Fig. 3. Visualization of Notch-dependent Su(H)-reporter activity (p12xSu(H)bs-lacZ) in embryos (single abdominal segment; dorsal up, anterior to left). (A-C) The reporter lacZ expression in stage 12 embryos. (A) A normal control embryo. (B) Notch^55e11 mutant embryo. (C) sanpodo^C55 mutant embryo. The reporter gene activity was dramatically reduced in B and C. (D-G) The lacZ reporter expression in the dbd lineage of stage 16 embryos. Arrows in D, E and G indicate DBDG. (D) In normal embryos strong nuclear staining is observed in DBDG but not in the neuron (encircled by dots). (E) When a constitutively active form of Notch was expressed in neurons (UAS- Notch^act/C155-GAL4), ectopic Su(H)-reporter activity was observed in the dbd neuron (dotted circle). (F) In the sanpodo mutation, which produces a double-neuron phenotype at the expense of the glial cell, the reporter activity is undetectable in cells of the dbd lineage cells (dotted circle). (G) Misexpression of gcm in neurons (UAS-gcm/C155-GAL4) does not activate the reporter in the dbd neuron that is transformed to a glial cell (dotted circle).

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