Figure 7

Mnx proteins promote normal MiP development and suppress acquisition of V2a interneuron and CaP characteristics. (A) Model depicting principal MiP (green) projection errors observed in the absence of Mnx proteins. MiPs often fail to project to their normal dorsal muscle targets and, instead, either project a V2a interneuron-like axon or a motor axon that projects alongside the CaP axon to ventral muscle. Combinations of these three projection errors account for the observed range of MiP phenotypes. By comparison, CaPs (blue) and V2a INs (purple) make normal projections. (B) Genetic pathways that account for observed MiP phenotypes. Mnx proteins, primarily Mnx2a and Mnx2b, promote MiP axogenesis by maintaining the late phase of Islet1 expression initiated by Nkx6. All three Mnx proteins (bracket) suppress acquisition of molecular and morphological features of V2a interneurons, and responsiveness to unknown signals that promote axon growth to ventral muscle.