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. 2005 Aug 25;102(36):12944–12949. doi: 10.1073/pnas.0502888102

Fig. 7.

Fig. 7.

N-cadherin 18A- and 18B-containing isoforms rescue R7 layer-specific targeting defects. The MARCM technique with a Tubulin-GAL4 driver was used to express UAS N-cadherin transgenes containing the 18A or 18B exons in single N-cadherin-null mutant R7 cells throughout pupal development. R7 targeting was examined at the adult stage. (A-C) Confocal images of adult R7 clones homozygous for N-cadM19 (A) or N-cadM19 expressing UAS N-cad 18B (B), or UAS N-cad 18A#1 (C). (Scale bar, 10 μm.) (D) Immunoblot analyses of adult flies expressing the indicated UAS N-cadherin constructs from a constitutive promoter (hsGAL4). N-cadherin was detected with an Ab against the cytoplasmic domain. Only the main C-terminal fragment (compare with Fig. 1) is shown. The band in the no UAS lane is endogenous N-cadherin. Anti-actin staining served as a loading control. (E) Summary of rescue experiments. Both 18A and 18B transgenes can restore correct layer selection to a substantial fraction of mutant R7 cells. Correct targeting of R7 cells of the indicated genotypes: N-cadM19 without rescue construct, 1 of 288; N-cadM19 with UAS N-cad 18A #1, 598 of 628; N-cadM19 with UAS N-cad 18B, 716 of 917; and N-cadM19with UAS N-cad 18A #2, 210 of 323. The R7 targeting of a second strong loss-of-function mutant, N-cad405, was also rescued by 18A and 18B transgenes (data not shown).