Strain dependency of TGFbeta1 function during embryogenesis

Autor:	S, Kallapur, I, Ormsby, T, Doetschman
Rok vydání:	1999
Předmět:	Male Mice Knockout Mice Inbred BALB C Mice Inbred C3H Genotype Mice Inbred Strains Mice SCID Embryo Transfer Mice Inbred C57BL Embryonic and Fetal Development Mice Blastocyst Species Specificity Pregnancy Transforming Growth Factor beta Animals Female Crosses Genetic
Zdroj:	Molecular reproduction and development. 52(4)
ISSN:	1040-452X
Popis:	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 x C57BL/6J/Ola 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 TGFbeta1 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 TGFbeta1 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.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=pmid________::f3b03c1e7e10b4f526168caf4ef2ab85 https://pubmed.ncbi.nlm.nih.gov/10092113 Zobrazit plný text záznamu Plný text