Impact of node ablation on the morphogenesis of the body axis and the lateral asymmetry of the mouse embryo during early organogenesis

Dev Biol. 1999 Jul 1;211(1):11-26. doi: 10.1006/dbio.1999.9276.

Abstract

The node of the mouse gastrula is the major source of the progenitor cells of the notochord, the floor plate, and the gut endoderm. The node may also play a morphogenetic role since it can induce a partial body axis following heterotopic transplantation. The impact of losing these progenitor cells and the morphogenetic activity on the development of the body axes was studied by the ablation of the node at late gastrulation. In the ablated embryo, an apparently intact anterior-posterior body axis with morphologically normal head folds, neural tube, and primitive streak developed during early organogenesis. Cell fate analysis revealed that the loss of the node elicits de novo recruitment of neural ectoderm and somitic mesoderm from the surrounding germ-layer tissues. This leads to the restoration of the neural tube and the paraxial mesoderm. However, the body axis of the embryo was foreshortened and somite formation was retarded. Histological and gene expression studies reveal that in most of the node-ablated embryos, the notochord in the trunk was either absent or interrupted, and the floor plate was absent in the ventral region of the reconstituted neural tube. The loss of the node did not affect the differentiation of the gut endoderm or the formation of the mid- and hindgut. In the node-ablated embryo, expression of the Pitx2 gene in the lateral plate mesoderm was no longer restricted to the left side but was found on both sides of the body or was completely absent from the lateral plate mesoderm. Therefore, the loss of the node results in the failure to delineate the laterality of the body axis. The node and its derivatives therefore play a critical role in the patterning of the ventral neural tube and lateral body axis but not of the anterior-posterior axis during early organogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Body Patterning / genetics*
  • Cell Differentiation
  • Cell Lineage
  • Embryonic and Fetal Development / genetics*
  • Gastrula / metabolism
  • Gene Expression Regulation, Developmental
  • Histocytochemistry
  • Homeodomain Proteins / genetics
  • In Situ Hybridization
  • Mesoderm / metabolism
  • Mice
  • Notochord / embryology
  • Nuclear Proteins*
  • Paired Box Transcription Factors
  • Transcription Factors / genetics

Substances

  • Homeodomain Proteins
  • Nuclear Proteins
  • Paired Box Transcription Factors
  • Transcription Factors
  • homeobox protein PITX1
  • homeobox protein PITX3
  • homeobox protein PITX2