Fig. 7. Bnl activity modulates GBE-lacZ expression. (A-D) Ectopic Bnl expression in the trachea causes up-regulation of GBE-lacZ expression. Lateral view of a portion of the DT of wild-type (A,B) and btl-GAL4/UAS-bnl (C,D) stage 16 embryos, carrying GBE-lacZ and double labelled for ß-gal (green; A,C) and Grh (red; B,D). GBE-lacZ expression is enhanced in most tracheal cells upon ectopic Bnl signalling (compare A and C), but Grh levels remain the same (compare B and D). (E-H) Ectopic expression of Bnl in single terminal cells results in increased levels of GBE-lacZ expression in this and neighbouring cells. Dorsal lateral views showing part of the DT and two dorsal branches of wild-type (E,F) and Term-GAL4/UAS-bnl (G,H) embryos carrying GBE-lacZ, and labelled for ß-gal (green, E,G), and lumenal antigen 2A12 and DSRF (both in red; overlaid with green in F and H). Ectopic Bnl signalling in terminal cells results in the expression of the terminal marker DSRF in additional cells (H) and in the same cells the level of GBE-lacZ expression is increased (G,H). (I-L) Bnl is required for GBE-lacZ expression. Lateral view of two tracheal segments in embryos mutant for pnt (I,J) and bnl (K,L) that carry GBE-lacZ. Double labelling for 2A12 (red) and ß-gal (green) shows that tracheal GBE-lacZ expression is reduced in bnl mutant embryos (K,L) as compared to the epidermal expression, or to the tracheal expression in pnt mutants (I,J), which represents wild-type levels. Scale bars: 10 µm.

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