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Questions and Answers
Suppressor-deficient TuMV-AS9-GFP can infect dcl4-2 mutants, which lack the contribution of Dicer-like protein 4 (DCL4) to gene silencing.
Suppressor-deficient TuMV-AS9-GFP can infect dcl4-2 mutants, which lack the contribution of Dicer-like protein 4 (DCL4) to gene silencing.
True
Suppressor-deficient TuMV-AS9-GFP can infect wild-type plants.
Suppressor-deficient TuMV-AS9-GFP can infect wild-type plants.
False
TuMV-GFP can establish local and systemic infection, including the inflorescence, of Arabidopsis plants, wild-type or mutants.
TuMV-GFP can establish local and systemic infection, including the inflorescence, of Arabidopsis plants, wild-type or mutants.
True
In N. benthamiana, infection of the meristems by potato virus X (PVX) is prevented by RDR6.
In N. benthamiana, infection of the meristems by potato virus X (PVX) is prevented by RDR6.
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Knockdown of RDR6 by RNA interference in N. benthamiana (rdr6i) did not rescue local and systemic infection by TuMV-AS9-GFP.
Knockdown of RDR6 by RNA interference in N. benthamiana (rdr6i) did not rescue local and systemic infection by TuMV-AS9-GFP.
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Arabidopsis Pumilio RNA binding protein 5 (APUM5) binds cucumber mosaic virus (CMV) and TuMV mRNA to promote translation.
Arabidopsis Pumilio RNA binding protein 5 (APUM5) binds cucumber mosaic virus (CMV) and TuMV mRNA to promote translation.
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Plant viruses can only infect the initially infected organ and cannot spread to other parts of the plant.
Plant viruses can only infect the initially infected organ and cannot spread to other parts of the plant.
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Susceptible hosts lack antiviral factors that could act against the virus.
Susceptible hosts lack antiviral factors that could act against the virus.
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Viral factors do not play a role in interfering with antiviral defence mechanisms.
Viral factors do not play a role in interfering with antiviral defence mechanisms.
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Genome-wide screens in yeast and Arabidopsis have not identified pro-viral and antiviral factors that affect virus replication at the cellular level.
Genome-wide screens in yeast and Arabidopsis have not identified pro-viral and antiviral factors that affect virus replication at the cellular level.
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Antiviral defence is not mediated by host factors that target viral nucleic acids or proteins.
Antiviral defence is not mediated by host factors that target viral nucleic acids or proteins.
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Compatible interactions occur between a virus and a non-host plant.
Compatible interactions occur between a virus and a non-host plant.
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Arabidopsis lacking eIF(iso)4E are immune to Tobacco Etch Virus (TEV) and Turnip Mosaic Virus (TuMV)
Arabidopsis lacking eIF(iso)4E are immune to Tobacco Etch Virus (TEV) and Turnip Mosaic Virus (TuMV)
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The lack of RNA translation in infected Arabidopsis prevents the formation of potyviral polyproteins and cell-to-cell movement, aiding resistance
The lack of RNA translation in infected Arabidopsis prevents the formation of potyviral polyproteins and cell-to-cell movement, aiding resistance
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Infected Arabidopsis plants analyzed with TuMV-GFP illustrate a one-step model of infection
Infected Arabidopsis plants analyzed with TuMV-GFP illustrate a one-step model of infection
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Antiviral defense responses can prevent infection from spreading, resulting in sufficient resistance to prevent observable symptoms, making the plant appear similar to a non-host
Antiviral defense responses can prevent infection from spreading, resulting in sufficient resistance to prevent observable symptoms, making the plant appear similar to a non-host
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Various techniques used to study plant-virus interactions include transient expression, transgenic expression, and virus mutagenesis
Various techniques used to study plant-virus interactions include transient expression, transgenic expression, and virus mutagenesis
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Turnip Mosaic Virus (TuMV) infection of Arabidopsis illustrates a two-step process: early suppression of antiviral defense, followed by establishment of local lesions
Turnip Mosaic Virus (TuMV) infection of Arabidopsis illustrates a two-step process: early suppression of antiviral defense, followed by establishment of local lesions
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True or false: Viruses encode proteins to execute all parts of the infection cycle.
True or false: Viruses encode proteins to execute all parts of the infection cycle.
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True or false: Antiviral immunity consists of host factors that target viral proteins or nucleic acids to facilitate virus infection.
True or false: Antiviral immunity consists of host factors that target viral proteins or nucleic acids to facilitate virus infection.
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True or false: Compatibility in plant-virus interactions is determined by the availability of pro-viral host factors.
True or false: Compatibility in plant-virus interactions is determined by the availability of pro-viral host factors.
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True or false: Susceptibility in plant-virus interactions is determined by the balance between antiviral defense and suppression of antiviral defense.
True or false: Susceptibility in plant-virus interactions is determined by the balance between antiviral defense and suppression of antiviral defense.
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True or false: Viral RNA translation is a host factor with antiviral activity against plant viruses.
True or false: Viral RNA translation is a host factor with antiviral activity against plant viruses.
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True or false: Antiviral gene silencing is a host factor with antiviral activity against plant viruses.
True or false: Antiviral gene silencing is a host factor with antiviral activity against plant viruses.
