Fecha de publicación: -- Fuente: PubMed "Tomato process" Nat Plants. 2026 Nov 5. doi: 10.1038/s41477-026-02458-7. Online ahead of print.ABSTRACTRNA silencing plays a central role in plant antiviral defence, in which viral RNA is processed into small RNAs (sRNAs) that guide Argonaute-mediated cleavage of viral transcripts. Among these, 22-nucleotide (nt) sRNAs are unique in their ability to trigger secondary sRNA production, thereby amplifying transitive silencing. In tomato, this 22-nt antiviral pathway is strongly activated upon virus infection through the upregulation of DCL2b, yet the underlying mechanism has remained unclear. miR6026, generated by DCL2b and targeting DCL2b itself, forms a feedback loop that fine-tunes this response. Here we show that tobacco mosaic virus (TMV) and tomato bushy stunt virus (TBSV) activate DCL2b transcription via the Dof16 transcription factor. Transcription of MIR6026 is also activated by both TMV and TBSV, while viral infection promotes DCL2b relocalization towards the cytoplasm, preventing pri-miR6026 processing into mature miR6026. This redistribution is associated with reduced phosphorylation of DCL2b at Tyr69, which weakens its interaction with importin-α and limits its nuclear localization. Notably, Arabidopsis DCL2 exhibits a similar virus-induced relocalization pattern, highlighting a conserved mechanism that enhances antiviral silencing during infection while minimizing off-target effects on host genes under normal conditions.PMID:42988911 | DOI:10.1038/s41477-026-02458-7