Gene Knockouts and Murine Development: (gene knockout/gene targeting/Mus/mammalian embryology/genetic redundancy).

A considerable quantity of data has been generated using the technique of in vivo gene knockout in mice, much of which is of relevance to the developmental biologist. Null mutations in Hox genes at the 3'-end of the clusters create complex irregularities at the rostral end of the embryo, including defects in the middle ear and the large blood vessels, suggesting that Hox genes may be involved in pattern specification of these structures in addition to the anteroposterior axis. Null mutations in oncogenes either cause wide pleiotropic effects, or act in a restricted manner on the haematopoietic system. Null mutations in growth factors and related molecules cause failure of proliferation in restricted areas of the embryo in some cases, but have little phenotype in others. There is as yet no null mutation which supports the idea that growth factors are involved in mesoderm induction in mammals. A surprising variety of genes have no null phenotype, or one less severe than might have been previously predicted on the basis of their known function in vitro and pattern of expression. This leads to the possibility that genetic redundancy exists in development.