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Strain dependency of TGFβ1 function during embryogenesis
Author(s) -
Kallapur Suhas,
Ormsby Ilona,
Doetschman Thomas
Publication year - 1999
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/(sici)1098-2795(199904)52:4<341::aid-mrd2>3.0.co;2-n
Subject(s) - biology , embryo , penetrance , embryogenesis , yolk sac , lethality , embryonic stem cell , genetics , phenotype , microbiology and biotechnology , andrology , gene , medicine
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/Ola × C57BL/6J/Ola × 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 TGFβ1 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 TGFβ1 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. Mol. Reprod. Dev. 52:341–349, 1999. © 1999 Wiley‐Liss, Inc.