Elongation of the main body axis in mouse is driven by self-renewing axial progenitors, initially located within the epiblast and subsequently repositioned to the tailbud. Within axial progenitors and surrounding cells, specific combinations of Hox transcription factors impart the positional information required for regional morphology. While the Hox genes are the ultimate effector molecules, it is the signals and molecules controlling combinatorial Hox expression that orchestrates how the main body axis is laid down. Revealing the identity of these molecules is fundamental to our understanding of developmental and evolutionary mechanisms. We have identified a novel mechanism that controls the timing of a major Hox code transition, the trunk-to-tail transition. The miR-196 family of microRNAs are embedded in Hox clusters and target Hox genes of the trunk region. Genetic deletion of miR-196 in mouse resulted in a predicted upregulation of this trunk Hox code, with a concomitant, yet unexpected, delay in the tail Hox code. Here we use in vitro pluripotent stem cell differentiation protocols, coupled with in vivo analyses, to demonstrate that miR-196 and Gdf11 signalling act synergistically in the timely activation of the tail Hox code and cessation of axis elongation.