Eukaryotic cells are continuously exposed to DNA damaging insults that can break or chemically modify their DNA. Double-strand breaks (DSBs) are particularly dangerous because their improper repair can directly lead to insertions, deletions, or major structural chromosomal rearrangements. DNA is packaged into a variety of chromatin domains, which each have specific molecular and biophysical properties that can influence the DSB response. Whereas euchromatin contains open, actively transcribed regions, heterochromatic regions mainly consist of compact, silent genomic regions. One major type of heterochromatin is facultative heterochromatin, which is essential to silence developmental genes throughout organismal development. Facultative heterochromatin is enriched for trimethylation of histone 3 lysine 27 (H3K27me3) as well as polycomb proteins, and accumulates in sub-nuclear foci, called polycomb bodies. Although the DNA repair response in euchromatic regions has been extensively studied, the repair response in polycomb-enriched chromatin remains largely unknown. We hypothesize that this heterochromatin subtype requires distinct chromatin- or DNA repair- responses to ensure safe DSB repair. To study the DSB response in polycomb chromatin, we here integrate a previously established inducible single DSB system (A. Janssen et al. G&D 2016) in Drosophila tissue in either euchromatin or polycomb chromatin. Using this system, we find that DSBs in polycomb chromatin employ the canonical repair pathways Homologous Recombination and Non-Homologous End-Joining. Moreover, chromatin analysis reveals local changes in the f-Het chromatin landscape specifically at the break site. We hypothesize that these DSB-induced chromatin changes are necessary to detect, access or process the DNA break. Together, our data indicate that DSBs in polycomb chromatin use canonical DSB repair pathways and require specific local chromatin changes for their faithful repair.