Defective neocortical development in Fyn-tyrosine-kinase-deficient mice
Defective neocortical development in Fyn-tyrosine-kinase-deficient mice
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DOI：
10.1097/00001756-200404090-00016
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发表时间：
2004-04
期刊：
影响因子：
1.7
通讯作者：
S. Yuasa;K. Hattori;T. Yagi
中科院分区：
文献类型：
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作者：
S. Yuasa;K. Hattori;T. Yagi
Fyn酪氨酸激酶参与了Reelin信号通路中DISABLED-1的酪氨酸磷酸化，而FYN的缺失有望导致一种卷轴样表型。因此，这项研究调查了Fyn缺陷小鼠的新皮质发育。溴脱氧尿嘧啶核苷标记显示，尽管较早生成的神经元正常放置，但较晚生成的神经元迁移不足。钙结合素和钙/钙调素依赖的蛋白激酶II免疫组织化学显示，II-III层神经元呈异常复层，但深层神经元几乎没有异常迹象。Fyn在晚期产生的迁移性皮质神经元的前导过程中有强烈表达。这些发现有力地表明，Fyn对于后来产生的神经元的迁移是必需的，但对于Reelin依赖的内向外层的形成是必不可少的。
Fyn tyrosine kinase is involved in the tyrosine-phosphorylation of Disabled-1 in the Reelin signaling pathway, and absence of Fyn is expected to result in a reeler-like phenotype. Thus, this study investigated neocortical development in Fyn-deficient mice. Bromodeoxyuridine labeling revealed the under-migration of later-generated neurons despite the normal placement of earlier-generated neurons. Calbindin- and -calcium/calmodulin-dependent protein kinase II-immunohistochemistry showed that layer II-III neurons were aberrantly stratified, but the neurons in the deeper layers showed little evidence of abnormality. Fyn was intensely expressed in the leading process of migratory cortical neurons generated in the later stage. These findings strongly suggest that Fyn is required for the migration of later-generated neurons, but that it is dispensable for the Reelin-dependent inside-out layer formation.