| First Author | Kallapur S | Year | 1999 |
| Journal | Mol Reprod Dev | Volume | 52 |
| Issue | 4 | Pages | 341-9 |
| PubMed ID | 10092113 | Mgi Jnum | J:53366 |
| Mgi Id | MGI:1332348 | Doi | 10.1002/(SICI)1098-2795(199904)52:4<341::AID-MRD2>3.0.CO;2-N |
| Citation | Kallapur S, et al. (1999) Strain dependency of TGFbeta1 function during embryogenesis. Mol Reprod Dev 52(4):341-9 |
| abstractText | There is incomplete penetrance to Tgfb1 knockout phenotypes. About 50% of Tgfb1 homozygous mutant (Tgfb1(-/- )) and 25% of Tgfb1 heterozygous (Tgfb1(+/-)) embryos die during embryogenesis. In a mixed NIH/OIa x C57BL/6J/OIa x 129 background partial embryonic lethality of the Tgfb1(-/- ) embryos occurs due to defective yolk sac vasculopoiesis and/or hematopoiesis. We show here that on a predominantly CF-1 genetic background, lack of TGF beta 1 causes a pre- morula lethality in about 50% of the null embryos. This partial lethality is not reversed by transfer of Tgfb1(-/- ) embryos to Tgfb1(+/+) hosts. The extent of embryonic lethality in Tgfb1(-/-) embryos ranges in a background dependent manner from 20% to 100%. Based on these and other studies it is clear that TGF beta 1 acts at two distinct phases of embryogenesis: pre-implantation development and yolk sac vasculogenesis/hematopoiesis. The susceptibility for the pre-implantation lethality depends on a small number of genetic modifiers since a small number of backcrosses onto the high susceptibility strain C57BL/6 leads to complete penetrance of the lethality. (C) 1999 Wiley-Liss, Inc. |
