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Developmental potential and survival of glycolysis‐deficient cells in fetal mouse chimeras
Author(s) -
Kelly Annemarie,
West John D.
Publication year - 2002
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.10085
Subject(s) - biology , chimera (genetics) , mesoderm , endoderm , microbiology and biotechnology , mutant , epiblast , gastrulation , wild type , null allele , yolk sac , amnion , embryo , cell type , gene targeting , embryonic stem cell , genetics , cell , fetus , embryogenesis , gene , pregnancy
Summary: Mouse embryos homozygous for a null allele of Gpi1 fail to complete gastrulation and die around E7.5. We produced E12.5 chimeric mouse conceptuses, composed of wild‐type and homozygous Gpi1 m/m null mutant cells to test whether the presence of wild‐type cells allowed mutant cells to survive and, if so, whether they survived better in some tissue locations than others. Fourteen homozygous Gpi1 m/m ↔ Gpi1 c/c chimeras were identified and these contained low levels of homozygous mutant cells in most tissues tested. Homozygous Gpi1 m/m cells contributed better to the yolk sac endoderm and placenta than to the epiblast derivatives tested (retinal pigment epithelium, brain, tail, amnion, and yolk sac mesoderm). The depletion of mutant cells confirms that the gene acts cell autonomously, but the GPI deficiency is not always cell‐lethal. When mixed with wild‐type cells in chimeras, homozygous mutant cells can differentiate into many different cell types and survive until at least E12.5. genesis 33:29–39, 2002. © 2002 Wiley‐Liss, Inc.