期刊
NUCLEIC ACIDS RESEARCH
卷 41, 期 8, 页码 4699-4708出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkt152
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资金
- Agence Nationale de la Recherche [ANR-08-BLAN-0082, ANR-10-LABX-40]
- Land Baden-Wurttemberg, Chica und Heinz Schaller Stiftung
- CellNetworks cluster of excellence
- Agence Nationale de la Recherche, Chica und Heinz Schaller Stiftung [ANR-08-BLAN-0082]
- Chica und Heinz Schaller Stiftung
Eukaryotic RNA quality control (RQC) uses both endonucleolytic and exonucleolytic degradation to eliminate dysfunctional RNAs. In addition, endogenous and exogenous RNAs are degraded through post-transcriptional gene silencing (PTGS), which is triggered by the production of double-stranded (ds)RNAs and proceeds through short-interfering (si)RNA-directed ARGONAUTE-mediated endonucleolytic cleavage. Compromising cytoplasmic or nuclear 5'-3' exoribonuclease function enhances sense-transgene (S)-PTGS in Arabidopsis, suggesting that these pathways compete for similar RNA substrates. Here, we show that impairing nonsense-mediated decay, deadenylation or exosome activity enhanced S-PTGS, which requires host RNA-dependent RNA polymerase 6 (RDR6/SGS2/SDE1) and SUPPRESSOR OF GENE SILENCING 3 (SGS3) for the transformation of single-stranded RNA into dsRNA to trigger PTGS. However, these RQC mutations had no effect on inverted-repeat-PTGS, which directly produces hairpin dsRNA through transcription. Moreover, we show that these RQC factors are nuclear and cytoplasmic and are found in two RNA degradation foci in the cytoplasm: siRNA-bodies and processing-bodies. We propose a model of single-stranded RNA tug-of-war between RQC and S-PTGS that ensures the correct partitioning of RNA substrates among these RNA degradation pathways.
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