Figure 6.

Model of non-cell autonomous induction of Diap-1 by cells with ligand-independent deregulated Hh activity. Drawn are three cells at a clonal boundary in the MF, one mutant cell (cell A) with deregulated Hh activity (blue) and two non-mutant cells (cells B and C; white to light red). The mutant cell accumulates CiA, which promotes autonomous N activity (purple arrow) and stimulates Dl expression (green arrow). Autonomous N signaling releases an unknown extracellular factor that promotes transcription of diap1 in the first signal-receiving non-mutant cell, cell B. In the same non-mutant cell, Dl induces non-cell autonomous N activity, which in turn promotes transcription of diap1 in the second non-mutant cell, cell C. In this manner, cells with deregulated Hh signaling transmit increased apoptosis resistance to neighboring cells by upregulation of Diap-1. When the MF moves into clones of deregulated Hh activity, GMR-driven hid expression (red) will be inhibited by increased Diap-1 levels, resulting in suppression of the GMR-hid eye phenotype. The white-to-red color gradient in cells B and C indicates the approaching hid-expressing wave driven by GMR