title: SAGA complex mediates the transcriptional up-regulation of antiviral RNA silencing.
abstract: Pathogen recognition and transcriptional activation of defense-related genes are crucial steps in cellular defense responses. RNA silencing (RNAi) functions as an antiviral defense in eukaryotic organisms. Several RNAi-related genes are known to be transcriptionally up-regulated upon virus infection in some host organisms, but little is known about their induction mechanism. A phytopathogenic ascomycete,Cryphonectria parasitica(chestnut blight fungus), provides a particularly advantageous system to study RNAi activation, because its infection by certain RNA viruses induces the transcription of dicer-like 2 (dcl2) and argonaute-like 2 (agl2), two major RNAi players. To identify cellular factors governing activation of antiviral RNAi inC. parasitica, we developed a screening protocol entailing multiple transformations of the fungus with cDNA of a hypovirus mutant lacking the RNAi suppressor (CHV1-Δp69), a reporter construct with a GFP gene driven by thedcl2promoter, and a random mutagenic construct. Screening for GFP-negative colonies allowed the identification ofsgf73, a component of the SAGA (Spt-Ada-Gcn5 acetyltransferase) complex, a well-known transcriptional coactivator. Knockout of other SAGA components showed that the histone acetyltransferase module regulates transcriptional induction ofdcl2andagl2, whereas histone deubiquitinase mediates regulation ofagl2but notdcl2Interestingly, full-scale induction ofagl2anddcl2by CHV1-Δp69 required both DCL2 and AGL2, whereas that by another RNA virus, mycoreovirus 1, required only DCL2, uncovering additional roles for DCL2 and AGL2 in viral recognition and/or RNAi activation. Overall, these results provide insight into the mechanism of RNAi activation.
authors.affiliation: Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama 710-0046, Japan.
authors.forename: Ida Bagus
authors.initials: IB
authors.lastname: Andika
authors.affiliation: Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama 710-0046, Japan.
authors.forename: Atif
authors.initials: A
authors.lastname: Jamal
authors.affiliation: Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama 710-0046, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Kondo
authors.affiliation: Agrivirology Laboratory, Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama 710-0046, Japan nsuzuki@okayama-u.ac.jp.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Suzuki
mesh_terms: D001203:Ascomycota / Q000235:genetics / Q000378:metabolism / Q000821:virology; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D000067148:Fungal Viruses / Q000235:genetics / Q000378:metabolism; D020868:Gene Silencing; D012367:RNA, Viral / Q000235:genetics / Q000378:metabolism; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D005656:Fungal Proteins; D012367:RNA, Viral; D014764:Viral Proteins
keywords: Cryphonectria parasitica; RNAi; antiviral defense; hypovirus; mycovirus