A key malformation in the homozygous <i>truncate</i> mouse mutants is a partial lack of the notochord in the embryo tail. In order to analyze if tail bud development was affected by the <i>truncate</i> (<i>tc</i>) mutation, serial semithin sections of tails of the homozygous mutant embryos were compared to the wild-type controls. In the wild-type embryos morphologically uniform mesenchyme of the tail bud was continuous via the medullary cord to the secondary neural tube, and via the tail cord to the notochord and the gut. In <i>truncate</i> embryos the tail cord was not continuous to the notochord, but to the additional lumen of the tail gut resulting in tail gut duplication. Toward the base of the tail two tail guts subsequently fused together or the additional one disappeared. If present in the tip of the tail, the notochord in <i>truncate</i> embryos ended near the ventral border of the secondary neural tube. The rest of the tail notochord was fragmented and the posterior ends of the fragments were frequently adjacent or even continuous to the neural tube. We suggest that the improper regionalization of the tail bud, where notochord is associated with the neural tube rather than with the tail gut, is related to the subsequent segmental lack of the notochord in <i>truncate</i> mutants.