The tail of all vertebrates, regardless of size and anatomical detail, derive from a post-anal extension of the embryo known as the tail bud. Formation, growth and differentiation of this structure are closely associated with the activity of a group of cells that derive from the axial progenitors that build the spinal cord and the muscle-skeletal case of the trunk. Gdf11 activity switches the development of these progenitors from a trunk to a tail bud mode by changing the regulatory network that controls their growth and differentiation potential. Recent work in the mouse indicates that the tail bud regulatory network relies on the interconnected activities of the Lin28/let-7 axis and the Hox13 genes. As this network is likely to be conserved in other mammals, it is possible that the final length and anatomical composition of the adult tail result from the balance between the progenitor-promoting and -repressing activities provided by those genes. This balance might also determine the functional characteristics of the adult tail. Particularly relevant is its regeneration potential, intimately linked to the spinal cord. In mammals, known for their complete inability to regenerate the tail, the spinal cord is removed from the embryonic tail at late stages of development through a Hox13-dependent mechanism. In contrast, the tail of salamanders and lizards keep a functional spinal cord that actively guides the tail’s regeneration process. I will argue that the distinct molecular networks controlling tail bud development provided a collection of readily accessible gene networks that were co-opted and combined during evolution either to end the active life of those progenitors or to make them generate the wide diversity of tail shapes and sizes observed among vertebrates.
