Fig. 6. Ssdp modifies the activity of Chip/Ap tetrameric complexes. Newly eclosed ap^GAL4/+ flies carrying one copy of each UAS transgene as shown. (A) ap^GAL4/+ flies exhibit no wing defects. (B) ap^GAL4/+; UAS-ChipFL/+. Overexpression of full-length Chip (ChipFL) reduces the levels of functional Chip/Ap complexes and results in wings that are small, unfused and with a poorly demarcated margin (arrow). These defects resemble those of hypomorphic ap mutants. (C) ap^GAL4/+;UAS-ChipFL/ssdp^L7.ssdp^L7 dominantly enhances the wing defects caused by Chip overexpression, leaving little or no organized wing tissue (arrow). (D) ap^GAL4/+;UAS-ChipLID:ApLIM/+. The fusion protein ChipLID:ApLIM results in formation of hyperactive complexes. Flies overexpressing ChipLID:ApLIM have blistered wings in which the dorsal and ventral surfaces fail to fuse, and which are held upward and away from the thorax in a fashion resembling LMO loss-of-function mutants. (E) ap^GAL4/+;UAS-ChipLID:ApLIM/ssdp^L7. Removal of one copy of ssdp from flies expressing ChipLID:ApLIM suppresses the blistered wing phenotype; the surfaces fuse properly, although the wings remained held up. (F) ap^GAL4/+;UAS-ChipLCCD/+. Expression of ChipLCCD, which lacks amino acids 387-426 and thus cannot bind Ssdp but is still capable of homo-dimerization and LIM interaction, results in more severe wing defects than expression of ChipFL, reducing the wing to a ribbon-like process with little discernible structure (arrow).

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