Normal embryonic development and cardiac morphogenesis in mice with Wnt1-Cre-mediated deletion of connexin43
Normal embryonic development and cardiac morphogenesis in mice with Wnt1-Cre-mediated deletion of connexin43
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DOI：
10.1002/dvg.20204
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发表时间：
2006-06-01
期刊：
影响因子：
1.5
通讯作者：
Willecke, K.
中科院分区：
文献类型：
--
作者：
Kretz, M.;Eckardt, D.;Willecke, K.
含有间隙连接蛋白connexin43 （Cx43）零突变的小鼠在出生后不久因心脏右心室流出道阻塞而死亡。这些心脏在肺出口底部显示出突出的小袋，即神经嵴细胞中cx43缺乏导致的形态学异常。为了检测Cx43在神经嵴细胞和衍生组织中的表达模式，并测试Cx43在神经嵴特异性缺失是否会导致Cx43缺失小鼠中出现的锥体缺陷，我们使用Wnt1-Cre转基因切除了Cx43。Cx43的完全缺失发生在神经嵴细胞和神经嵴衍生组织中。然而，神经嵴细胞中特异性缺乏Cx43的小鼠心脏与对照组没有区别。因此，Cx43缺失小鼠的心脏形态异常很可能不是由神经嵴细胞中缺乏Cx43引起的。
Mice harboring a null mutation in the gap junction protein connexin43 (Cx43) die shortly after birth due to an obstruction of the right ventricular outflow tract of the heart. These hearts exhibit prominent pouches at the base of the pulmonary outlet, i.e., morphological abnormalities that were ascribed to Cx43-deficiency in neural crest cells. In order to examine the Cx43 expression pattern in neural crest cells and derived tissues and to test whether neural crest-specific deletion of Cx43 leads to the conotruncal defects seen in Cx43null mice, we ablated Cx43 using a Wnt1-Cre transgene. Deletion of Cx43 was complete and occurred in neural crest cells as well as in neural crest-derived tissues. Nevertheless, hearts of mice lacking Cx43 specifically in neural crest cells were indistinguishable from controls. Thus, the morphological heart abnormalities of Cx43 null mice are most likely not caused by lack of Cx43 in neural crest cells.