Résumé
In plants, transgenes can be silenced at both the transcriptional [1] and post-transcriptional levels [2]. Methylation of the transgene promoter correlates with transcriptional gene silencing (TGS) [3] whereas methylation of the coding sequence is associated with post-transcriptional gene silencing (PTGS) [4]. In animals, TGS requires methylation and changes in chromatin conformation [5]. The involvement of methylation during PTGS in plants is unclear and organisms with non-methylated genomes such as Caenorhabditis elegans or Drosophila can display RNAinterference (RNAi), a silencing process mechanistically related to PTGS [6]. Here, we crossed Arabidopsis mutants impaired in a SWI2/SNF2 chromatin component (ddm1[7]) or in the major DNA methyltransferase (met1[8] and E. Richards, personal communication) with transgenic lines in which a reporter consisting of the cauliflower mosaic virus 35S promoter fused to the β-glucuronidase (GUS) gene (35S–GUS) was silenced by TGS or PTGS. We observed an efficient release of 35S–GUS TGS by both the ddm1 and met1 mutations and stochastic release of 35S–GUS PTGS by these two mutations during development. These results show that DNA methylation and chromatin structure are common regulators of TGS and PTGS.