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
.