BROAD-COMPLEX TRANSCRIPTION FACTORS REGULATE THORACIC MUSCLE ATTACHMENT IN DROSOPHILA

The Broad-Complex, a 20-hydroxyecdysone-regulated gene, is essential f or the development of many tissues during metamorphosis. In Broad-Comp lex mutants of the rbp complementation group, dorsoventral indirect ni ght muscles (DVM) are largely absent, and the dorsal longitudinal indi rect night 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 hypothesiz ed 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 relat ive, BRC-Z4. formation of muscle primordia from imaginal myoblasts app ears normal in rbp mutants. However, the myotendinous junctions linkin g the DVM to the dorsal epidermis are weak, and the muscles detach dur ing pupal life and subsequently degenerate. The data indicate that rbp mutations disrupt the cell-cell interactions between developing muscl es and epidermal tendon cells as they recognize and attach to one anot her. Using a BRC-Z1-specific monoclonal antibody, we show that both th e developing muscles and epidermal tendon cells express BRC-Z1 at the time of pupation, before mutant muscles begin to detach. We conclude t hat 20-hydroxyecdysone acts through the Broad-Complex to control the d evelopment of thoracic myotendinous junctions. (C) 1997 Academic Press .