Fine structural study of cell migration in the early mesoderm of normal and mutant mouse embryos (<i>T</i>-locus:<i>t</i>9/<i>t</i>9)

Abstract

ABSTRACT Mouse embryos homozygous for the t9-allele exhibit an enlarged primitive streak, scanty mesoderm, and aberrant axial organization by the eighth day of development and die by the tenth day. Light and electron microscopic observations of sections through mesodermal cells of these mutant embryos reveal sheet-like arrangements of cells rather than the array of stellate individual cells seen in mesoderm of normal embryos. The abnormal mesodermal cells usually display lobate pseudopodia instead of the filiform pseudopodia typical of normal mesodermal cells. These lobopodia do not possess the subsurface microfilaments characteristic of filopodia. Cellular junctions such as those regularly seen between adjacent filpopodia of normal mesodermal cells occur only very rarely between neighboring lobopodia of mutant mesodermal cells. The deficiency of mesoderm may be due to the failure of cells to form the cellular associations typical of gastrulation and to move normally from the primitive streak which consequently becomes enlarged due to the accumulation of apparently immobilized cells. Those few cells which do attain the proper location nevertheless do not appear well-differentiated. Their abnormalities of cell shape, cellular translocation, and cellular interactions may be related to a lack of microfilament cytostructure and surface adhesiveness.