Fig. 8. A model for Gdf11 function in controlling Hox gene expression and rostrocaudal identity in the spinal cord. (A) Normally, the onset of Gdf11 expression begins after most of the cervical progenitor cells leave the stem zone, and therefore, only progenitor cells designated for caudal levels receive the Gdf11 signal. Fgf and Gdf11 work together to define Hox gene expression domains in the caudal spinal cord. (B) Gdf11 electroporation increases the level of Gdf11 and, thus, results in a rostral displacement of Hoxc6-Hoxc10 domains. (C) In Gdf11^-/- embryos, only the Fgf signal remains. This causes severe caudal displacement and expansion in Hoxc10 and Hoxc9 domains, respectively, and a lesser effect in Hoxc6 and Hoxc8 domains. (D) A model for Gdf11 function in the control of Hox gene expression and RC identity of the spinal cord. Smad2 mediates the function of Gdf11 in promoting caudal Hox gene expression. Although high levels of Gdf11 can activate the Smad1/5/8 pathway in vitro, the significance of this pathway in vivo requires further examination.