Youcai mosaic virus
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ABSTRACT:
PROVIDER: PRJNA110829 | ENA |
REPOSITORIES: ENA
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Project description:Using a crucifer-infecting strain of Tobacco Mosaic Virus (TMV-Cg) and Arabidopsis thaliana as a model system, we analyzed the viral small RNA profile in wild-type plants as well as rdr mutants by applying small RNA deep sequencing technology. Over 100,000 TMV-Cg-specific small RNA reads, mostly of 21- (78.4%) and 22-nucleotide (12.9%) in size and originating predominately (79.9%) from the genomic sense RNA strand, were captured at an early infection stage, yielding the first high-resolution small RNA map for a plant virus. The TMV-Cg genome harbored multiple, highly reproducible small RNA-generating hot spots that corresponded to regions with no apparent local hairpin-forming capacity. Significantly, both the rdr1 and rdr6 mutants exhibited globally reduced levels of viral small RNA production as well as reduced strand bias in viral small RNA population, revealing an important role for these host RDRs in viral siRNA biogenesis. In addition, an informatics analysis showed that a large set of host genes could be potentially targeted by TMV-Cg-derived siRNAs for posttranscriptional silencing, raising the interesting possibility for a hidden layer of widespread virus-host interactions that may contribute to viral pathogenicity and host specificity. Profiling of TMV-Cg derived small RNAs in systemically infected tissues of wild type (Col-0) Arabidopsis as well as the rdr1and rdr6 mutants, at 3 days post-infection.
2009-03-24 | E-GEOD-12918 | biostudies-arrayexpress
Project description:Using a crucifer-infecting strain of Tobacco Mosaic Virus (TMV-Cg) and Arabidopsis thaliana as a model system, we analyzed the viral small RNA profile in wild-type plants as well as rdr mutants by applying small RNA deep sequencing technology. Over 100,000 TMV-Cg-specific small RNA reads, mostly of 21- (78.4%) and 22-nucleotide (12.9%) in size and originating predominately (79.9%) from the genomic sense RNA strand, were captured at an early infection stage, yielding the first high-resolution small RNA map for a plant virus. The TMV-Cg genome harbored multiple, highly reproducible small RNA-generating hot spots that corresponded to regions with no apparent local hairpin-forming capacity. Significantly, both the rdr1 and rdr6 mutants exhibited globally reduced levels of viral small RNA production as well as reduced strand bias in viral small RNA population, revealing an important role for these host RDRs in viral siRNA biogenesis. In addition, an informatics analysis showed that a large set of host genes could be potentially targeted by TMV-Cg-derived siRNAs for posttranscriptional silencing, raising the interesting possibility for a hidden layer of widespread virus-host interactions that may contribute to viral pathogenicity and host specificity.
2009-03-24 | GSE12918 | GEO
Project description:Strigolactones (SLs) are plant hormones that regulate diverse developmental processes and environmental responses in plants. It has been discovered that SLs play an important role in regulating plant immune resistance to pathogens, but there are currently no reports on their role in the interaction between Nicotiana benthamiana and Tobacco mosaic virus (TMV). In this study, the exogenous application of SLs weakened the resistance of N. benthamiana to TMV, promoting TMV infection, whereas the exogenous application of Tis108, an SL inhibitor, resulted in the opposite effect. Virus-induced gene silencing (VIGS) inhibition of two key SL synthesis enzyme genes, NtCCD7 and NtCCD8, enhanced the resistance of N. benthamiana to TMV. Additionally, we conducted a screening of N. benthamiana related to TMV infection. TMV-infected plants treated with SLs were compared to the control by using RNA-seq. KEGG enrichment analysis and weighted gene co-expression network analysis (WGCNA) of differentially expressed genes (DEGs) suggested that plant hormone signaling transduction may play a significant role in the SL-TMV-N. benthamiana interactions. This study reveals new functions of SLs in regulating plant immunity and provides a reference for controlling TMV diseases in production.
2024-08-16 | GSE272661 | GEO
Project description:In this study we used vascular specific promoters and a translating ribosome affinity purification strategy to identify phloem-associated translatome responses to infection by tobacco mosaic virus (TMV) in the systemic host Arabidopsis thaliana ecotype Shahdara. Three different promoter:FLAG-RPL18 lines were used. These included two phloem specific promoters (pSUC2 and pSULTR2;2) as well as the more ubiquitously expressed cauliflower mosaic virus 35S promoter (p35S). Immunopurification of ribosome-mRNA complexes was accomplished by the method described in Reynoso et al. (Plant Functional Genomics: Methods and Protocols, 185-207; 2015). The dataset includes samples from the leaves of 5-week-old plants inoculated with TMV (1 mg/mL) or mock inoculated with sterile water.
