Genetic Determinants of Plant-Virus Interactions

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 wild-type plants.

TuMV-GFP can establish local and systemic infection, including the inflorescence, of Arabidopsis plants, wild-type or mutants.

In N. benthamiana, infection of the meristems by potato virus X (PVX) is prevented by RDR6.

Knockdown of RDR6 by RNA interference in N. benthamiana (rdr6i) did not rescue local and systemic infection by TuMV-AS9-GFP.

Arabidopsis Pumilio RNA binding protein 5 (APUM5) binds cucumber mosaic virus (CMV) and TuMV mRNA to promote translation.

Plant viruses can only infect the initially infected organ and cannot spread to other parts of the plant.

Susceptible hosts lack antiviral factors that could act against the virus.

Viral factors do not play a role in interfering with antiviral defence mechanisms.

Genome-wide screens in yeast and Arabidopsis have not identified pro-viral and antiviral factors that affect virus replication at the cellular level.

Antiviral defence is not mediated by host factors that target viral nucleic acids or proteins.

Compatible interactions occur between a virus and a non-host plant.

Arabidopsis lacking eIF(iso)4E are immune to Tobacco Etch Virus (TEV) and Turnip Mosaic Virus (TuMV)

The lack of RNA translation in infected Arabidopsis prevents the formation of potyviral polyproteins and cell-to-cell movement, aiding resistance

Infected Arabidopsis plants analyzed with TuMV-GFP illustrate a one-step model of infection

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

Various techniques used to study plant-virus interactions include transient expression, transgenic expression, and virus mutagenesis

Turnip Mosaic Virus (TuMV) infection of Arabidopsis illustrates a two-step process: early suppression of antiviral defense, followed by establishment of local lesions

True or false: Viruses encode proteins to execute all parts of the infection cycle.

True or false: Antiviral immunity consists of host factors that target viral proteins or nucleic acids to facilitate virus infection.

True or false: Compatibility in plant-virus interactions is determined by the availability of pro-viral host factors.

True or false: Susceptibility in plant-virus interactions is determined by the balance between antiviral defense and suppression of antiviral defense.

True or false: Viral RNA translation 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.

Plant virus genome replication is independent of host resources and factors.

Plants do not respond to virus infection through mechanisms such as autophagy, ubiquitination, mRNA decay, and gene silencing.

Viral factors and pro-viral host factors work in opposition during the infection cycle.

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 antagonistic activity of antiviral factors does not suggest a two-step model to explain plant-virus interactions.

Infection of a plant by a virus initiates in multiple cells.