Supplemental Figure 1
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Fig. S1. Loss of Ser function results in selective upregulation of Wg and induction of cell death in the ventral eye. Targeted misexpression of SerDN was used to abolish Ser function in the eye using an ey-GAL4 driver. (A,A′) Loss-of-function of Ser results in loss of ventral eye (A) and ectopic induction of Wg on the ventral eye margin (arrow; A′). (B-D) In the Ser-mutant background, increasing levels of Wg signaling by misexpressing wg (ey>SerDN+wg; C) and arm (ey>SerDN+arm) results in enhancement of the loss of ventral eye phenotype to no-eye, whereas reducing Wg signaling by misexpressing Sgg (ey>SerDN+SggA9), an antagonist of Wg signalling, results in significant rescue of the loss of ventral eye phenotype. (E,E′) Abolishing Ser function in the eye (ey>SerDN) resulted in the selective loss of ventral eye cells by the induction of cell death, as shown by TUNEL- positive cells nuclei on the ventral eye margin (arrow). Blocking cell death by misexpressing diap1 (ey>SerDN +diap1) results in significant rescue of the ventral eye loss.
