CBP/p300 is a transcriptional co-activator that is recruited to enhancers b
y various DNA-binding proteins, including proteins whose activity is contro
lled by extracellular signals. Here, we report that Drosophila CBP loss-of-
function mutants show specific defects which mimic those seen in mutants th
at lack the extracellular signal Dpp or its effector Mad. Furthermore, we f
ind that CEP loss severely compromises the ability of Dpp target enhancers
to respond to endogenous or exogenous Dpp, Finally, we show that CBP binds
to the C-terminal domain of Mad. Our results provide evidence that CBP func
tions as a co-activator during Dpp signalling, and they suggest that Mad ma
y recruit CBP to effect the transcriptional activation of Dpp-responsive ge
nes during development.