The elbow (elB) gene encodes a conserved nuclear protein with a single zinc finger. Expression of ElB is restricted to a specific subset of tracheal cells, namely the dorsal branch and the lateral trunks. Stalled or aberrant migration of these branches is observed in elB mutant embryos. Conversely, ElB misexpression in the trachea gave rise to absence of the visceral branch and an increase in the number of cells forming the dorsal branch. These results imply that the restricted expression of ElB contributes to the specification of distinct branch fates, as reflected in their stereotypic pattern of migration. As elB loss-of-function tracheal phenotypes are reminiscent of defects in Dpp signaling, the relationship between ElB and the Dpp pathway was examined. By using pMad antibodies that detect the activation pattern of the Dpp pathway, we show that Dpp signaling in the trachea is not impaired in elB mutants. In addition, expression of the Dpp target gene kni was unaltered. The opposite is true as well, because expression of elB is independent of Dpp signaling. ElB thus defines a parallel input, which determines the identity of the lateral trunk and dorsal branch cells. No ocelli (Noc) is the Drosophila protein most similar to ElB. Mutations in noc give rise to a similar tracheal phenotype. Noc is capable of associating with ElB, suggesting that they can function as a heterodimer. ElB also associates with the Groucho protein, indicating that the complex has the capacity to repress transcription of target genes. Indeed, in elB or noc mutants, expanded expression of tracheal branch-specific genes was observed.