Segmentation defects of notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice

被引:77
作者
Zhang, N
Norton, CR
Gridley, T
机构
[1] Jackson Lab, Bar Harbor, ME 04609 USA
[2] Van Andel Res Inst, Grand Rapids, MI USA
关键词
segmentation clock; somite formation; presomitic mesoderm; fringe genes; Radical fringe knockout mice;
D O I
10.1002/gene.10081
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:21 / 28
页数:8
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