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 beta-actin promoter exhibit duplicated axes or a severely dorsalised phenotype. Although the transgene was introduced into fertilised eggs all duplications occurred within a single amnion and, therefore, arose from the production of more than one primitive streak at the time of gastrulation. 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 anteriorly, there was a reduction in tissue rostral to the anterior limit of the notochord, and no duplicated expression domain of the forebrain marker Hesx1 was observed. Anterior truncations were evident in dorsalised transgenic embryos containing a single axis. These results are discussed in the light of the effects of ectopic Xwnt8 in Xenopus embryos, where its early expression leads to complete axis duplication but expression after the mid-blastula transition causes anterior truncation. It is proposed that while ectopic Cwnt8C in the mouse embryo can duplicate the primitive streak and node this only produces incomplete axis duplication because specification of the anterior aspect of the axis, as opposed to maintenance of anterior character, is established by interaction with anterior primitive endoderm rather than primitive streak derivatives.
Pöpperl
H
H
Laboratory of Developmental Neurobiology, MRC National Institute for Medical Research, Mill Hill, London, UK.
Schmidt
C
C
Wilson
V
V
Hume
C R
CR
Dodd
J
J
Krumlauf
R
R
Beddington
R S
RS
D000199:Actins / Q000235:genetics; D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins; D019521:Body Patterning / Q000235:genetics*; D002645:Chickens; D003598:Cytoskeletal Proteins; D004475:Ectoderm / Q000502:physiology*; D005775:Gastrula; D015870:Gene Expression; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D011401:Promoter Regions, Genetic / Q000235:genetics; D016548:Prosencephalon / Q000196:embryology*; D011506:Proteins / Q000235:genetics / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D012097:Repressor Proteins; D000072056:Transcription Factor HES-1; D051153:Wnt Proteins; D029961:Zebrafish Proteins
D000199:Actins; D051792:Basic Helix-Loop-Helix Proteins; D003598:Cytoskeletal Proteins; D018398:Homeodomain Proteins; D011506:Proteins; D012333:RNA, Messenger; D012097:Repressor Proteins; D000072056:Transcription Factor HES-1; D051153:Wnt Proteins; D029961:Zebrafish Proteins; C489736:HESX1 protein, human; C489734:Hes1 protein, mouse; C489733:Hesx1 protein, mouse; C094521:wnt8a protein, zebrafish; C078493:HES1 protein, human