Abstract
The Broad-Complex, a 20-hydroxyecdysone-regulated gene, is essential for the development of many tissues during metamorphosis. In Broad-Complex mutants of the rbp complementation group, dorsoventral indirect flight muscles (DVM) are largely absent, and the dorsal longitudinal indirect flight muscles, tergotrochanteral muscles, and remaining DVM often select incorrect attachment sites. The Broad-Complex encodes a family of zinc-finger-containing transcription factors, and it is hypothesized that Broad Complex proteins containing the Z1 zinc-finger pair (BRC-Z1) mediate rbp+ function. We provide additional strong support for this hypothesis by showing that heat-shock-induced BRC-Z1 expression rescues the thoracic muscle defects of rbp mutants completely. BRC-Z4 induction can also rescue the thoracic musculature, but BRC-Z2 and -Z3 can not. Thus, the effect is specific to BRC-Z1 and its closest relative, BRC-Z4. Formation of muscle primordia from imaginal myoblasts appears normal in rbp mutants. However, the myotendinous junctions linking the DVM to the dorsal epidermis are weak, and the muscles detach during pupal life and subsequently degenerate. The data indicate that rbp mutations disrupt the cell-cell interactions between developing muscles and epidermal tendon cells as they recognize and attach to one another. Using a BRC-Z1-specific monoclonal antibody, we show that both the developing muscles and epidermal tendon cells express BRC-Z1 at the time of pupation, before mutant muscles begin to detach. We conclude that 20-hydroxyecdysone acts through the Broad-Complex to control the development of thoracic myotendinous junctions.
