The targeted disruption of the MYPT1 gene results in embryonic lethality
The targeted disruption of the MYPT1 gene results in embryonic lethality
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DOI：
10.1007/s11248-005-3453-3
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发表时间：
2005-06-01
影响因子：
3
通讯作者：
Nakano, T
中科院分区：
文献类型：
--
作者：
Okamoto, R;Ito, M;Nakano, T
肌球蛋白磷酸酶(MP)是一种主要的磷酸酶，负责肌球蛋白II调节轻链的去磷酸化。MYPT1是平滑和非肌肉MP的靶亚单位，负责MP的激活和调节。为了确定MP的生理作用，我们通过基因打靶产生了MYPT1缺陷小鼠。与野生型小鼠相比，杂合子小鼠的MYPT1表达水平没有变化，也没有明显的表型。没有一只F2小鼠的MYPT1基因缺失是纯合的，这表明MYPT1基因的靶向破坏导致了胚胎死亡。胚胎致死点在7.5DPC之前。这些发现表明MYPT1在小鼠胚胎发生中是必不可少的。
Myosin phosphatase (MP) is a major phosphatase responsible for the dephosphorylation of the regulatory light chain of myosin II. MYPT1, a target subunit of smooth and nonmuscle MP, is responsible for activation and regulation of MP. To identity the physiological roles of MP, we have generated MYPT1-deficient mice by gene targeting. The heterozygous mice showed no changes in expression levels of MYPT1 and no distinct phenotype compared to wild-type mice was observed. None of the F2 mice were homozygous for the MYPT1 deletion, indicating that the targeted disruption of the MYPT1 gene resulted in embryonic lethality. The point of embryonic lethality is before 7.5 dpc. These findings indicate that MYPT1 is essential for mouse embryogenesis.