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Members of the large family of Hox transcription factors are encoded by geneswhose tightly regulated expression in development and in space within differentembryonic tissues confer positional identity from the neck to the tips of thelimbs. Many structures of the face, head, and heart10 develop from cellpopulations expressing few or no Hox genes. Hoxb1 is the member of itschromosomal cluster expressed in the most rostral domain during vertebratedevelopment, but never by the multipotent neural crest cell population anteriorto the cerebellum. We have developed a novel floxed transgenic mouse line,CAG-Hoxb1,-EGFP (CAG-Hoxb1), which upon recombination by Cre recombinaseconditionally induces robust Hoxb1 and eGFP overexpression. When induced withinthe neural crest lineage, pups die at birth. A variable phenotype develops fromE11.5 on, associating frontonasal hypoplasia/aplasia, micrognathia/agnathia,major ocular and forebrain anomalies, and cardiovascular malformations. Neuralcrest derivatives in the body appear unaffected. Transcription of effectors ofdevelopmental signaling pathways (Bmp, Shh, Vegfa) and transcription factors(Pax3, Sox9) is altered in mutants. These outcomes emphasize that repression ofHoxb1, along with other paralog group 1 and 2 Hox genes, is strictly necessaryin anterior cephalic NC for craniofacial, visual, auditory, and cardiovasculardevelopment.

Ectopic expression of Hoxb1 induces cardiac and craniofacial malformations