Transcriptional enhancer factor 1 disruption by a retroviral gene trap leads to heart defects and embryonic lethality in mice.

Z Chen, GA Friedrich, P Soriano - Genes & development, 1994 - genesdev.cshlp.org
Z Chen, GA Friedrich, P Soriano
Genes & development, 1994genesdev.cshlp.org
We have used a retroviral gene trap in embryonic stem (ES) cells to derive a recessive
embryonic lethal mouse strain, ROSA beta-geo5. Mutant embryos display an enlarged
pericardial cavity, bradycardia, a dilated fourth ventricle in the brain, and die between
embryonic days 11 and 12. Whereas heart development in the mutant embryos is extensive,
the ventricular wall is abnormally thin with a reduced number of trabeculae. Cloning of the
trapped gene indicates that proviral insertion creates a null mutation in the transcriptional …
We have used a retroviral gene trap in embryonic stem (ES) cells to derive a recessive embryonic lethal mouse strain, ROSA beta-geo5. Mutant embryos display an enlarged pericardial cavity, bradycardia, a dilated fourth ventricle in the brain, and die between embryonic days 11 and 12. Whereas heart development in the mutant embryos is extensive, the ventricular wall is abnormally thin with a reduced number of trabeculae. Cloning of the trapped gene indicates that proviral insertion creates a null mutation in the transcriptional enhancer factor 1 (TEF-1) gene. Although transcription of a number of muscle-specific genes believed to be TEF-1 targets appears normal, the defect in cardiogenesis is likely attributable to diminished transcription of one or several cardiac-specific genes.
genesdev.cshlp.org