Molecular Characterization and Pathogenicity of an Infectious cDNA Clone of Youcai Mosaic Virus on Solanum nigrum.

Virus infections cause devastative economic losses for various plant species, and early diagnosis and prevention are the most effective strategies to avoid the losses. Exploring virus genomic evolution and constructing virus infectious cDNA clones is essential to achieve a deeper understanding of the interaction between host plant and virus. Therefore, this work aims to guide people to better prevent, control, and utilize the youcai mosaic virus (YoMV). Here, the YoMV was found to infect the Solanum nigrum under natural conditions. Then, an infectious cDNA clone of YoMV was successfully constructed using triple-shuttling vector-based yeast recombination. Furthermore, we established phylogenetic trees based on the complete genomic sequences, the replicase gene, movement protein gene, and coat protein gene using the corresponding deposited sequences in NCBI. Simultaneously, the evolutionary relationship of the YoMV discovered on S. nigrum to others was determined and analyzed. Moreover, the constructed cDNA infectious clone of YoMV from S. nigrum could systematically infect the Nicotiana benthamiana and S. nigrum by agrobacterium-mediated infiltration. Our investigation supplied a reverse genetic tool for YoMV study, which will also contribute to in-depth study and profound understanding of the interaction between YoMV and host plant.

Sugarcane streak mosaic virus P1 protein inhibits unfolded protein response through direct suppression of bZIP60U splicing.

The unfolded protein response (UPR) is a cell-designated strategy that maintains the balance of protein folding in the endoplasmic reticulum (ER). UPR features a network of signal transduction pathways that reprogram the transcription, mRNA translation, and protein post-translational modification to relieve the ER stresses from unfolded/misfolded proteins. Infection with plant viruses can induce the UPR, and activated UPR often promotes plant viral infections in turn. However, the mechanism used by plant viruses to balance UPR and achieve robust infection remain largely unknown. In this study, P1SCSMV was identified as a virus-encoded RNA silencing suppressor (VSR). Heterologous overexpression of P1SCSMV via potato virus X (PVX) was found lead to programmed cell death (PCD) in Nicotiana benthamiana. Furthermore, P1SCSMV was also found to inhibit the PVX infection-triggered UPR by downregulating UPR-related genes and directly induced the distortion and collapse of the ER polygonal meshes on PVX-P1SCSMV infected N. benthamiana. Moreover, self-interaction, VSR activity, UPR inhibition, and cell death phenotype of P1SCSMV were also found to be dependent on its bipartite nuclear localization signal (NLS) (251RKRKLFPRIPLK262). P1SCSMV was found to directly bind to the stem-loop region of NbbZIP60U via its NLS and inhibit the UPR pathways, ultimately resulting in a PCD phenotype in PVX-P1SCSMV infected N. benthamiana leaves. This study also revealed the balancing role of potyviruses encoded P1SCSMV in the UPR pathway to achieve robust viral infection. This may represent a novel virulence strategy for plant viruses.

Sugarcane Streak Mosaic Virus P1 Attenuates Plant Antiviral Immunity and Enhances Potato Virus X Infection in Nicotiana benthamiana.

The sugarcane streak mosaic virus (SCSMV) is the most important disease in sugarcane produced in southern China. The SCSMV encoded protein 1 (P1SCSMV) is important in disease development, but little is known about its detailed functions in plant-virus interactions. Here, the differential accumulated proteins (DAPs) were identified in the heterologous expression of P1SCSMV via a potato virus X (PVX)-based expression system, using a newly developed four-dimensional proteomics approach. The data were evaluated for credibility and reliability using qRT-RCR and Western blot analyses. The physiological response caused by host factors that directly interacted with the PVX-encoded proteins was more pronounced for enhancing the PVX accumulation and pathogenesis in Nicotiana benthamiana. P1SCSMV reduced photosynthesis by damaging the photosystem II (PSII). Overall, P1SCSMV promotes changes in the physiological status of its host by up- or downregulating the expression of host factors that directly interact with the viral proteins. This creates optimal conditions for PVX replication and movement, thereby enhancing its accumulation levels and pathogenesis. Our investigation is the first to supply detailed evidence of the pathogenesis-enhancing role of P1SCSMV, which provides a deeper understanding of the mechanisms behind virus-host interactions.