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Abstract
Citrus tristeza virus (CTV) is phloem-restricted in natural citrus hosts. The 23 kDa protein (p23) encoded by the virus is an RNA silencing suppressor and a pathogenicity determinant. Expression of p23, or its N-terminal 157 amino acid fragment comprising the zinc-finger and flanking basic motifs, driven by the constitutive 35S promoter of cauliflower mosaic virus incites CTV-like symptoms and other aberrations in transgenic citrus. To better define the role of p23 in CTV pathogenesis, we compared the phenotypes of Mexican limes transformed with p23-derived transgenes from the severe T36 or the mild T317 CTV isolates under the control of the phloem-specific promoter from commelina yellow mottle virus (CoYMV) or the 35S promoter. Expression of the constructs restricted to the phloem incited a phenotype resembling CTV-specific symptoms (vein clearing and necrosis, and stem pitting), but not the non-specific aberrations (like mature leaf epinasty and yellow pinpoints, growth cease and apical necrosis) observed when p23 was ectopically expressed. Furthermore, vein necrosis and stem pitting in Mexican lime appeared specifically associated with p23 from T36. Phloem-specific accumulation of the p23Δ158-209(T36) fragment was sufficient to incite the same anomalies, indicating that the region comprising the N-terminal 157 amino acids of p23 is responsible (at least in part) for the vein clearing, stem pitting and possibly vein corking in this host.
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Concepts
Persian lime, Rutaceae, Bacteria, Amino acid, Acid, Citrus, Protein, Gene
MeSH headings
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