Abstract

Mycoviruses are known to be difficult to cure in fungi but their spontaneous loss occurs commonly. The unexpected disappearance of mycoviruses can be explained by diverse reasons, from methodological procedures to biological events such as posttranscriptional silencing machinery. The long-term effects of a virus infection on the host organism have been well studied in the case of human viruses; however, the possible residual effect on a fungus after the degradation of a mycovirus is unknown. For that, this study analyses a possible residual effect on the transcriptome of the pathogenic fungus Fusarium circinatum after the loss of the mitovirus FcMV1. The mycovirus that previously infected the fungal isolate was not recovered after a 4-year storage period. Only 14 genes were determined as differentially expressed and were related to cell cycle regulation and amino acid metabolism. The results showed a slight acceleration in the metabolism of the host that had lost the mycovirus by the upregulation of the genes involved in essential functions for fungal development. The analysis also revealed a weak expression in the annotated genes of the RNA silencing machinery. To our knowledge, this is the first time that a potential residual effect on the host transcriptome caused by the past infection of a mycovirus is reported.

Highlights

  • Mycoviruses are ubiquitous in fungi [1], generally causing cryptic and persistent infections [2,3]

  • The raw sequencing data have been deposited in the National Center for Biotechnology Information (NCBI) Sequence

  • The spontaneous loss of mycoviruses after a storage period is well known by mycovirus researchers, as far as we are aware this is the first time that a potential residual effect on the host transcriptome caused by a past infection of a mycovirus is reported

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Summary

Introduction

Mycoviruses are ubiquitous in fungi [1], generally causing cryptic and persistent infections [2,3]. The mycoviruses associated with this phenomenon have been reported in several plant pathogenic fungi, including Ophiostoma novo-ulmi, Botrytis spp., and Fusarium graminearum [11]. The model case of virocontrol of a forest disease is that of Cryphonectria parasitica hypovirus 1 (CHV1), the mycovirus of the highly destructive fungus of chestnut blight Cryphonectria parasitica. This hypovirus is used successfully as a biocontrol agent against chestnut blight in Europe and United States [12,13]. It has been demonstrated how a small DNA mycovirus of the necrotrophic pathogen

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