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Fig. 6. dachshund acts strongly to activate Fmrf expression in combination with ap and BMP signaling. Small inset panels show close-ups of Fmrf expression in the ap-cluster. (A-D) Misexpression within the peptidergic compartment using c929-GAL4. Misexpression of dac alone does not trigger ectopic Fmrf-lacZ (A), but co-misexpression of both dac and ap triggers ectopic Fmrf-lacZ in the Plc cells (B). Both endogenous and ectopic Fmrf-lacZ expression is dependent upon BMP signaling, as only SE2 cells express Fmrf in wit mutants (C; c929-GAL4, Fmrf-lacZ/UAS-ap; wit^A12, UAS-dac/wit^B11). Misexpression of dac and ap together with BMP activation triggers extensive ectopic Fmrf-lacZ expression (D; c929-GAL4, Fmrf-lacZ/UAS-tkv^A, UAS-sax^A; UAS-ap, UAS-dac/+). dAp, Crz and Tvb cells (inset) all express Fmrf (D). (E-G) Misexpression within all postmitotic neurons using elav^GAL4. Misexpression of dac alone triggers Fmrf-lacZ expression in a small subset of posterior cells (E), but co-misexpression of both dac and ap triggers extensive ectopic Fmrf-lacZ expression (F). Staining for Fmrf-lacZ (green) and pMad (magenta) reveals that ectopic Fmrf-lacZ cells are all pMad-positive (G). Misexpression of dac and ap in RP motor neurons using HB9-GAL4 triggers ectopic proFmrf expression (H). (I-L) Misexpression in ap-neurons. Misexpression of dac alone does not trigger ectopic Fmrf-lacZ (I), but together with BMP activation (J) and ap (K), all ap-neurons, except the vAp neurons, are triggered to express Fmrf-lacZ. (L) Both ectopic and endogenous Fmrf expression is dependent upon eya (L; ap^GAL4, eya^Cli-IID/eya¹⁰, UAS-tkv^A, UAS-sax^A; UAS-ap, UAS-dac/+).

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