Summary diagrams.

<p>(A) R7, R1/6 and the cone cells form an equivalence group. Manipulations of the RTK/N pathways can freely transform fates between the R7, R1/6 and the cone cell types. Any cell can form any of the three fates depending on the signals that it receives. (B) N activates a repressor of photoreceptor development that DER cannot overcome but Sev can. In the upper level, the wild type situation is depicted. Here we infer that a DER activating signal from the R2 (red arrow) specifies the R1 precursor as a photoreceptor (R1/6 type). In the middle level, when N is ectopically active in the R1 precursor in the absence of sev, the DER activating signal is unable to specify the R1 precursor as a photoreceptor. In the lower level, when N is ectopically active in the R1 precursor in the presence of the <i>sev</i> gene, the cell is specified as a photoreceptor (R7 type). (C) A model of fate R1/6/7/cone cell specification. (i) The precluster cells express low levels of <i>Dl</i> (black arrows). (ii) Cells are recruited into defined niches; the first three being those on the R5/8/2 face. Three cells occupy these positions and Dl from the precluster activates mild N signaling (weak shade of gray), which provides a weak block to photoreceptor specification. Spitz expressed by R2/5 (red arrows) activates DER in the cells in the R1/6 position and overcomes the N block. (C) R1/6 begin differentiation as photoreceptors and express high levels of Dl as cells join the niches of the two flanking cone cells. The cell in the R7 position and these presumptive cone cells receive Dl from R1/6 and N is activated to high levels (dark gray). This provides a potent barrier to photoreceptor specification and also activates <i>sev</i> transcription. Binding of Sev to Boss on R8 provides high-level RTK activity (blue arrow). (iv) The RTK signaling specifies the R7 precursor as photoreceptor and the concomitant presence of activated N directs the R7 rather than the R1/6 photoreceptor type. R7 proceeds to express high levels of Dl, as do the two cone cells and R3. As the subsequent cone cells join, they receive these Dl signals and activate both the barrier to photoreceptor differentiation and <i>sev</i> expression. (V) None of the cone cell precursors contact R8 so none have activated Sev, and Spitz diffusing from R2/5 is unable to trigger the photoreceptor fate because of the high N activity.