L'inactivation épigénétique post-transcriptionnelle chez les végétaux : un mécanisme de résistance aux virus.

Abstract

Le développement de la transgénèse a permis de découvrir des phénomènes originaux d’inactivation de l’expression des gènes fondés sur la reconnaissance d’homologies de séquences. Bien qu’héritables par la mitose et par la méiose (comme des mutations classiques), ces phénomènes d’inactivation de gènes sont fréquemment réversibles (contrairement aux mutations) car ils n’impliquent aucune modification de la séquence nucléotidique de l’ADN. Les inactivations sont dues, soit à des modifications chimique et/ou structurale de l’ADN – altérant quantitativement ou qualitativement la transcription –, soit à des processus posttranscriptionnels aboutissant à la dégradation spécifique d’une population d’ARN. Plusieurs équipes ont démontré le rôle de ces processus dans le contrôle des transposons. Récemment, notre équipe a montré que les processus posttranscriptionnels permettaient aux plantes de se protéger contre certaines infections virales.

Post-transcriptional gene silencing (PTGS) in plants and quelling in fungi are transgene-induced silencing phenomena, resulting from the degradation of transgene RNAs and homologous endogenous RNAs. PTGS shows similarities with RNAi in animals, a phenomenon induced by injection of double-stranded RNA (dsRNA) or introduction of transgenes expressing dsRNA. First, PTGS and RNAi both involve dsRNA. Second, they can be dissected into three steps: localized initiation, propagation of a sequence-specific systemic signal, maintenance in silenced tissues. Finally, they both correlate with the accumulation of 25nt sense and anti-sense RNAs. Genetic dissection and cloning of genes regulating PTGS, quelling and RNAi confirmed the links between these three phenomena. Indeed, all three involve a putative RNA-dependent-RNA polymerase and a protein similar to the translation initiator factor eIF2C. However some differences can be noticed. In particular, PTGS in plants requires two genes, SGS3 (encoding a protein of unknown function) and MET1 (encoding a DNA-methyltransferase), which are not required for RNAi. Indeed, the genomes of C. elegans and Drosophila (two organisms undergoing RNAi) lack both methylation and orthologs of the SGS3 gene). Several experiments revealed that PTGS is a general mechanism of virus resistance. In particular, we showed that Arabidopsis mutants impaired in PTGS are hypersensitive to infection by the virus CMV. However, many viruses have developed strategies to counteract PTGS and therefore succeed to infect plants. Because viruses may act as targets, inducers or inhibitors of PTGS, the success and the extent of virus infection therefore depends on the competition between plant PTGS defenses and virus counteracting effects.