Decapentaplegic (DPP) is a member of the TGFβ family of signalling molecules that is implicated in patterning many structures, including the wing of Drosophila. In the wing, three target genes of DPP have been identified. These are expressed at different positions relative to the source of DPP, consistent with regulation in a concentration-dependent manner. Target-gene expression depends on the receptor, Thick veins (TKV), and the positively acting Mad/Medea transcription factors. Two recent papers add another wrinkle to the story in the form of a putative transcriptional repressor, Brinker, that is negatively regulated by DPP. brinker was identified by Jazwinski et al.1xThe Drosophila gene brinker reveals a novel mechanism of Dpp target gene regulation. Jazwinska, A. et al. Cell. 1999; 96: 563–573Abstract | Full Text | Full Text PDF | PubMed | Scopus (200)See all References in a screen for embryonic lethal mutations because it caused a phenotype similar to ectopic activation of DPP signalling. Campbell and Tomlinson2xTransducing the Dpp morphogen gradient in the wing of Drosophila: regulation of Dpp targets by brinker. Campbell, G. and Tomlinson, A. Cell. 1999; 96: 553–562Abstract | Full Text | Full Text PDF | PubMedSee all References identified the same gene through an enhancer-trap line that was expressed in a DPP-responsive manner in the developing wing. Both groups observed that clones of cells mutant for brinker resulted in phenotypes characteristic of ectopic DPP signalling. The phenotypes were autonomous to the mutant clone, showing that brinker did not affect production of DPP. Furthermore, ectopic expression of DPP target-genes was induced even when the brinker mutation was combined with mutations that prevented transduction of the DPP signal. This suggested that brinker functions to inhibit the DPP target genes directly. As brinker expression is negatively regulated by DPP signalling, one model that emerges is that DPP induces expression of its target-genes by blocking transcription of brinker. The fact that the phenotypes associated with brinker mutant cells are characteristic of those produced by low, rather than high, levels of DPP activity suggests that repression of brinker is only sufficient to confer effects of intermediate DPP levels. Direct activation of target genes via Mad/Medea is probably required for maximal effects. The amino-acid sequence of Brinker does not reveal homology to known repressors so future experiments will need to determine whether it indeed functions as a DNA-binding transcriptional repressor. In the meantime, a search for vertebrate homologues will almost certainly begin: given the conservation between DPP and TGFβ signalling in other organisms it seems highly likely that brinker relatives will operate elsewhere.