DEFECTS IN SOMITE FORMATION IN LUNATIC FRINGE DEFICIENT MICE

Segmentation in vertebrates first arises when the unsegmented paraxial mesoderm subdivides to form paired epithelial spheres called somites( 1,2). The Notch signalling pathway is important in regulating the form ation and anterior-posterior patterning of the vertebrate somite(3-7). One component of the Notch signalling pathway in Drosophila is the fr inge gene, which encodes a secreted signalling molecule required for a ctivation of Notch during specification of the wing margins-(8-11). He re we show that mice homozygous for a targeted mutation of the lunatic fringe (Lfng) gene, one of the mouse homologues(12,13) of fringe, hav e defects in somite formation and anterior-posterior patterning of the somites. Somites in the mutant embryos are irregular in size and shap e, and their anterior-posterior patterning is disturbed. Marker analys is revealed that in the presomitic mesoderm of the mutant embryos, sha rply demarcated domains of expression of several components of the Not ch signalling pathway are replaced by even gradients of gene expressio n. These results indicate that Lfng encodes an essential component of the Notch signalling pathway during somitogenesis in mice.