Dicer functions transcriptionally and posttranscriptionally in a multilayer antiviral defense

In antiviral RNA interference (RNAi), Dicer plays a primary role in processing double-stranded RNA (dsRNA) molecules into small-interfering RNAs (siRNAs) that guide Argonaute effectors to posttranscriptional suppression of target viral genes. Here, we show a distinct role for Dicer in the siRNA-inde...

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Published in:Proceedings of the National Academy of Sciences - PNAS Vol. 116; no. 6; p. 2274
Main Authors: Andika, Ida Bagus, Kondo, Hideki, Suzuki, Nobuhiro
Format: Journal Article
Language:English
Published: United States 05.02.2019
Subjects:
Ascomycota - genetics
Ascomycota - metabolism
Ascomycota - virology
Disease Resistance - genetics
Disease Resistance - immunology
Fungal Proteins - genetics
Fungal Proteins - metabolism
Gene Expression Regulation, Fungal
Host-Pathogen Interactions - genetics
Mutation
Phenotype
Ribonuclease III - genetics
Ribonuclease III - metabolism
RNA Processing, Post-Transcriptional
Transcription, Genetic
Virus Diseases - genetics
Virus Diseases - virology
Viruses
Cryphonectria parasitica
fungal virus
RNA silencing
antiviral defense
SAGA
ISSN:1091-6490, 1091-6490
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Summary:In antiviral RNA interference (RNAi), Dicer plays a primary role in processing double-stranded RNA (dsRNA) molecules into small-interfering RNAs (siRNAs) that guide Argonaute effectors to posttranscriptional suppression of target viral genes. Here, we show a distinct role for Dicer in the siRNA-independent transcriptional induction of certain host genes upon viral infection in a filamentous fungus. Previous studies have shown that the two key players, dicer-like 2 ( ) and argonaute-like 2 ( ), of antiviral RNAi in a phytopathogenic ascomycete, , are highly transcriptionally induced upon infection with certain RNA mycoviruses, including the positive-stranded RNA hypovirus mutant lacking the RNAi suppressor ( hypovirus 1-Δp69, CHV1-Δp69). This induction is regulated by the Spt-Ada-Gcn5 acetyltransferase (SAGA) complex, a well-known transcriptional coactivator. The present study shows that diverse host genes, in addition to and , were up-regulated more than 10-fold by SAGA upon infection with CHV1-Δp69. Interestingly, DCL2, but not AGL2, was essential for SAGA-mediated global gene up-regulation. Moreover, deletion of certain virus-induced genes enhanced a CHV1-Δp69 symptom (growth rate) but not its accumulation. Constitutive, modest levels of expression drastically reduced viral siRNA accumulation but were sufficient for full-scale up-regulation of host genes, suggesting that high induction of and siRNA production are not essential for the transcriptional up-regulation function of DCL2. These data clearly demonstrate the dual functionality of DCL2: as a dsRNA-specific nuclease in posttranscriptional antiviral RNA silencing and as a key player in SAGA-mediated host gene induction, which independently represses viral replication and alleviates virus-induced symptom expression.
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ISSN:1091-6490
1091-6490
DOI:10.1073/pnas.1812407116