Fig. 2. The no soul gene encodes a winged helix domain-containing protein that belongs to the foxi1 subfamily. (A) ABI automated sequencer-produced chromatographs showing that the Ser¹⁹⁴ is mutated to Pro in the no soul mutant. (B) Comparative model showing that the predicted conformations of the native and mutated segment are different. The ab initio modeled segment is in green (the rest of the protein is shown in brown), the proline mutation is shown in the ball-and-stick style (red), and the bound DNA is blue. In the mutant model, the C terminus of the recognition helix is shortened by one turn and the loop connecting the recognition helix to the subsequent ß strand is shifted significantly relative to the native model. These conformational changes decrease the extent of interactions between the protein and DNA, assuming DNA is positioned as in the template structures. (C) Sequence alignment between no soul/foxi1, Xenopus (xfoxi1c), mouse (Mfkh10) and the winged helix domain of genesis that was used for comparative structure modeling. The winged helix motif and the position of the no soul mutation are marked. (D) Confocal image showing the control and the foxi1 morpholino-injected embryos. Although motor neurons are normal, epibranchial placode-derived visceral sensory neurons are defective as in the no soul mutant. mV/mVII/mX, the Vth, VIIth and Xth motor neurons; OT, ocular and trochlear motor nuclei; VII, geniculate ganglion; IX, petrosal ganglion; X, nodose ganglion.