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Fig. 5. Expression of nuclear effectors of the Egfr pathway prevents R8 differentiation. (A-H) Misexpression clones. sca-GAL4 was used to induce expression of UAS-Egfr^act, UAS-pnt-P1 or UAS-ro in R8. Third instar clones (A-E,G) are negatively marked by the absence of ßgal (green). (A-C) Misexpression of UAS-Egfr^act in R8. Expression of Sens (A), Ro (B) and Boss (C), are not disrupted, suggesting that robust activation of the Egfr pathway at the level of the cell membrane is not sufficient to perturb R8 differentiation. UAS-Egfr^act induced predicted phenotypes in other tissues (not shown), indicating that the transgene was active in this assay. (D-F) Misexpression of UAS-pnt-P1 in R8. (D,E) Apical (D) and basal (E) expression of Sens (red). Sens-expressing nuclei are not evenly spaced and are apically displaced. (F) Adult retinal sections at the level of R8 show ommatidia with a variably reduced number of photoreceptors and a lack of small rhabdomeres, consistent with a disruption of R8 differentiation and similar to sens loss-of-function phenotypes (arrow). Compare area of clone (below solid line) to neighboring wild-type tissue (above solid line). (G-H) Misexpression of UAS-ro in R8. (G) Expression of Sens (red) is initially wild type in appearance but is reduced by the fourth column of R8 differentiation and absent by the sixth column. (H) At the level of R8, no small rhabdomeres are detected within the clone (below solid line), phenocopying sens loss of function.

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