The development of the Drosophila wing disc requires the activities of the BMP and TGFβ signalling pathways. BMP signalling is critical for the correct growth and patterning of the disc, whereas the related TGFβ pathway is mostly required for growth. The BMP and TGFβ pathways share a common co-receptor (Punt) and a nuclear effector (Medea), and consequently it is likely that these pathways can interfere with each other during normal development. In this work we focus on the spatial activation domains and requirements for TGFβ signalling during wing disc development. We found that the phosphorylation of Smad2, the specific transducer for TGFβ signalling, occurs in a generalised manner in the wing disc. It appears that the expression of the four candidate TGFβ ligands (Activinβ, Dawdle, Maverick and Myoglianin) in the wing disc is required to obtain normal levels of TGFβ signalling in this tissue. We show that Baboon, the specific receptor of the TGFβ pathway, can phosphorylate Mad, the specific transducer of the BMP pathway, in vivo. However, this activation only occurs in the wing disc when the receptor is constitutively activated in a background of reduced expression of Smad2. In the presence of Smad2, the normal situation during wing disc development, high levels of activated Baboon lead to a depletion in Mad phosphorylation and to BMP loss-of-function phenotypes. Although loss of either babo or Smad2 expression reduce growth in the wing blade in a similar manner, loss of Smad2 can also cause phenotypes related to ectopic BMP signalling, suggesting a physiological role for this transducer in the regulation of Mad spatial activation.
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