Disease relevance of TBSVgp5

• The P19 protein of tomato bushy stunt virus (TBSV) is a multifunctional pathogenicity determinant involved in suppression of posttranscriptional gene silencing, virus movement, and symptom induction [1].
• The contribution of individual genes was determined by bioassays with an infectious clone of wild-type TBSV, with p19/p22 mutant derivatives, and by expression of individual TBSV genes from a heterologous potato virus X (PVX) vector [2].
• The presence of DI RNAs in tombusvirus-infected plants reduces the accumulation of helper virus RNA and results in the development of attenuated symptoms similar to those caused by tombusviruses defective in p19, the posttranscriptional gene silencing (PTGS) suppressor [3].
• The three-dimensional structure of an siRNA bound to the tombusvirus p19 protein--a suppressor of gene silencing--provides a first glimpse into how plant viruses can defeat their host's anti-viral RNAi defenses [4].
• Here, the role of both CP and p19 in the systemic spread has been reevaluated by utilizing transgenic N. benthamiana plants expressing the movement protein (MP) of Red clover necrotic mosaic virus and chimeric TBSV mutants that express CP of Turnip crinkle virus [5].

High impact information on TBSVgp5

• A normally labile intermediate in the miRNA biogenesis/RNA-induced silencing complex (RISC) assembly pathway, miRNA*, accumulated specifically in the presence of suppressors (P1/HC-Pro, p21, or p19) that inhibited miRNA-guided cleavage of target mRNAs [6].
• Transcription of sg mRNA2 in tombusviruses allows for expression of the p19 suppressor of gene silencing and p22 movement proteins [7].
• Molecular mechanism of RNA silencing suppression mediated by p19 protein of tombusviruses [8].
• In this study, we analyzed the influence of two nested genes (p19 and p22) of tomato bushy stunt virus (TBSV) on disease symptoms in systemically infected plants and in local lesion hosts [2].
• Wild-type TBSV or p19-defective mutants initially show a similar infection course in Nicotiana benthamiana, but the absence of an active P19 results in viral RNA degradation followed by recovery from infection [9].

Biological context of TBSVgp5

• Thus, our results provide evidence that elicitation of the necrotic phenotype requires the presence of the wt p33 in addition to the p19 protein of tombusviruses [10].
• We have investigated the importance of two small nested genes (p19 and p22) located near the 3' end of the genome of tomato bushy stunt virus (TBSV) for infectivity in several hosts [11].
• The effect of p19 was not saturated in cells that had received up to four individual T-DNAs and persisted until leaf senescence [12].
• Two alpha-helical 'reading heads' project from opposite ends of the p19 homodimer and position pairs of tryptophans for stacking over the terminal base pairs, thereby measuring and bracketing both ends of the siRNA duplex [13].

Other interactions of TBSVgp5

• Associated with this differentially regulated suppression was a greatly reduced expression of both the p19 protein, which is responsible for severe symptoms, and the p22 protein, which is associated with cell-to-cell movement of the virus [14].

Analytical, diagnostic and therapeutic context of TBSVgp5

• Genetic dissection of tomato bushy stunt virus p19-protein-mediated host-dependent symptom induction and systemic invasion [15].

References