MECHANISMS OF TUMORIGENESIS IN DROSOPHILA

Using Drosophila, our research focuses on the Jun N-terminal Kinase (JNK) pathway's roles in regeneration and tumorigenesis. JNK induces apoptosis in damaged cells and promotes proliferation via paracrine signaling, impacting the JAK/STAT, Wingless, and Decapentaplegic pathways. We've identified JNK's significance in tumorigenesis, studying its effects in mutations like scribble, erupted, and polyhomeotic. Moreover, we've revealed how overgrowing tumor cells can restrict normal tissue growth. Additionally, JNK induces senescence in Drosophila cells, secreting growth signals that influence neighboring tissue. We're also investigating chromatin remodeling during tissue regeneration and found that retrotransposons impact chromatin accessibility. Our work sheds light on cellular processes in regeneration, tumorigenesis, and chromatin dynamics.