Poly(A) tail length regulation by mRNA deadenylases is critical for suppression of transposable elements

Abstract

Transposons are mobile genetic elements that can impair the host genome stability and integrity. In plants, suppression of transposons is thought to be mediated mainly by small RNAs; however, the role of RNA decay in posttranscriptional repression of transposons is unknown. Here we show that RNA deadenylation is critical for controlling transposons in Arabidopsis. Previously, we demonstrated that transposon RNAs often harbor structural aberrancy owing to its inherently suboptimal codon usage and ribosome stalling. Such RNA aberrancy is monitored and resolved by RNA decay which is initiated by removal of poly(A) tail or deadenylation. The CCR4-NOT complex is a primary RNA deadenylase in Arabidopsis, and we found that it is required for stable repression of transposons. Intriguingly, RNA deadenylation controls transposons that are not targeted by cytoplasmic secondary small RNAs, which implies a target-specific regulation of transposon by the host. Our study suggests a previously unknown mechanism for transposon repression mediated by RNA deadenylation and unveils a complex nature of the host strategy to maintain the genome integrity.