Cdx2 is essential for axial elongation in mouse development.
Inactivation of Cdx2 leads to preimplantation embryonic lethality. Rescue of the implantation defect by tetraploid fusion established that Cdx2 is necessary for trophoblastic development, vasculogenesis in the yolk sac mesoderm, allantoic growth, and chorioallantoic fusion. "Rescued" Cdx2 mutants die at late gastrulation stages because of failure of placental development. Cdx2 is also needed for the completion of the normal process of gastrulation and tail bud elongation. Presegmental paraxial mesoderm is severely restricted in amount and somites posterior to somite 5 are abnormal. The Cdx2 mutation, like mutations impairing Wnt and Fgf signaling, causes posterior truncations and disturbs axial patterning of the embryonic structures, indicated by changes in the Hox expression domains. The gene appears to be important in the integration of the pathways controlling embryonic axial elongation, and anterior-posterior patterning.
Chawengsaksophak
Kallayanee
K
Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario, Canada M5G 1X5.
de Graaff
Wim
W
Rossant
Janet
J
Deschamps
Jacqueline
J
Beck
Felix
F
D000818:Animals; D001755:Blastocyst / Q000378:metabolism*; D019521:Body Patterning / Q000502:physiology*; D000071616:CDX2 Transcription Factor; D004475:Ectoderm / Q000378:metabolism; D004707:Endoderm / Q000378:metabolism; D005775:Gastrula / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D005801:Genes, Homeobox / Q000502:physiology; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism*; D008648:Mesoderm / Q000378:metabolism; D051379:Mice / Q000196:embryology*; D010641:Phenotype; D011123:Polyploidy; D013234:Stem Cells / Q000378:metabolism; D014157:Transcription Factors; D014327:Trophoblasts / Q000378:metabolism
D000071616:CDX2 Transcription Factor; C487514:Cdx2 protein, mouse; D018398:Homeodomain Proteins; D014157:Transcription Factors