Fig. 3. Bgb phenotypes. (A-D) SEMs of adult eyes. Posterior is to the left and dorsal is up. All flies were reared at 25^oC. (A) lz^ts1; Bgb^D/+. The Bgb^D mutant enhances lz^ts1 on the posterior side of the eye (compare with Fig. 1B). (B) lz^ts1; Df(3L)Bgb^K4/+. The Bgb^K4 deletion enhances the lz^ts1 eye phenotype. (C) lz^R1. The lz null eye is very smooth and does not show any ommatidial organization. (D) lz^ts1; Df(3L)Bgb^K4/Bgb^D. Rare escapers of this genotype have a phenotype resembling a lz null eye. (E-M) Embryonic phenotype of Bgb and run mutants. Anterior is to the left and dorsal is up. Embryos were stained with mAb22C10 (E-J) or -Engrailed antibody (K-M). (E) Wild-type stage-15 embryo. mAb22C10 recognizes neurons of the chordotonal organs (box). These are easily identified on the basis of their stereotypical arrangement and position in abdominal segments A1-A7. (F) A schematic diagram of the lateral chordotonal neurons based on that by Campos-Ortega and Hartenstein (1997). Within each wild-type cluster (WT panel) the axon of the single lateral chordotonal neuron, lch1, pioneers the segmental nerve (SN) to its target in the midline. The remaining five lateral chordotonal neurons, lch5, follow the intersegmental nerve (ISN) to their target in the midline. In Bgb mutant embryos (Bgb panel), the axon of the lch1 neuron incorrectly follows the ISN to the midline. In this and subsequent panels an arrowhead indicates the absence of the lch1 axon in its normal position. This axon does not join the SN, but instead aberrantly turns toward the ISN and follows this incorrect path to the midline. The ventral sensilla, vp5, has an apical projection (asterisk in F and H to distinguish this structure from the axon of the lch1 neuron). (G,H) Lateral chordotonal neurons of (G) wild-type and (H) Bgb^D/Bgb^D stage-15 embryos. (G) The axons of the lch1 neurons correctly follow the SN to the midline (arrow). (H) In the mutants, axons of the lch1 neurons do not follow the SN (arrowheads), but incorrectly project towards the lch5 and follow the ISN to the midline. In this genetic background the phenotype is not fully expressed and only 2 of the 3 lateral chordotonal clusters shown have this defect. (I) Lateral chordotonal neurons of Bgb^D/Df(3L)Bgb^K4 stage-15 embryo. In these mutants, the axons of the lch1 neurons aberrantly project towards the lch5 and do not follow the SN to the midline (arrowheads). This phenotype is similar to, but stronger than, that seen in (H). (J) Lateral chordotonal neurons of run^YP17/run^YP17 stage-15 embryo. Only two sets of lateral chordotonal neurons are seen within the region corresponding to the previous panels because of a lack of segments in this mutant (Gergen and Wieschaus, 1986). The axon of one of the lch1 neurons shown misprojects and does not follow the SN to the midline (arrowhead). (K) Wild-type stage-11 embryo. Engrailed protein is expressed as a 14 stripe pattern in the posterior compartment of each segment. (L) Bgb^D/Bgb^D stage-11 embryo. Engrailed expression is as seen in wild type. (M) run^YP17/run^YP17 stage-11 embryo. These embryos show a segmentation phenotype, not seen in Bgb mutants.

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