Deletion of Pax7 changes the tunica muscularis of the mouse esophagus from an entirely striated into a mixed phenotype.

The mechanisms responsible for the different amounts of striated muscle in mammalian esophagi are still enigmatic. A recent ultrastructural analysis in mouse esophagus pointed to a particular role of satellite cells during postnatal growth of striated muscle. The aim of this study was to investigate satellite cell development and the influence of Pax7 on this process. Developing and adult esophagi of wild-type and mice carrying a targeted mutation in Pax7 were analyzed by electron microscopy. We found a gene dose-dependent delayed development of striated muscle and a severe loss of satellite cells in Pax7(+/-) and Pax7(-/-) esophagi. In contrast to the entirely striated wild-type esophagus, Pax7(-/-) mutants developed a mixed phenotype with predominantly smooth muscle caudally. We conclude that Pax7-dependent myogenic progenitor cells are of prime importance for striated muscle formation and the degree of smooth-to-striated muscle conversion during esophageal ontogeny. Copyright 2009 Wiley-Liss, Inc.