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Mechanisms of RNA virus induced plant death

ABSTRACT: The changes of small RNA profile have been studied in tomato and wild tomato plants to understand the host reponse to the infection of a non-coding viral RNA infection.

ORGANISM(S): Solanum habrochaites Solanum lycopersicum Solanum lycopersicum x Solanum habrochaites

PROVIDER: GSE102373 | GEO | 2019/12/01

REPOSITORIES: GEO

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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. This model is hosted on BioModels Database and identified by: MODEL1307270000 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:The plant response may be triggered by various factors, including pathogens, non-pathogenic microbes, and natural or synthetic molecules, such as salicylic acid (SA), benzo(1,2,3)-Thiadiazole-7-Carbothioic Acid S-Methyl Ester (BTH) that are considered as plant resistance inducers. Resistance inducers mobilize the plant for the synthesis of defense compounds, but they are not directly toxic for the plant. The BTH is an analogue of SA, a molecule naturally synthesized in the plant during systemic acquired resistance (SAR). In this study, we hypothesized that challenging the plant with resistance inducer causes an increase in the level of proteins associated with defence response to external stimuli with primary metabolism and that the action of the choline derivative of the BTH (in the form of the ionic liquid) during induction of resistance in tomato plants is mediated by to some extent similar signaling pathways as it is in the case of unmodified BTH compound. Therefore, this study aimed to identify global proteome changes occurring in tomato plants exposed to resistance inducers as well as to identify common pathways associated with the plant's defense response to (+)ssRNA viruses induced upon both, viral infection and prior resistance inducer treatment. The effect of ionic liquids on changes in plant proteome is not described in the literature. The ionic character of compounds offers a great advantage of using them as the plant resistance inducer. The high chemical and thermal stability, as well as low volatility, guarantees safe application in fields. For that reason, comparing the action of the resistance inducer in the form of an ionic liquid with the core compound (BTH) will help to elucidate the mode of action of ionic liquid derivatives in plant resistance induction. To this end, two RNA-type viruses from different families were tested: tomato mosaic virus (ToMV, Virgaviridae) and potato virus Y (PVY, Potyviridae). The most affected processes presented in the results were: photosynthesis, regulation of oxidative stress, metabolism of glutathione and chitin, cell wall reorganization. The increased impact on the regulation of primary metabolism in inducer-treated plants (both for BTH and cholinium ionic liquid derivative). The response to ToMV and PVY was more intense when infected plants were pre-treated with inducers. The increased abundances of defense priming proteins with changes in cell wall organization may block virus transport from infected spots to other tissue of the host plant so that the losses caused by the disease will be lower.