Transposons are mobile genetic elements that can cause fatal mutations in the genomes. To counteract these genome invaders, host genomes have evolved elaborate mechanisms which involve short interfering (si)-RNAs. In plants, RNA-DEPENDENT RNA POLYMERASE 6 (RDR6)-SUPPRESSOR OF GENE SILENCING 3 (SGS3) complex serves as a detector of non-self RNAs that selectively recognizes and duplexes the transposon RNAs which are then later processed to siRNAs. Transposon-derived siRNAs triggers both post-transcriptional repression and priming of epigenetic silencing. However, the regulatory mechanisms for the selective recognition of transposon RNAs and the initiation of siRNA-mediated epigenetic silencing are still unknown. Here we show that transposon RNAs undergo frequent ribosome stalling presumably owing to their unfavourable codon sequence usage, which eventually causes the RNA truncation and the localization to stress granules. The cleavage of RNAs is a critical prerequisite for RDR6 recognition of its targets. We found that transposon RNAs are more prone to RNA truncation likely mediated through translation-dependent RNA decay pathways. Stress granules are membrane-less cytoplasmic organelles, where RDR6 and SGS3 are located. We observed that SGS3 forms liquid droplets in vitro presumably through prion-like domains. Stress granules are known to contain weakly translating RNAs and indeed our stress granule-enriched RNA-seq revealed that transposon RNAs are strongly enriched in the stress granules. In short, the host genome detects transposons by their reduced translational status which leads to RNA truncation and stress granule localization that both contribute to selective targeting of transposon RNAs to the siRNA production pathway. Our study provides a novel insight into the regulatory mechanisms for the recognition of invasive genetic elements and the initiation of epigenetic silencing essential for the maintenance of genome integrity.