| First Author | Zhang N | Year | 2002 |
| Journal | Genesis | Volume | 33 |
| Issue | 1 | Pages | 21-8 |
| PubMed ID | 12001066 | Mgi Jnum | J:77247 |
| Mgi Id | MGI:2181244 | Doi | 10.1002/gene.10081 |
| Citation | Zhang N, et al. (2002) Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice. Genesis 33(1):21-8 |
| abstractText | Summary: The Notch signaling pathway is important in regulating formation and anterior-posterior patterning of somites in vertebrate embryos. Here we show that distinct segmentation defects are displayed in embryos mutant for the Notch pathway genes Notch1, Lunatic fringe (Lfng), Delta-like 1 (Dll1), and Delta-like 3 (Dll3). Lfng-deficient mice and Dll3-deficient mice exhibit very similar defects, and marker analysis suggests that progression of the segmentation clock is disrupted in Dll3 mutants. We also show that Radical fringe (Rfng)-deficient mice exhibit no obvious phenotypic defects. To assess whether the absence of a phenotype in Rfng-deficient mice was the result of functional redundancy with the Lfng gene, we generated Lfng/Rfng double homozygous mutant mice. These mice exhibit the skeletal defects normally observed in Lfng-deficient mice, but we detected no obvious synergistic or additive effects in the double mutant animals. genesis 33:21-28, 2002. |
