Does the T gene determine the anteroposterior axis of a mouse embryo?

Jpn J Genet. 1990 Oct;65(5):287-97. doi: 10.1266/jjg.65.287.

Abstract

The t complex in the mouse is essential to embryonic development. The semidominant mutation, T, is embryonic lethal in homozygotes. In T/T embryos, proper morphogenetic movement is hindered, causing the number of mesodermal cells to be reduced. The other effect of T mutation is shortening of the tail in heterozygotes, T/+ and T/t. t is a series of recessive mutations in the t complex. A detailed examination of tail shortening indicated the T and t mutations to exert various effects, such as the derangement of the pattern of necrosis, fusion or duplication of the neural tube and gut. The most severely affected structure is the notochord. The t mutation augments the effect of T mutation in the formation of normal notochord. A gradient of phenotypic severity along anteroposterior axis of an embryo appeared to exist correlative to the dosage of the T gene. Should the products of the T gene be responsible for inducing mesoderm and the establishment of the anteroposterior axis of an embryo, diverse effects of the T mutation on embryogenesis can be explained collectively.

MeSH terms

  • Animals
  • Embryo, Mammalian / anatomy & histology*
  • Embryonic and Fetal Development / genetics*
  • Genes, Lethal*
  • Homozygote
  • Mesoderm / cytology
  • Mice
  • Morphogenesis
  • Mutation
  • Phenotype