| First Author | Van de Putte T | Year | 2001 |
| Journal | Mech Dev | Volume | 102 |
| Issue | 1-2 | Pages | 33-44 |
| PubMed ID | 11287179 | Mgi Jnum | J:69359 |
| Mgi Id | MGI:1934490 | Doi | 10.1016/s0925-4773(01)00279-9 |
| Citation | Van de Putte T, et al. (2001) Mice with a homozygous gene trap vector insertion in mgcRacGAP die during pre-implantation development. Mech Dev 102(1-2):33-44 |
| abstractText | In a phenotypic screen in mice using a gene trap approach in embryonic stem cells, we have identified a recessive loss-of-function mutation in the mgcRacGAP gene. Maternal protein is present in the oocyte, and mgcRacGAP gene transcription starts at the four-cell stage and persists throughout mouse pre-implantation development. Total mgcRacGAP deficiency results in pre-implantation lethality. Such E3.5 embryos display a dramatic reduction in cell number, but undergo compaction and form a blastocoel. At E3.0-3.5, binucleated blastomeres in which the nuclei are partially interconnected are frequently observed, suggesting that mgcRacGAP is required for normal mitosis and cytokinesis in the pre-implantation embryo. All homozygous mutant blastocysts fail to grow out on fibronectin-coated substrates, but a fraction of them can still induce decidual swelling in vivo. The mgcRacGAP mRNA expression pattern in post-implantation embryos and adult mouse brain suggests a role in neuronal cells. Our results indicate that mgcRacGAP is essential for the earliest stages of mouse embryogenesis, and add evidence that CYK-4-like proteins also play a role in microtubule-dependent steps in the cytokinesis of vertebrate cells. In addition, the severe phenotype of null embryos indicates that mgcRacGAP is functionally non-redundant and cannot be substituted by other GAPs during early cleavage of the mammalian embryo. |
