PT  - JOURNAL ARTICLE
AU  - Angel Emilio Martínez de Alba
AU  - Ana Beatriz Moreno
AU  - Marc Gabriel
AU  - Allison C. Mallory
AU  - Aurélie Christ
AU  - Rémi Bounon
AU  - Sandrine Balzergue
AU  - Sebastien Aubourg
AU  - Daniel Gautheret
AU  - Martin D. Crespi
AU  - Hervé Vaucheret
AU  - Alexis Maizel
TI  - In plants, decapping prevents RDR6-dependent production of small interfering RNAs from endogenous mRNAs
AID  - 10.1101/013912
DP  - 2015 Jan 01
TA  - bioRxiv
PG  - 013912
4099  - http://biorxiv.org/content/early/2015/01/16/013912.short
4100  - http://biorxiv.org/content/early/2015/01/16/013912.full
AB  - Cytoplasmic degradation of endogenous RNAs is an integral part of RNA quality control (RQC) and often relies on the removal of the 5’ cap structure and their subsequent 5’ to 3’ degradation in cytoplasmic processing (P-)bodies. In parallel, many eukaryotes degrade exogenous and selected endogenous RNAs through post-transcriptional gene silencing (PTGS). In plants, PTGS depends on small interfering (si)RNAs produced after the conversion of single-stranded RNAs to doublestranded RNAs by the cellular RNA DEPENDENT RNA POLYMERASE 6 (RDR6) in cytoplasmic siRNA-bodies. PTGS and RQC compete for transgene-derived RNAs, but it is unknown whether this competition also occurs for endogenous transcripts. Here, we show that the lethality of decapping mutants is suppressed by impairing RDR6 activity. We also show that upon decapping impairment hundreds of endogenous mRNAs give rise to a new class of siRNAs, a subset of which depends on RDR6 for their production. We observe that, in vivo, P- and siRNA-bodies often are juxtaposed and remain associated while moving in an actin-dependent manner, potentially allowing for cross-talk of the two machineries. Our results suggest that the decapping of aberrant endogenous RNA in P-bodies limits their entry into the PTGS pathway and prevents the subsequent deleterious consequences arising from this entry. We anticipate that the siRNAs identified in decapping mutants represent a subset of a larger ensemble of endogenous siRNAs. We call them rqc-siRNAs due to their over-accumulation when RQC processes are impaired.