There is no living organism that does not contain transposons, and they make up a significant fraction, and in some instances, the vast majority of the genome in a given species. Owing to their proliferation propensity, these mobile genetic elements can create genetic variability providing selective benefits, but they also have a mutagenic potential. Therefore, host genomes have evolved epigenetic surveillance mechanisms to recognize and silence transposons. If maintenance of silencing is rather well understood, little is know about how the host recognize transposons as non-self elements and initiate silencing as they invade the genome. Also, although several examples indicate that a variety of environmental factors can reverse transposon silencing, how such factors interfere with the silencing machinery is largely unknown. The proposed research project will make use of our recent discovery of active endogenous retrotransposons in Arabidopsis to decipher genetically the mechanisms involved in initiating silencing of a transposon. In parallel, we will characterize how DNA-methylation associated silencing can be efficiently re-established once it has been lost, and use a genome-wide approach to determine the extent of this phenomenon. Finally, we intend to determine the genome-wide impact of a stress on transposon silencing and to genetically identify and characterize the molecular bases of stress-induced release of silencing at transposons. Our studies have the potential to bring general insights into how transposons have been so successful in colonizing host genomes, how they are kept under tight control and can be unleashed thereby contributing to genome plasticity and environmental adaptation.