Transgenic mouse with endogenous endoglin gene disruption

Abstract

Transgenic mice are genetically engineered for a deficiency in endoglin production. These mice may have a homozygous or hemizygous disruption of the endogenous endoglin gene. Homozygous mice exhibit a lack of endoglin production. The failure to produce endoglin results in arrested development of the vascular system of the mouse and no survival beyond E11.5. These mice and cells derived therefrom provide useful reagents for understanding the development and pathology of the mammalian vascular system.

We claim:  
     
         1 . A transgenic mouse embryo homozygous for endogenous endoglin gene disruption.  
     
     
         2 . The transgenic mouse embryo of  claim 2 , wherein the disruption results in a lack of expression of the endoglin gene product.  
     
     
         3 . The transgenic mouse embryo of  claim 2 , wherein the lack of expression of the endoglin gene product results in arrested development of the vascular system of the mouse.  
     
     
         4 . The transgenic mouse embryo of  claim 1 , wherein the disruption results from insertion of a selectable marker gene sequence or other heterologous sequence into the genome by homologous recombination.  
     
     
         5 . The transgenic mouse embryo of  claim 4 , wherein the selectable marker gene sequence comprises a gene conferring neomycin resistance.  
     
     
         6 . The transgenic mouse embryo of  claim 4 , wherein the disruption results in a lack of expression of the endoglin gene product.  
     
     
         7 . The transgenic mouse embryo of  claim 6 , wherein the lack of expression of the endoglin gene product results in arrested development of the vascular system of the mouse.  
     
     
         8 . A cell derived from the mouse embryo of  claim 1 .  
     
     
         9 . A cell derived from the mouse embryo of  claim 7 .  
     
     
         10 . A cell derived from a transgenic mouse embryo homozygous for endogenous endoglin gene disruption, said disruption resulting from insertion of a selectable marker gene sequence or other heterologous sequence into the genome by homologous recombination, wherein the disruption results in a lack of expression of the endoglin gene product, and wherein the lack of expression of the endoglin gene product results in arrested development of the vascular system of the mouse embryo.  
     
     
         11 . A transgenic mouse or mouse embryo hemizygous for disruption of an endogenous endoglin gene.  
     
     
         12 . The transgenic mouse or mouse embryo of  claim 11 , wherein the disruption results from insertion of a selectable marker gene sequence or other heterologous sequence into the genome by homologous recombination.  
     
     
         13 . The transgenic mouse or mouse embryo of  claim 12 , wherein the selectable marker gene sequence comprises a gene conferring neomycin resistance.  
     
     
         14 . A cell derived from the mouse or mouse embryo of  claim 11 .  
     
     
         15 . A cell derived from the mouse or mouse embryo of  claim 13 .  
     
     
         16 . A mouse embryonic stem cell hemizygous for disruption of an endogenous endoglin gene.  
     
     
         17 . The mouse embryonic stem cell of  claim 16 , wherein the disruption results from insertion of a selectable marker gene sequence or other heterologous sequence into the genome by homologous recombination.  
     
     
         18 . The mouse embryonic stem cell of  claim 17 , wherein the selectable marker gene sequence comprises a gene conferring neomycin resistance.