Attacking the defenders: plant viruses fight back.
Levy Avner,Dafny-Yelin Mery,Tzfira Tzvi
Trends in microbiology
Plants use RNA silencing mechanisms and produce short-interfering RNA (siRNA) molecules in a defense response against viral infection. To counter this defense response, viruses produce suppressor proteins, which can block the host silencing pathway or interfere with its function in plant cells. The targets for many viral suppressors and the mechanisms by which they function in plant cells are still largely unknown. Recent reports describe that the 2b suppressor of the Cucumber mosaic virus binds ARGONAUTE and that the P0 suppressor of Polerovirus targets ARGONAUTE to degradation. Another report has revealed that the V2 suppressor of tomato yellow mosaic virus binds the coiled-coil protein suppressor of the gene-silencing SGS3 homolog. These reports provide novel insight into the mechanisms developed by viruses to disable the defense system of the plant.
Arabidopsis SGS2 and SGS3 genes are required for posttranscriptional gene silencing and natural virus resistance.
Mourrain P,Béclin C,Elmayan T,Feuerbach F,Godon C,Morel J B,Jouette D,Lacombe A M,Nikic S,Picault N,Rémoué K,Sanial M,Vo T A,Vaucheret H
Posttranscriptional gene silencing (PTGS) in plants resuits from the degradation of mRNAs and shows phenomenological similarities with quelling in fungi and RNAi in animals. Here, we report the isolation of sgs2 and sgs3 Arabidopsis mutants impaired in PTGS. We establish a mechanistic link between PTGS, quelling, and RNAi since the Arabidopsis SGS2 protein is similar to an RNA-dependent RNA polymerase like N. crassa QDE-1, controlling quelling, and C. elegans EGO-1, controlling RNAi. In contrast, SGS3 shows no significant similarity with any known or putative protein, thus defining a specific step of PTGS in plants. Both sgs2 and sgs3 mutants show enhanced susceptibility to virus, definitively proving that PTGS is an antiviral defense mechanism that can also target transgene RNA for degradation.
The epigenetic factor FVE orchestrates cytoplasmic SGS3-DRB4-DCL4 activities to promote transgene silencing in .
Sun Di,Li Yanjun,Ma Zeyang,Yan Xingxing,Li Niankui,Shang Baoshuan,Hu Xiaomei,Cui Kai,Koiwa Hisashi,Zhang Xiuren
Posttranscriptional gene silencing (PTGS) is a regulatory mechanism to suppress undesired transcripts. Here, we identified (), a well-known epigenetic component, as a new player in cytoplasmic PTGS. Loss-of-function mutations substantially reduced the accumulation of transgene-derived small interfering RNAs (siRNAs). FVE interacts with suppressor of gene silencing 3 (SGS3), a master component in PTGS. FVE promotes SGS3 homodimerization that is essential for its function. FVE can bind to single-stranded RNA and double-stranded RNA (dsRNA) with moderate affinities, while its truncated form FVE-8 has a significantly increased binding affinity to dsRNA. These affinities affect the association and channeling of SGS3-RNA to downstream dsRNA binding protein 4 (DRB4)/Dicer-like protein 2/4 (DCL2/4) complexes. Hence, FVE, but not FVE-8, biochemically enhances the DRB4/DCL2/4 activity in vitro. We surmise that FVE promotes production of transgene-derived siRNAs through concertedly tuning SGS3-DRB4/DCL2/4 functions. Thus, this study revealed a noncanonical role of FVE in PTGS.