Resistance to viruses of potato: current status and prospects

The potato (Solanum tuberosum), one of the most important food crops in the world, is infected by various viruses, nine of which have great economic significance, causing substantial losses in the yield and quality of the crop. To minimize consequences of virus infections, in developed countries specific phytosanitary measures have been established and are being improved to monitor the spread of viruses and certify seed potato material using virus diagnostics and production of virus-free potato cultivars. However, in the longer-term, the development and deployment of potato cultivars resistant to viruses would be a priority. Some new potato cultivars and lines resistant to many viruses have already been generated using either traditional breeding methods or genetic engineering. For this purpose, natural resistance genes, primarily from wild Solanum species, or virus derived nucleotide sequences have been used as sources of resistance. However, these approaches have essential limitations because the acquired resistance is highly specific (against individual viruses only), is not durable, can be overcome by viruses and, finally due to regulatory bans on genetically modified organisms. Recently developed new genome editing technologies with the potential to be a powerful tool for gene design open up broad opportunities for development of next-generation resistance genes. The most promising approaches are (1) site-directed mutagenesis of the genes conferring specific resistance to make their action much broader and (2) the use of non-specific (nonhost) resistance to generate plants resistant to unrelated viruses and, in some cases, to other pathogens and even abiotic stresses. Identification of genes involved in mechanisms of non-host resistance is just beginning. The cell nucleus is a new source of novel factors involved in various signaling pathways resulting in defence response to virus infection. This review focuses on the approaches and challenges related to the development of potato plants resistant to virus infections

A Family of Plasmodesmal Proteins with Receptor-Like Properties for Plant Viral Movement Proteins

Plasmodesmata (PD) are essential but poorly understood structures in plant cell walls that provide symplastic continuity and intercellular communication pathways between adjacent cells and thus play fundamental roles in development and pathogenesis. Viruses encode movement proteins (MPs) that modify these tightly regulated pores to facilitate their spread from cell to cell. The most striking of these modifications is observed for groups of viruses whose MPs form tubules that assemble in PDs and through which virions are transported to neighbouring cells. The nature of the molecular interactions between viral MPs and PD components and their role in viral movement has remained essentially unknown. Here, we show that the family of PD-located proteins (PDLPs) promotes the movement of viruses that use tubule-guided movement by interacting redundantly with tubule-forming MPs within PDs. Genetic disruption of this interaction leads to reduced tubule formation, delayed infection and attenuated symptoms. Our results implicate PDLPs as PD proteins with receptor-like properties involved the assembly of viral MPs into tubules to promote viral movement

Insight on genes affecting tuber development in potato upon <i>Potato spindle tuber viroid</i> (PSTVd) infection

Potato (Solanum tuberosum L) is a natural host of Potato spindle tuber viroid (PSTVd) which can cause characteristic symptoms on developing plants including stunting phenotype and distortion of leaves and tubers. PSTVd is the type species of the family Pospiviroidae, and can replicate in the nucleus and move systemically throughout the plant. It is not well understood how the viroid can affect host genes for successful invasion and which genes show altered expression levels upon infection. Our primary focus in this study is the identification of genes which can affect tuber formation since viroid infection can strongly influence tuber development and especially tuber shape. In this study, we used a large-scale method to identify differentially expressed genes in potato. We have identified defence, stress and sugar metabolism related genes having altered expression levels upon infection. Additionally, hormone pathway related genes showed significant up- or down-regulation. DWARF1/DIMINUTO, Gibberellin 7-oxidase and BEL5 transcripts were identified and validated showing differential expression in viroid infected tissues. Our study suggests that gibberellin and brassinosteroid pathways have a possible role in tuber development upon PSTVd infection

Two Plant Viral Suppressors of Silencing Require the Ethylene-Inducible Host Transcription Factor RAV2 to Block RNA Silencing

RNA silencing is a highly conserved pathway in the network of interconnected defense responses that are activated during viral infection. As a counter-defense, many plant viruses encode proteins that block silencing, often also interfering with endogenous small RNA pathways. However, the mechanism of action of viral suppressors is not well understood and the role of host factors in the process is just beginning to emerge. Here we report that the ethylene-inducible transcription factor RAV2 is required for suppression of RNA silencing by two unrelated plant viral proteins, potyvirus HC-Pro and carmovirus P38. Using a hairpin transgene silencing system, we find that both viral suppressors require RAV2 to block the activity of primary siRNAs, whereas suppression of transitive silencing is RAV2-independent. RAV2 is also required for many HC-Pro-mediated morphological anomalies in transgenic plants, but not for the associated defects in the microRNA pathway. Whole genome tiling microarray experiments demonstrate that expression of genes known to be required for silencing is unchanged in HC-Pro plants, whereas a striking number of genes involved in other biotic and abiotic stress responses are induced, many in a RAV2-dependent manner. Among the genes that require RAV2 for induction by HC-Pro are FRY1 and CML38, genes implicated as endogenous suppressors of silencing. These findings raise the intriguing possibility that HC-Pro-suppression of silencing is not caused by decreased expression of genes that are required for silencing, but instead, by induction of stress and defense responses, some components of which interfere with antiviral silencing. Furthermore, the observation that two unrelated viral suppressors require the activity of the same factor to block silencing suggests that RAV2 represents a control point that can be readily subverted by viruses to block antiviral silencing

Umbravirus

The genomes of umbraviruses consist of one linear segment of positive-sense single-stranded RNA (ssRNA). Umbraviruses differ from other plant viruses in that they do not encode a coat protein (CP), and no viral particles are formed in infected plants. To compensate for the lack of virus particles, umbraviruses depend for survival on an assistor virus, which is always a member of the family Luteoviridae. For transmission between plants, the CP of the luteovirus forms aphid-transmissible hybrid virus particles encapsidating umbraviral RNA. Satellite RNAs are also associated with some umbraviruses. Umbravirus genomes encode an RNA-dependent RNA polymerase and two other proteins. One of these is a cell-to-cell movement protein that can mediate transport of viral RNA through plasmodesmata. The other, the ORF3 protein, binds to RNA to form filamentous ribonucleoprotein (RNP) particles. This serves to stabilize RNA and facilitate its long-distance movement through the phloem. The ORF3 protein enters the cell nucleus targeting the nucleolus. There is a correlation between the ORF3 protein nucleolar localization and its ability to form the RNP particles and transport viral RNA long distances. Information on the biological properties of umbraviruses, such as host range and mode of aphid transmission as well as on the control measures, is presented