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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >MARCKS deficiency in mice leads to abnormal brain development and perinatal death.
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MARCKS deficiency in mice leads to abnormal brain development and perinatal death.

机译：小鼠的MARCKS缺乏症会导致异常的大脑发育和围产期死亡。

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摘要

The MARCKS protein is a widely distributed cellular substrate for protein kinase C. It is a myristoylprotein that binds calmodulin and actin in a manner reversible by protein kinase C-dependent phosphorylation. It is also highly expressed in nervous tissue, particularly during development. To evaluate a possible developmental role for MARCKS, we disrupted its gene in mice by using the techniques of homologous recombination. Pups homozygous for the disrupted allele lacked detectable MARCKS mRNA and protein. All MARCKS-deficient pups died before or within a few hours of birth. Twenty-five percent had exencephaly and 19% had omphalocele (normal frequencies, < 1%), indicating high frequencies of midline defects, particularly in cranial neurulation. Nonexencephalic MARCKS-deficient pups had agenesis of the corpus callosum and other forebrain commissures, as well as failure of fusion of the cerebral hemispheres. All MARCKS-deficient pups also displayed characteristic lamination abnormalities of the cortex and retina. These studies suggest that MARCKS plays a vital role in the normal developmental processes of neurulation, hemisphere fusion, forebrain commissure formation, and formation of cortical and retinal laminations. We conclude that MARCKS is necessary for normal mouse brain development and postnatal survival.
机译：MARCKS蛋白是蛋白激酶C广泛分布的细胞底物。它是一种肉豆蔻酰蛋白，其结合钙调蛋白和肌动蛋白的方式可被蛋白激酶C依赖性磷酸化逆转。它还在神经组织中高表达，特别是在发育过程中。为了评估MARCKS的可能发育作用，我们使用同源重组技术破坏了其在小鼠中的基因。等位基因纯合的幼犬缺乏可检测的MARCKS mRNA和蛋白质。所有缺乏MARCKS的幼崽在出生前或出生后几个小时内死亡。 25％的人有脑脊液抽出，19％的人有卵泡破裂（正常频率，<1％），表明中线缺损的发生频率很高，尤其是在颅神经中。无脑型MARCKS缺陷的幼仔有call体和其他前脑连合的发育不全，以及大脑半球融合失败。所有缺乏MARCKS的幼犬也表现出皮质和视网膜的特征性层压异常。这些研究表明，MARCKS在神经的正常发育过程，半球融合，前脑连合形成以及皮质和视网膜叠层的形成中起着至关重要的作用。我们得出结论，MARCKS对于正常的小鼠大脑发育和产后生存是必需的。

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