An imbalance in cell-cell signalling can cause over-proliferation or apoptosis. Endocytosis - which involves sorting ligand-bound receptors into vesicles for degradation - keeps cell-cell signalling in check. Protein sorting requires the vacuolar protein sorting (Vps) proteins, and vps25 mutant mosaics in the Drosophila eye have three distinct phenotypes: non-autonomous cell proliferation, non-autonomous resistance to apoptosis and cell-autonomous cell death. Bergmann and colleagues (p. 1871)have investigated the mechanisms behind these phenotypes by making detailed observations of vps25 mosaics, so extending recent published findings on this gene. They report that non-autonomous proliferation in vps25mutant mosaics is caused by inappropriate Notch signalling via JAK/STAT, and that cells surrounding vps25 clones are resistant to apoptosis due to increased Diap1 (Drosophila inhibitor of apoptosis protein 1) levels. As for cell-autonomous cell death, this is caused not only by Dronc-mediated apoptosis (clones lacking both vps25 and Ark can die), but probably involves JNK and Hippo. In light of this, the authors discuss the possibilities of using vps25 mosaics for modelling cancer.

© 2006.
2006