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Developmental potential and survival of glycolysis-deficient cells in fetal mouse chimeras

Annemarie Kelly1, John D West

  • 1Genes and Development Group, Department of Reproductive and Developmental Sciences, University of Edinburgh, United Kingdom.

Genesis (New York, N.Y. : 2000)
|May 10, 2002
PubMed

Insights

Mice lacking Gpi1 die early, but when mixed with normal cells, homozygous Gpi1 mutant cells can survive and differentiate, especially in the yolk sac and placenta.

Area of Science:

  • Developmental Biology
  • Genetics

Background:

  • Gpi1 encodes glucose-6-phosphate isomerase, essential for embryonic development.
  • Null mutations in Gpi1 lead to embryonic lethality around embryonic day 7.5 due to gastrulation failure.

Purpose of the Study:

  • To investigate if wild-type cells can rescue homozygous Gpi1 mutant cells.
  • To determine if Gpi1 mutant cells show differential survival in various tissue locations within chimeric embryos.

Main Methods:

  • Creation of chimeric mouse embryos by combining wild-type and Gpi1 null mutant cells.
  • Analysis of cell contribution and survival of homozygous Gpi1 mutant cells at embryonic day 12.5.

Main Results:

  • Homozygous Gpi1 mutant cells were found at low levels in most tissues of chimeric conceptuses.
  • Mutant cells contributed more effectively to yolk sac endoderm and placenta compared to epiblast derivatives.
  • The gene acts cell autonomously, but GPI deficiency is not universally cell-lethal in chimeras.

Conclusions:

  • Wild-type cells can support the survival and differentiation of Gpi1-deficient cells.
  • Gpi1 mutant cells exhibit tissue-specific survival advantages, thriving better in extraembryonic tissues.
  • GPI deficiency is not strictly cell-lethal when compensated by wild-type cells in a chimeric environment.

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