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Plant virus genome replication is independent of host resources and factors.
Plant virus genome replication is independent of host resources and factors.
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Plants do not respond to virus infection through mechanisms such as autophagy, ubiquitination, mRNA decay, and gene silencing.
Plants do not respond to virus infection through mechanisms such as autophagy, ubiquitination, mRNA decay, and gene silencing.
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Viral factors and pro-viral host factors work in opposition during the infection cycle.
Viral factors and pro-viral host factors work in opposition during the infection cycle.
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The establishment of virus infection is not genetically determined by the availability of pro-viral factors and the balance between plant defense and viral suppression of defense responses.
The establishment of virus infection is not genetically determined by the availability of pro-viral factors and the balance between plant defense and viral suppression of defense responses.
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The antagonistic activity of antiviral factors does not suggest a two-step model to explain plant-virus interactions.
The antagonistic activity of antiviral factors does not suggest a two-step model to explain plant-virus interactions.
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Infection of a plant by a virus initiates in multiple cells.
Infection of a plant by a virus initiates in multiple cells.
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Study Notes
- Two-step model for plant-virus interactions: compatibility determined by availability of pro-viral host factors, absence of which results in incompatibility (Fig. 1B)
- Arabidopsis is susceptible to Tobacco Etch Virus (TEV) and Turnip Mosaic Virus (TuMV), but mutants lacking eIF(iso)4E (translation initiation factor) are immune (Lellis et al., 2002; Wang et al., 2013)
- Lack of RNA translation likely prevents formation of potyviral polyproteins and possibly cell-to-cell movement, aiding resistance
- Infected Arabidopsis plants, when analyzed with green-fluorescence protein-tagged TuMV (TuMV-GFP), illustrate a two-step model of infection: early suppression of antiviral defence determines the level of susceptibility and the potential for spread to the entire plant
- Antiviral defence responses can prevent infection from spreading, resulting in sufficient resistance to prevent observable symptoms, making the plant appear similar to a non-host (Garcia-Ruiz et al., 2015; Lellis et al., 2002; Qu et al., 2008)
- Plant-virus interactions involve various viral proteins and host factors, each with unique roles: (H. GARCIA-RUIZ) RPP8 protein binding, TCV CP, A. thaliana; (NBR1) Autophagy cargo receptor (TuMV and WMV), A. thaliana; (TYLCCV) RFP1 ubiquitination, BC1, N. tabacum; (AMV) PSBP kinase, CP, N. benthamiana; (TMV) Helicase, N protein phosphatase, N. tabacum 'Xanthi'; (PVX) Rx1, Rx2, NA, PVX CP, S. tuberosum; (ToMV) Tm-2, Tm-22, NA, TMV MP, S. lycopersicum; (TCV) RPP8 protein binding, CP, A. thaliana; (TSWV) Tsw, NSs, Capsicum chinense; (TSWV) Sw5b, NS, S. tuberosum
- Various techniques are used to study plant-virus interactions: transient expression, transgenic expression, localization, cloning, genetic analysis, and virus mutagenesis.
- Several viruses are mentioned: Alfalfa Mosaic Virus (AMV), Bamboo Mosaic Virus (BaMV), Barley Stripe Mosaic Virus (BSMV), Brome Mosaic Virus (BMV), Cabbage Leaf Curl Virus (CaLCuV), Cauliflower Mosaic Virus (CaMV), Cotton Leaf Curl Multan Virus (CLCuMuV), Cymbidium Ringspot Virus (CymRSV), Cucumber Mosaic Virus (CMV), Cucumber Necrosis Virus (CNV), Maize Chlorotic Mottle Virus (MCMV), Melon Necrotic Spot Virus (MNSV), Mungbean Yellow Mosaic India Virus (MYMIV), Oilseed Rape Mosaic Virus (ORMV), Pepper Mild Mottle Virus (PMMoV), Pepper Mottle Virus (PepMV), Potato Virus A (PVA), Potato Virus X (PVX), Potato Virus Y (PVY), Rice Stripe Virus (RSV), Soybean Mosaic Virus (SMV), Sugarcane Mosaic Virus (SCMV), Tobacco Etch Virus (TEV), Tobacco Mosaic Virus (TMV), Tobacco Rattle Virus (TRV), Tomato Bushy Stunt Virus (TBSV), Tomato Mosaic Virus (ToMV), Tomato Ringspot Virus (ToRSV), Tomato Yellow Leaf Curl Virus (TYLCV), Tomato Spotted Wilt Virus (TSWV), Tomato Yellow Leaf Curl Virus (ToYLCV), Turnip Crinkle Virus (TCV), Turnip Mosaic Virus (TuMV), Turnip Yellow Mosaic Virus (TYMV), Watermelon Mosaic Virus (WMV).
- Infection of Arabidopsis by TuMV-GFP illustrates a two-step process: early suppression of antiviral defence, followed by establishment of local lesions (Fig. 2A).
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Description
Explore the genetic determinants and mechanisms underlying the interactions between plants and viruses. Learn about how viruses encode proteins and utilize host factors for their infection cycle, as well as the host's antiviral immunity. Delve into the two-step model determining compatibility in plant-virus interactions.
