期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2019
卷号：116
期号：6
页码：2274-2281
DOI：10.1073/pnas.1812407116
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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 ( dcl2 ) and argonaute-like 2 ( agl2 ), of antiviral RNAi in a phytopathogenic ascomycete, Cryphonectria parasitica , are highly transcriptionally induced upon infection with certain RNA mycoviruses, including the positive-stranded RNA hypovirus mutant lacking the RNAi suppressor ( Cryphonectria 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 dcl2 and agl2 , 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 dcl2 expression drastically reduced viral siRNA accumulation but were sufficient for full-scale up-regulation of host genes, suggesting that high induction of dcl2 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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