Survival and normal function of glycolysis-deficient mouse oocytes

A Kelly, J D West

Research output: Contribution to journalArticlepeer-review

Abstract

Mouse embryos homozygous for a null allele of Gpi1 which encodes the glycolytic enzyme glucose phosphate isomerase fail to complete gastrulation and die at about embryonic day 7.5, but mutant cells can survive in fetal chimaeras in which they are mixed with wild-type cells. An adult female mouse chimaera, composed of wild-type cells and homozygous Gpi1(-/-) null mutant cells, was produced to test whether the presence of wild-type cells in the ovary allowed mutant oocytes to survive and function. This mouse produced 28 offspring, eight of which were derived from homozygous Gpi1(-/-) null oocytes. DNA in situ hybridization also showed that some Gpi1(-/-) follicle cells were able to survive in chimaeric ovarian follicles. It is likely that the survival of mutant follicle cells and fully functional mutant oocytes was mediated by the presence of wild-type cells that could provide metabolic intermediates and so bypass the block in the glycolytic pathway. Wild-type cumulus cells probably supported the growing GPI-deficient oocytes via metabolic co-operation, by passing ATP and other glycolytic products through gap junctions. It was concluded that female mouse germ cells and ovarian follicle cells do not need an intact endogenous glycolytic pathway if they can obtain appropriate metabolites from an exogenous source.

Original languageEnglish
Pages (from-to)469-73
Number of pages5
JournalReproduction
Volume124
Issue number4
Publication statusPublished - Oct 2002

Keywords

  • Anemia, Hemolytic, Congenital Nonspherocytic
  • Animals
  • Cell Communication
  • Cell Survival
  • Chimera
  • Female
  • Glucose-6-Phosphate Isomerase
  • Glycolysis
  • Mice
  • Mice, Mutant Strains
  • Mutation
  • Oocytes
  • Ovarian Follicle

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