Mycoviruses, RNA Silencing, and Viral RNA Recombination

Abstract

In contrast to viruses of plants and animals, viruses of fungi, mycoviruses, uniformly lack an extracellular phase to their replication cycle. The persistent, intracellular nature of the mycovirus life cycle presents technical challenges to experimental design. However, these properties, coupled with the relative simplicity and evolutionary position of the fungal host, also provide opportunities for examining fundamental aspects of virus–host interactions from a perspective that is quite different from that pertaining for most plant and animal virus infections. This chapter presents support for this view by describing recent advances in the understanding of antiviral defense responses against one group of mycoviruses for which many of the technical experimental challenges have been overcome, the hypoviruses responsible for hypovirulence of the chestnut blight fungus Cryphonectria parasitica. The findings reveal new insights into the induction and suppression of RNA silencing as an antiviral defense response and an unexpected role for RNA silencing in viral RNA recombination.

Gene silencing and gene expression in phytopathogenic fungi using a plant virus vector

“…Like animal and plant viruses, mycoviruses are also inducers, targets, and suppressors of RNAi involved in the antiviral defense response (23). In the case of Cryphonectria parasitica, the RNAi-based response against hypovirus infection contributed to hypovirus RNA recombination.…”

Multiple approaches for the detection and characterization of viral and plasmid symbionts from a collection of marine fungi

“…This phenomenon is particularly relevant in some yeasts, where co-evolution with ecologically relevant virus presence (causing the advantageous "killer" phenotype) has brought to the absence of the silencing machinery altogether (Drinnenberg et al, 2011), and therefore sRNA approaches would have failed any detection in these specific fungal species. It is also true that mycoviruses show the ability to suppress the RNA silencing antiviral response (Nuss, 2011). This could also be another explanation for the differences observed in generating sRNA from specific viruses particularly in the case of the isolate MUT4330, which is unique for hosting six different virus specie behaving very differently in respect to generating vsRNA: in this case it is safe to assume that indeed it is a virus encoded factor which determines the different specific outcome for each species.…”

A Novel Victorivirus from a Phytopathogenic Fungus, Rosellinia necatrix, Is Infectious as Particles and Targeted by RNA Silencing

“…These technical aspects include availability of reverse genetics systems for hypoviruses (family Hypoviridae) (18,19), transfection protocols for mycoreoviruses (family Reoviridae) (12), and host genome manipulability, i.e., homologous-recombination-based gene disruption and multiple gene transformation techniques (20)(21)(22)(23). Importantly, great advances have been made in our understanding of RNA silencing (RNAi) as an antiviral host defense mechanism in this fungus (24). Like many other filamentous ascomycetous fungi (25), C. parasitica carries two Dicer-like genes (dcl-1 and dcl-2), four Argonaute-like genes (agl-1 to agl-4), and four RdRp genes (rdr-1 to rdr-4) as possible key RNA silencing components.…”