Transposable elements (TEs) are abundant and dynamic components of genomes, capable of both disrupting and shaping genetic information. To investigate these dual roles, our team explores how host genomes regulate TEs, how these controls evolve during development, and how some TEs may be repurposed by the host. Using Drosophila melanogaster as a model, we combine genetics, epigenomics, molecular and cellular biology, and developmental approaches to address three main questions:

1. How is TE silencing established and preserved through development?
   We aim to understand how transposable element repression is initiated during development and how this repression is maintained over time in differentiated cells. In this context, using the Drosophila ovarian soma as a model, we combine genetic tools and live imaging to explore the temporal dynamics of piRNA-mediated silencing and to assess the stability and memory of this repression across developmental stages.

2. Exploring the biological significance of TE expression during development
   Some TEs escape silencing and are expressed in specific developmental windows or tissues. To better understand these events, we explore their functional consequences, their potential roles in developmental processes, and the host regulatory circuits that allow or restrict them. Through this work, we contribute to redefining TEs not only as threats but also as possible developmental actors.

3. From soma to germline: decoding the infectious potential of endogenous retroviruses
   Some retrotransposons, known as endogenous retroviruses (ERVs), retain genes reminiscent of infectious retroviruses, including envelope-like proteins. In particular, in Drosophila, several of these elements are expressed specifically in somatic follicle cells and have the potential to invade the germline. Our objective is to understand the molecular mechanisms that enable such intercellular transfer, with a particular focus on the role of TE-encoded proteins and their interaction with host factors. To this end, we use genetic, molecular, and proteomic approaches to uncover how endogenous retroelements exploit cellular environments to ensure their propagation.