植物病 DNA病毒 感染细胞非感染细胞 Infected cell Non-infected Cell 毒入侵 RNA病毒 RNA virus 诱导产 MMUNIZATION 免疫 7DCL4 扩放 生的 SMD1 Stabilizatio i CH3- 短距离扩散 次生 扩放 Passenger ,. o@降解 RNADNA virus SDE3 transcription SIRNA stational 诱导系统抗性 The figure shows how primary viRNAs (1st) are amplified into secondary viRNAs(2nd)in the RDR6-dependent pathway. Aberrant (ab)viral mRNAs lacking a cap or polya tail (AAA) can enter RNA-dependent RNA polymerase pathways independently of 1st viRNA synthesis. A DCL4-dependent silencing signal (arbitrarily depicted as free 21 nucleotide viRNAs )moves through the plasmodesmata(P)to immunize neighboring cells Movement may be enhanced through further rounds of amplification involving viral transcripts that enter immunized cells. VSRs and potential endogenous silencing suppressors(red ) represent genetic rather than direct physical interactions with host silencing components植物病 毒入侵 诱导产 生的 次生 siRNA The figure shows how primary viRNAs (1st) are amplified into secondary viRNAs (2nd) in the RDR6-dependent pathway. Aberrant (ab) viral mRNAs lacking a cap or polyA tail (AAA) can enter RNA-dependent RNA polymerase pathways independently of 1st viRNA synthesis. A DCL4-dependent silencing signal (arbitrarily depicted as free 21 nucleotide viRNAs) moves through the plasmodesmata (P) to immunize neighboring cells. Movement may be enhanced through further rounds of amplification involving viral transcripts that enter immunized cells. VSRs and potential endogenous silencing suppressors (red) represent genetic rather than direct physical interactions with host silencing components