TRANSCRIPTIONAL ENHANCER FACTOR-1 DISRUPTION BY A RETROVIRAL GENE TRAP LEADS TO HEART-DEFECTS AND EMBRYONIC LETHALITY IN MICE
TRANSCRIPTIONAL ENHANCER FACTOR-1 DISRUPTION BY A RETROVIRAL GENE TRAP LEADS TO HEART-DEFECTS AND EMBRYONIC LETHALITY IN MICE
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DOI：
10.1101/gad.8.19.2293
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发表时间：
1994-10-01
影响因子：
10.5
通讯作者：
SORIANO, P
中科院分区：
文献类型：
--
作者：
CHEN, Z;FRIEDRICH, GA;SORIANO, P
我们在胚胎干细胞（ES）中使用逆转录病毒基因陷阱获得了一种隐性胚胎致死小鼠菌株ROSA β -geo5。突变胚胎表现为心包腔增大、心动过缓、第四脑室扩张，并在胚胎第11至12天死亡。而突变胚胎的心脏发育范围广泛，心室壁异常薄，小梁数量减少。捕获基因的克隆表明，前病毒插入在转录增强因子1 （TEF-1）基因中产生零突变。尽管许多被认为是TEF-1靶点的肌肉特异性基因的转录似乎正常，但心脏发生的缺陷可能是由于一个或几个心脏特异性基因的转录减少。
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, brachycardia, 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.