Fig. 7. Dpp signal transduction and Sal expression are inhibited in cells lacking HS polymerase activity. Staining with PS1 antisera allows visualization of pMad generated by Dpp signaling activity. Cells mutant for ttv (A), sotv (B) or ttv and sotv (C), show reduced pMad levels (arrows in A and C or arrowhead in B) regardless of whether the clones are situated in the anterior or posterior compartments, suggesting that Dpp signaling is compromised independently of Hh. Low levels of pMad can be detected within clones in the vicinity of the clone boundaries, suggesting that Dpp signaling can still occur in mutant cells, although with reduced effectiveness or range. Sal responds to a high threshold of Dpp signaling and is expressed in the wing pouch centered on the AP boundary. However, in ttv (D), sotv (E) and ttv, sotv (F) mutant cells, Sal expression is reduced independently of whether clones lie in the anterior or posterior compartment (arrows). Loss of Sal in anterior clones is a direct result of loss of Dpp signaling rather than an indirect consequence of compromised Hh signaling, since it occurs in a domain beyond the effective range of Hh. Sal staining persists in ttv and sotv clones that overlap the AP boundary (arrowheads), suggesting that Dpp can signal in an autocrine or paracrine fashion, even in mutant cells.