Open AccessThe ORF2 protein of Fusarium graminearum virus 1 suppresses the transcription of FgDICER2 and FgAGO1 to limit host antiviral defences
Author(s) -
Yu Jisuk,
Park Ju Yeon,
Heo JeongIn,
Kim KookHyung
Publication year - 2020
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12895
Subject(s) - biology , rna interference , rna silencing , rna , small hairpin rna , mutant , small interfering rna , transcription (linguistics) , gene silencing , green fluorescent protein , open reading frame , microbiology and biotechnology , virology , gene , genetics , peptide sequence , linguistics , philosophy
Summary The filamentous fungus Fusarium graminearum possesses an RNA‐interference (RNAi) pathway that acts as a defence response against virus infections and exogenous double‐stranded (ds) RNA. Fusarium graminearum virus 1 (FgV1), which infects F. graminearum , confers hypovirulence‐associated traits such as reduced mycelial growth, increased pigmentation and reduced pathogenicity. In this study, we found that FgV1 can suppress RNA silencing by interfering with the induction of FgDICER2 and FgAGO1 , which are involved in RNAi antiviral defence and the hairpin RNA/RNAi pathway in F. graminearum . In an FgAGO1 ‐ or FgDICER2 ‐promoter/GFP‐reporter expression assay the green fluorescent protein (GFP) transcript levels were reduced in FgV1‐infected transformed mutant strains. By comparing transcription levels of FgDICER2 and FgAGO1 in fungal transformed mutants expressing each open reading frame (ORF) of FgV1 with or without a hairpin RNA construct, we determined that reduction of FgDICER2 and FgAGO1 transcript levels requires only the FgV1 ORF2‐encoded protein (pORF2). Moreover, we confirmed that the pORF2 binds to the upstream region of FgDICER s and FgAGO s in vitro . These combined results indicate that the pORF2 of FgV1 counteracts the RNAi defence response of F. graminearum by interfering with the induction of FgDICER2 and FgAGO1 in a promoter‐dependent manner.