 proteins.

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