Members of the Notch family of transmembrane receptors mediate a numbe
r of developmental decisions in invertebrates. In order to study Notch
function in a vertebrate organism, we have mutated the Notch1 gene of
the mouse. Notch1 gene function is required for embryonic survival in
the second half of gestation. In the first half of gestation, we have
found no effect of the mutation on the normal programs of neurogenesi
s, myogenesis or apoptosis. We conclude that Notch1 function is not es
sential for these processes, at least in early postimplantation develo
pment. However, we have found that somitogenesis is delayed and disorg
anized in Notch1 mutant embryos. We propose that Notch1 normally coord
inates the process of somitogenesis, and we provide a model of how thi
s might occur.