13-P096 Regulation of spinal neurogenesis by receptor tyrosine phosphatase PTPγ

agus, stomach, pre-umbilical intestine, post-umbilical intestine, hindgut), but overall it was significantly shorter compared with controls. In talpid3 gut, although neural crest-derived ENS precursors (shown with HNK-1 immunohistochemistry) and TuJ1-positive enteric neurons were distributed along the length of the gut, similar to controls, there were dramatic differences in their patterning across the gut wall. Also, the organisation of smooth muscle actin (SMA) was considerably altered in talpid3 mutants, with SMA staining absent in the esophagus, but distributed across the entire wall of the intestine. Our results suggest that although neural crest cells are able to migrate and differentiate in talpid3 gut, their patterning within the gut is dramatically perturbed. In addition, overall gut length is significantly reduced and SMA-positive cells either fail to differentiate or, if present, fail to be organised into circular muscle layers. Thus, these findings suggest that perturbation of Hh signalling in the talpid3 chicken embryo results in malformation of the gastrointestinal tract, disorganised gut smooth muscle, and disrupted patterning of the ENS.