The C2 protein of tomato yellow leaf curl Sardinia virus acts as a pathogenicity determinant and a 16-amino acid domain is responsible for inducing a hypersensitive response in plants

• Published in: Virus research Vol. 215; pp. 12 - 19
• Main Authors: Matić, Slavica, Pegoraro, Mattia, Noris, Emanuela
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 02.04.2016
• Subjects: Agrobacterium - genetics; Agroinfiltration; amino acids; Arabidopsis - immunology; Arabidopsis - virology; Arabidopsis thaliana; Begomovirus - pathogenicity; Cell Death; Gene Expression; genes; Host-Pathogen Interactions; hydrogen peroxide; Hypersensitive response; Lycopersicon esculentum; Nicotiana - immunology; Nicotiana - virology; Nicotiana benthamiana; Nicotiana tabacum; pathogenicity; Pathogenicity determinant; Plant Cells - physiology; Plant Cells - virology; Plant Diseases - immunology; Plant Diseases - virology; plant diseases and disorders; plant viruses; Salicylic acid; Tomato yellow leaf curl Sardinia virus; Tomato yellow leaf curl virus; Transformation, Genetic; transgenic plants; TYLCSV; viral proteins; Viral Proteins - genetics; Viral Proteins - metabolism; Virulence Factors - genetics; Virulence Factors - metabolism; Pathogenicity determinant; Salicylic acid; Hypersensitive response; Agroinfiltration; TYLCSV; C2
• ISSN: 0168-1702; 1872-7492
• DOI: 10.1016/j.virusres.2016.01.014

•The C2 protein of TYLCSV induces a hypersensitive response (HR) in Nicotiana spp and A​rabidopsis.•TYLCSV V2 and Rep counteract the C2-mediated HR in co-agroinfiltration experiments.•A domain of 16 amino acids (aa 85–100) of TYLCSV C2 is responsible for inducing HR.•Salicylic acid and temperature are involved in the HR induced by TYLCSV C2. The role of the C2 protein in the pathogenicity of tomato yellow leaf curl Sardinia virus (TYLCSV) was investigated. Here we report that Agrobacterium-mediated transient expression of TYLCSV C2 resulted in a strong hypersensitive response (HR) in Nicotiana benthamiana, N. tabacum, and Arabidopsis thaliana, with induction of plant cell death and production of H2O2. Since HR is not evident in plants infected by TYLCSV, it is expected that TYLCSV encodes a gene (or genes) that counters this response. HR was partially counteracted by co-agroinfiltration of TYLCSV V2 and Rep, leading to chlorotic reaction, with no HR development. Considering that the corresponding C2 protein of the closely related tomato yellow leaf curl virus (TYLCV) did not induce HR, alignment of the C2 proteins of TYLCSV and TYLCV were carried out and a hypervariable region of 16 amino acids was identified. Its role in the induction of HR was demonstrated using TYLCSV-TYLCV C2 chimeric genes, encoding two TYLCSV C2 variants with a complete (16 aa) or a partial (10 aa only) swap of the corresponding sequence of TYLCV C2. Furthermore, using NahG transgenic N. benthamiana lines compromised in the accumulation of salicylic acid (SA), a key regulator of HR, only a chlorotic response occurred in TYLCSV C2-infiltrated tissue, indicating that SA participates in such plant defense process. These findings demonstrate that TYLCSV C2 acts as a pathogenicity determinant and induces host defense responses controlled by the SA pathway.