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Effects of rat Axin domains on axis formation in Xenopus embryos
Author(s) -
Fukui Akimasa,
Kishida Shosei,
Kikuchi Akira,
Asashima Makoto
Publication year - 2000
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.2000.00536.x
Subject(s) - xenopus , wnt signaling pathway , mutant , microbiology and biotechnology , biology , endoderm , adenomatous polyposis coli , gsk 3 , signal transduction , gene , genetics , cellular differentiation , colorectal cancer , cancer
Wnt signaling plays an important role in axis formation in early vertebrate development. Axin is one Wnt signaling regulator that inhibits this pathway. The effects of the injection of mRNA of several rat Axin (rAxin) mutants on axis formation in Xenopus embryos were examined. It was found that rAxin mutants containing only a regulation of G‐protein signaling (RGS) domain fragment or with deletion of the RGS domain induced axis formation. Because the RGS domain is a major adenomatous polyposis coli gene product (APC)‐binding domain, APC association with glycogen synthase kinase 3β (GSK3β) on the Axin molecule may be important in inhibition of axis formation. The ventralizing activities of wild‐type rAxin and a mutant in which the Di shevelled and A x in (DIX) domain was deleted (ΔDIX mutant) were examined. Histological examination and gene expression revealed that the ventralizing activity of the ΔDIX mutant was weaker than that of wild‐type rAxin. This finding suggests that the C‐terminus of rAxin contributes to the inhibition of Wnt signaling in Xenopus embryos. Furthermore, an rAxin mutant that contained both the RGS and GSK3β‐binding domains affected both the dorsal and ventral sides of blastomeres, mediated ectodermal fate and induced expansion of notochord and/or endoderm, but did not induce axis formation.