2017-07-17 | GSE97662 | GEO
Project description:Transgenic expression of viral proteins in natural host plants is a useful simplified system with the potential to understand the individual effect of each viral component. Transgenic expression of movement (MP) and a variant from coat protein (CPT42W) in tobacco, a TMV natural host, produces severe morphological changes, altered miRNAs accumulation and poor fertility. We used microarrays to characterize the gene expression changes caused by the co-expression of TMV capsid and movement proteins in Nicotiana tabacum comparing two isogenic lines MPxCPT42W and mpxcpT42W* (a line with both transgenes spontaneously silenced and with normal phenotype). Leaf tissues from 6-week old tobacco plants MPxCPT42W and mpxcpT42W* were collected for RNA extraction and hybridization on Affymetrix microarrays. We collected pools of three plants (one biological replicate) and analyzed three independent biological replicates for each transgenic line.
2012-12-01 | E-GEOD-37905 | biostudies-arrayexpress
Project description:Transgenic expression of viral proteins in natural host plants is a useful simplified system with the potential to understand the individual effect of each viral component. Transgenic expression of movement (MP) and a variant from coat protein (CPT42W) in tobacco, a TMV natural host, produces severe morphological changes, altered miRNAs accumulation and poor fertility. We used microarrays to characterize the gene expression changes caused by the co-expression of TMV capsid and movement proteins in Nicotiana tabacum comparing two isogenic lines MPxCPT42W and mpxcpT42W* (a line with both transgenes spontaneously silenced and with normal phenotype).
2012-12-01 | GSE37905 | GEO
Project description:TMV-resistant (N), -susceptible (n), and enhanced susceptible mutant sun1-1 (N) tomato were grown in asceptic conditions in growth chambers (25º, 16hr/8hr light dark). 4-5 week old tomato were treated with TMV leaf sap or mock leaf sap, and leaf tissue was collected after 3, 9, and 27 hours. RNA was isolated from each sample (leaf tissue from one plant/one treatment/one timepoint), using standard TIGR protocols, and 25ug of total RNA was labeled using TIGR indirect labeling protocols. The experiment was repeated three times. Keywords: Direct comparison
2007-09-01 | GSE8233 | GEO
Project description:TMV, Nicotiana tabacum cv. Xanthi (Tobacco) Transcriptome
| PRJNA665939 | ENA
Project description:Viral siRNA generated from antiviral RNA silencing machinery was profiled using small RNA sequencing from Phalaenopsis orchid mixed infected with CymMV and ORSV
2020-01-01 | GSE94083 | GEO
Project description:Heldt2012 - Influenza Virus Replication
The model describes the life cycle of influenza A virus in a mammalian cell including the following steps: attachment of parental virions to the cell membrane, receptor-mediated endocytosis, fusion of the virus envelope with the endosomal membrane, nuclear import of vRNPs, viral transcription and replication, translation of the structural viral proteins, nuclear export of progeny vRNPs and budding of new virions. It also explicitly accounts for the stabilization of cRNA by viral polymerases and NP and the inhibition of vRNP activity by M1 protein binding. In short, the model focuses on the molecular mechanism that controls viral transcription and replication.
This model is described in the article:
Modeling the intracellular dynamics of influenza virus replication to understand the control of viral RNA synthesis.
Heldt FS, Frensing T, Reichl U.
J Virol.
Abstract:
Influenza viruses transcribe and replicate their negative-sense RNA genome inside the nucleus of host cells via three viral RNA species. In the course of an infection, these RNAs show distinct dynamics, suggesting that differential regulation takes place. To investigate this regulation in a systematic way, we developed a mathematical model of influenza virus infection at the level of a single mammalian cell. It accounts for key steps of the viral life cycle, from virus entry to progeny virion release, while focusing in particular on the molecular mechanisms that control viral transcription and replication. We therefore explicitly consider the nuclear export of viral genome copies (vRNPs) and a recent hypothesis proposing that replicative intermediates (cRNA) are stabilized by the viral polymerase complex and the nucleoprotein (NP). Together, both mechanisms allow the model to capture a variety of published data sets at an unprecedented level of detail. Our findings provide theoretical support for an early regulation of replication by cRNA stabilization. However, they also suggest that the matrix protein 1 (M1) controls viral RNA levels in the late phase of infection as part of its role during the nuclear export of viral genome copies. Moreover, simulations show an accumulation of viral proteins and RNA toward the end of infection, indicating that transport processes or budding limits virion release. Thus, our mathematical model provides an ideal platform for a systematic and quantitative evaluation of influenza virus replication and its complex regulation.
With the current parameter set, the model reproduces an infection at a multiplicity of infection (MOI) of 10. Figure 2A of the paper is reproduced here, with parameters kDegRnp and kSynP changed to zeros.
Initial conditions and parameter changes that were used to obtain specific figures in the article can be found in Table A2.
The model has the correct value for kAttLo as 4.55e-04. The value of this parameter mentioned as 4.55e-02 in Table 1 of the paper is incorrect. This is checked with the author.
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2024-09-02 | BIOMD0000000463 | BioModels