Long Terminal Repeat (LTR) retrotransposon represent a class of transposable elements (TEs) found in nearly all eukaryotic genomes. In Drosophila melanogaster, 11% of the genome is made up of LTR retrotransposons and their remnants. TEs can persist in a species only if they are capable of transposing into the germline lineage. Interestingly, errantiviruses, a subclass of LTR retrotransposons, which share structural and functional similarities with vertebrate endogenous retroviruses (ERV), persist in the Drosophila genome despite being expressed exclusively in somatic cells of the ovary. The transposition cycle of errantivirus and the mechanisms that enable them to transit from somatic cells to germ cells, and thus invade the genome of subsequent generations, remain enigmatic. To elucidate these mechanisms, this study will focus on a specific Drosophila errantivirus, ZAM. We created conditions in which the control of ZAM was abolished leading to its de novo reactivation in somatic gonadal cells and subsequent invasion of the germline (Yoth et al., 2023). Using this model and a combination of genetic, biochemical, and imaging approaches, my PhD project aims to dissect the molecular mechanisms involved in ERV infection and transposition.