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Fig. 4. dachshund and eyes absent are both important for Fmrf expression but play different roles. Expression of proFmrf (A-D,M,N), morphology of ap-axons at the thoracic midline (E-H), innervation of the DNH using ap^GAL4; UAS-myc-EGFP^F (green) and anti-Glutactin to visualize the DNH (red) (E'-H'), and pMad expression in the ap-cluster (I-L,R,S) in late-stage-17 embryos. In the wild type (A), proFmrf expression is readily observed in the six lateral Tv neurons in thoracic segments T1 to T3 and in the two anterior, medial SE2 neurons. (A,E,E',I) In controls (ap^GAL4/+; UAS-myc-EGFP^F/+), ap-neurons project close to the midline (E) and innervate the DNH (E'), and pMad staining is evident in the Tv cell of the ap-cluster (I). (B,F,F',J) In dac mutants (dac³/dac⁴), the expression of proFmrf is weak and partly lost in Tv cells (B). However, in dac mutants (ap^GAL4, dac⁴/dac³; UAS-myc-EGFP^F/+), there is entirely wild-type midline and DNH innervation (F,F'), and pMad staining of Tv cells (J). (C,G,G',K) In eya mutants (eya^Cli-IID/eya¹⁰) proFmrf expression is detected in only 32% of Tv neurons, and this is reduced to 6% by removing one copy of ap (C). In eya mutants (ap^GAL4, eya^Cli-IID/eya¹⁰; UAS-myc-EGFP^F/+), TV axonal projections reach the midline (G) but fail to innervate the DNH (G', only 19% of DNH). Only 26% of Tv neurons express pMad (K). (D,H,H',L) Cell-autonomous reintroduction of eya (ap^GAL4, eya^Cli-IID/eya¹⁰; UAS-myc-EGFP^F/UAS-eya) rescues proFmrf (D), DNH innervation (H') and Tv pMad expression (L). (M,R) Direct activation of the BMP pathway in eya mutants (ap^GAL4, eya^Cli-IID/eya¹⁰, UAS-tkv^A, UAS-sax^A; UAS-myc-EGFP^F/+) only partly restores proFmrf (M), although pMad is expressed in most ap-cluster neurons and is rescued to 100% in Tv cells (R). (N,S) Providing gbb cell-autonomously in eya mutants (ap^GAL4, eya^Cli-IID/eya¹⁰, UAS-gbb; UAS-myc-EGFP^F/+) fails to restore either proFmrf (N) or pMad (S). (O,P,Q) Expression of -lacZ reveals abdominal ap-axon projections in the stage 16-17 embryo. In the control (apC--lacZ), dAp and vAp neurons project axons within the ipsilateral ap-fascicle and do not cross the midline (O). In two different eya mutant VNCs (eya^Cli-IID/eya¹⁰; apC--lacZ), the dAp axons frequently (96%) cross the midline (P, arrow, Q). However, they join the contralateral ap fascicle and appear to project anteriorly, like wild-type dAp axons (Q, arrowhead). (T) Relative proFmrf staining intensity in wild type, dac mutant (dac³/dac⁴) and dac rescue (ap^GAL4, dac⁴/dac³; UAS-dac/+) late-stage-17 Tv neurons. dac mutants have reduced proFmrf expression and the dac rescue shows increased intensity, probably due to overexpression of dac. Percentages presented in white were obtained in a wild-type ap background, whereas those presented in green correspond to an ap heterozygous (ap^GAL4/+) background.

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