Hox genes are key regulator of embryonic development in all animals with bilateral symmetry. Their products are transcription factors that activate and repress downstream genes. The nature of Hox targets is mostly unknown in vertebrates.

In the cranial neural crest, a transient cell population of the vertebrate embryo, Hox genes act by restricting the differentiation potential of these cells. Both neural crest populations that emigrate from the cranial or trunk portions of the neural tube differentiate into a variety of cell types (including neurons glia and melanocytes). However, only the cranial neural crest can differentiate into the bone and cartilage producing cells, which will make most of the skeleton of the face and the neck. This specific property of the cranial neural crest is not understood and it inversely correlates with the expression of Hox genes; in support of this view, fate mapping studies trace the development of the facial skeleton back to the cranial neural crest originating from Hox-negative areas of the neural tube.

By applying a combination of functional, genomics and transcriptional approaches to the developing mouse embryo, the lab is focused in understanding how Hox genes control the differentiation of the cranial neural crest and, more in general, how they direct morphogenesis in the vertebrate embryo.