Andreas Gewies, Mercedes Castineiras-Vilarino, Uta Ferch, Nina Jährling, Katja Heinrich, Ulrike Hoeckendorf, Gerhard K. H. Przemeck, Matthias Munding, Olaf Groß, Timm Schroeder, Marion Horsch, E. Loraine Karran, Aneela Majid, Stefan Antonowicz, Johannes Beckers, Martin Hrabé de Angelis, Hans-Ulrich Dodt, Christian Peschel, Irmgard Förster, Martin J. S. Dyer, Jürgen Ruland

Members of the PRDM protein family have been shown to play important roles during embryonic development. Previous in vitro and in situ analyses indicated a function of Prdm6 in cells of the vascular system. To reveal physiological functions of Prdm6, we generated conditional Prdm6-deficient mice. Complete deletion of Prdm6 results in embryonic lethality due to cardiovascular defects associated with aberrations in vascular patterning. However, smooth muscle cells could be regularly differentiated from Prdm6-deficient embryonic stem cells and vascular smooth muscle cells were present and proliferated normally in Prdm6-deficient embryos. Conditional deletion of Prdm6 in the smooth muscle cell lineage using a SM22-Cre driver line resulted in perinatal lethality due to hemorrhage in the lungs. We thus identified Prdm6 as a factor that is essential for the physiological control of cardiovascular development.