A fundamental process in embryonic development is the establishment of body axes, including the anteroposterior (A-P) axis, the dorsoventral (D-V) axis, and the left-right (L-R) axis. Back to 1940s, when signaling pathways and molecular mechanisms behind axis formation remained a mystery, a spontaneous mutation called Kinky (FuKi) at the mouse Fused locus attracted attention due to its impact on a variety of developmental processes, especially on the formation of embryonic A-P axis(Gluecksohn-Schoenheimer 1949). Around 1990s, two other spontaneous alleles of the mouse Fused gene, Fused (FuFu) and Knobbly (FuKb), and one transgenic insertional mutant FuTg1 were identified (Jacobs-Cohen et al. 1984; Perry et al. 1995; Mary et al. 1996), all showing defects in the formation of embryonic axis. These Axinnull mutants normally led to lethality at embryonic day 8–10, and in addition to causing embryonic axis duplications, they also led to...
KeywordsEmbryonic Axis Destruction Complex Tumor Suppressor Adenomatous Polyposis Coli Axin Protein Suppressor Adenomatous Polyposis Coli
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