LAUSR

to be faithfully maintained for normal homeostatic tissue functions. How cells integrate developmental and signalling-dependent instructions to acquire or alter transcriptional states remains a fundamental question in developmental biology. Polycomb and Trithorax group members act as epigenetic regulators to maintain target gene silencing or activation, respectively. Remarkably, tissues are capable of restoring homeostasis upon damage or stress, with inherent chromatin alterations supporting dynamic regulation of cell states. We are investigating how developmental and signalling pathways translate into modulating chromatin states underlying distinct tissue responses. Signalling pathways modulate developmental and regenerative processes but can also be exploited by cancer cells to promote tissue invasion and growth advantage. Motivated by the parallels between the two processes, we identified context-specific features that can discriminate regenerative from tumorigenic states. We explored the contribution of ectopic signalling pathways to promote tumour development upon impaired Polycomb silencing. We employed quantitative analyses to measure the effect of JNK, JAK/STAT and Notch pathways in a Drosophila epithelial tumour model and found that these pathways support tumour growth. Furthermore, JAK/STAT signalling functions in parallel to JNK, while Notch signalling relies on JNK. We thus defined a signalling hierarchy in tumours that is distinct from the sequential activation determined during tissue regeneration. Furthermore, we are also developing novel methods for tissuespecific chromatin profiling of rare cell populations. These approaches overcome the current limitations of small tissue amounts, and can be generally applicable to a diverse array of organisms and developmental stages. The combination of emerging technologies with powerful genetics in a real tissue context will support mechanistic insights driving chromatin alterations during development and homeostasis.