Transcriptional control and exploitation of an immune-responsive family of retrotransposons in Arabidopsis

Abstract

Mobilization of transposable elements (TEs) in plants has been recognized as a driving force of evolution and adaptation, in particular by providing genes with regulatory modules that impact their transcription. In this study, we employed an ATCOPIA93 Long terminal repeats (LTR) promoter-GUS fusion to show that this retrotransposon behaves like an immune-responsive gene during plant defense in Arabidopsis. We also showed that the reactivation of the endogenous ATCOPIA93 copy \"EVD\", in the presence of bacterial stress, is not only negatively regulated by DNA methylation but also by Polycomb-mediated silencing--a mode of repression typically found at protein-coding and microRNA genes. Interestingly, one of the ATCOPIA93-derived soloLTRs is located upstream of the disease resistance gene RPP4 and is devoid of either DNA methylation or H3K27m3 marks. Through loss-of-function experiments, we demonstrated that this soloLTR is required for proper expression of RPP4 during plant defense, thus linking the responsiveness of ATCOPIA93 to biotic stress and the co-option of its LTR for plant immunity.