| First Author | Kelly A | Year | 2002 |
| Journal | Genesis | Volume | 33 |
| Issue | 1 | Pages | 29-39 |
| PubMed ID | 12001067 | Mgi Jnum | J:268696 |
| Mgi Id | MGI:6272681 | Doi | 10.1002/gene.10085 |
| Citation | Kelly A, et al. (2002) Developmental potential and survival of glycolysis-deficient cells in fetal mouse chimeras. Genesis 33(1):29-39 |
| abstractText | 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 Gpi1m/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 Gpi1m/m<-->Gpi1c/c chimeras were identified and these contained low levels of homozygous mutant cells in most tissues tested. Homozygous Gpi1m/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. |
