MISEXPRESSION OF CWNT8C IN THE MOUSE INDUCES AN ECTOPIC EMBRYONIC AXIS AND CAUSES A TRUNCATION OF THE ANTERIOR NEUROECTODERM

Transgenic embryos expressing Cwnt8C under the control of the human be ta-actin promoter exhibit duplicated axes or a severely dorsalised phe notype. Although the transgene was introduced into fertilised eggs all duplications occurred within a single amnion and, therefore, arose fr om the production of more than one primitive streak at the time of gas trulation, Morphological examination and the expression of diagnostic markers in transgenic embryos suggested that ectopic Cwnt8C expression produced only incomplete axis duplication: axes were always fused ant eriorly, there was a reduction in tissue rostral to the anterior limit of the notochord, and no duplicated expression domain of the forebrai n marker Hesx1 was observed, Anterior truncations were evident in dors alised transgenic embryos containing a single axis, These results are discussed in the light of the effects of ectopic Xwnt8 in Xenopus embr yos, where its early expression leads to complete axis duplication but expression after the midblastula transition causes anterior truncatio n, It is proposed that while ectopic Cwnt8C in the mouse embryo can du plicate the primitive streak and node this only produces incomplete ax is duplication because specification of the anterior aspect of the axi s, as opposed to maintenance of anterior character, is established by interaction with anterior primitive endoderm rather than primitive str eak derivatives.