Fig. 1. nrv2 and ATP mutations cause tracheal length and diameter defects. When compared with wild-type (WT) animals (A,C-E), nrv2 (B,F-I) and ATP (M-O) mutant trachea have increased length, diameter expansions and missing lumen segments. The tracheal defects in nrv2 homozygotes can be completely rescued by expressing the nrv2.2 isoform using the e22c-Gal4 driver (J,K) or partially rescued using the btl-Gal4 driver (L). Similarly, expression of the nrv2.1 isoform by the e22C-Gal4 driver could also completely rescue all tracheal defects in nrv2 mutants (Fig. 6H), whereas the btl-Gal4 driver produced only the same partial rescue seen with nrv2.2 (data not shown). (A-C,F,J,L,M,O) Lateral views of the dorsal trunk (DT) and transverse connective (TC). (D,G,K,N) Ventral views of the ganglionic branches (GB). (E,H,I) Dorsal views of the dorsal trunk. The animal in H lacks both zygotic and maternal nrv2. All images are of stage 16 embryos, except E,H,I, which show stage 15 embryos. Examples of lumenal gap regions are indicated with brackets. UAS-nrv2.1 or UAS-nrv2.2 expressed under the control of the e22c driver rescued the nrv2 tracheal phenotype to wild type in 8/9 and 19/21 animals respectively. Genotypes: (A,C-E) Oregon R; (B,F,G,I) nrv2^nwu3; (H) nrv2^nwu3/nrv2^-23B from nrv2^nwu3 germline clone (glc); (J,K) nrv2^k13315e22C-Gal4/nrv2^l(2)k04223 UAS nrv2.2; (L) nrv2^l(2)k04223 btl-Gal4/nrv2^l(2)k04223 UAS nrv2.2; (M,N) ATP⁰⁴⁶⁹⁴; (O) ATP^DTS1R1. Scale bar: in B, 10 µm for A,B; in O, 5 µm for C,F,J,L,M,O; in N, 5 µm for D,G,K,N; in E, 10 µm for E,H,I.