Gastrulation in the mouse: assessment of cell populations in the epiblast of tw18/tw18 embryos

Abstract

Homozygous tW18 embryos die prior to organogenesis. They develop gross abnormalities shortly after primitive streak formation. Anatomically, the lesion appears to be confined to the mesoderm with that tissue showing ultrastructural deficiencies and abnormal migration (Spiegelman & Bennett, 1974), and failing to develop in teratomas produced from mutant embryos (Artzt & Bennett, 1972). Analysis of growth rate by determining cell number increase, and by mapping mitotic activity and planes of cleavage in the epiblast shows that the mutant embryos are small but paradoxically show overall a very high mitotic activity, approximately double that of their normal litter mates. They also show a marked disorientation of the planes of cleavage in most of the epiblast. In pre-primitive streak embryos, before gross abnormality is detectable, two types of embryo can be found. One group constitutes the small embryos which also show the mitotic disturbances characteristic of the later stage mutants. The second group, larger embryos, do not show mitotic abnormalities. The tW18 allele thus seems to act several hours before primitive streak formation. Since there is no difference in the amount of cell between mutant and normal embryos until 6.75 days p.c. it seems that arrest in division is the cause of the elevated mitotic index in mutants. Significantly a small region of the epiblast in mutant embryos is free of the mitotic abnormalities characteristic of the tissue as a whole. This region is the so-called proliferative zone (Snow, 1977) and the data suggest that it may be from this region that some of the ectoderm of the later embryos is produced.