Electronic Journal of Biotechnology ISSN: 0717-3458
  © 2004 by Universidad Católica de Valparaíso -- Chile
Vol. 7 No. 3, Issue of December 15, 2004
 

 


Figure 2. A model for RNA-based TGS and PTGS. Steps involving dsRNA and steps that are affected by viral suppressors of PTGS and in various PTGS mutants are shown. TGS may be triggered directly by transcription of inverted repeat sequences in the nucleus and methylation of homologous promoter regions in the genome. In addition, dsRNA and other aberrant RNAs formed in the nucleus may be transported to the cytoplasm and enter the PTGS pathway. Two modes of dsRNA production lead to PTGS in the cytoplasm: first, virus induced gene silencing mediated by the viral RdRP, and second, transgene-induced gene silencing mediated by cellular RdRP. The dsRNA from either of these sources can be targeted by a putative dsRNA specific ribonuclease which generates 21-25 nt RNAs of both polarities (smRNAs). These smRNAs are incorporated into a ribonuclease and act as guides for sequence-specific degradation of homologous RNAs. dsRNAs from the cytoplasm may trigger methylation of homologous genomic sequences by transfer of a signal molecule into the nucleus. Similarly, PTGS can induce locally and then spread through the organism via production and transport of a mobile silencing signal. The signaling molecules are not known. HC-Pro suppresses gene silencing at a step upstream of the accumulation of the small RNAs but downstream of the mobile silencing signal, probably via activation of an endogenous cellular suppressor of PTGS, rgs-Cam. The PVX p25 suppressor of PTGS prevents the accumulation and / or transport of the mobile silencing signal, probably by interfering with the cellular RdRP branch of the pathway.


Supported by UNESCO / MIRCEN network