Publication | Open Access
Fertile Hypomorphic <i>ARGONAUTE</i> (<i>ago1</i>) Mutants Impaired in Post-Transcriptional Gene Silencing and Virus Resistance
621
Citations
34
References
2002
Year
Viral ReplicationViral Polymerase MechanismGeneticsMolecular BiologyMolecular GeneticsGenomicsPlant Molecular BiologyTranscriptional RegulationResistance Mutation (Virology)Virus GeneViral GeneticsRna ProcessingVirus ResistanceVirologyGene ExpressionPost-transcriptional Gene SilencingFunctional GenomicsBiologyDevelopmental BiologyArabidopsis Ago1 MutantsRna InterferenceNatural SciencesPlants PtgsGenetic MechanismMedicine
Post‑transcriptional gene silencing (PTGS) in plants, also called cosuppression or quelling, is mediated by PAZ/PIWI proteins such as AGO1 and is analogous to RNAi in animals, but Arabidopsis ago1 mutants exhibit severe developmental defects and sterility. This study isolates hypomorphic ago1 mutants that remain fertile. The fertile hypomorphic ago1 mutants are defective in PTGS, are more sensitive to AGO1 perturbation than development, and display hypersensitivity to viral infection, supporting PTGS as a plant antiviral defense.
Transgene-induced post-transcriptional gene silencing (PTGS) results from specific degradation of RNAs that are homologous with the transgene transcribed sequence. This phenomenon, also known as cosuppression in plants and quelling in fungi, resembles RNA interference (RNAi) in animals. Indeed, cosuppression/quelling/RNAi require related PAZ/PIWI proteins (AGO1/QDE-2/RDE-1), indicating that these mechanisms are related. Unlike Neurospora crassa qde-2 and Caenorhabditis elegans rde-1 mutants, which are morphologically normal, the 24 known Arabidopsis ago1 mutants display severe developmental abnormalities and are sterile. Here, we report the isolation of hypomorphic ago1 mutants, including fertile ones. We show that these hypomorphic ago1 mutants are defective for PTGS, like null sgs2, sgs3, and ago1 mutants, suggesting that PTGS is more sensitive than development to perturbations in AGO1. Conversely, a mutation in ZWILLE/PINHEAD, another member of the Arabidopsis AGO1 gene family, affects development but not PTGS. Similarly, mutations in ALG-1 and ALG-2, two members of the C. elegans RDE-1 gene family, affect development but not RNAi, indicating that the control of PTGS/RNAi and development by PAZ/PIWI proteins can be uncoupled. Finally, we show that hypomorphic ago1 mutants are hypersensitive to virus infection, confirming the hypothesis that in plants PTGS is a mechanism of defense against viruses.
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