Nuk controls pathfinding of commissural axons in the mammalian central nervous system
Nuk controls pathfinding of commissural axons in the mammalian central nervous system
复制标题
DOI：
10.1016/s0092-8674(00)80075-6
复制
发表时间：
1996-07-12
期刊：
影响因子：
64.5
通讯作者：
Klein, R
中科院分区：
文献类型：
--
作者：
Henkemeyer, M;Orioli, D;Klein, R
已经提出Eph家族受体酪氨酸激酶控制轴突导向和成束。为了解决Eph家族成员Nuk的生物学功能，在小鼠生殖系中产生了两种突变：蛋白质无效等位基因（Nuk（1））和编码缺乏酪氨酸激酶和C-末端结构域的Nuk-β gal融合受体的等位基因（Nuk（lacZ））。在Nuk（1）纯合子脑中，形成前连合后束的大部分轴突异常迁移到脑底，导致皮质神经元无法连接两个颞叶。这些结果表明，Nuk，一种结合跨膜配体的受体，在哺乳动物中枢神经系统中特定轴突的寻路中起着关键和独特的作用。
Eph family receptor tyrosine kinases have been proposed to control axon guidance and fasciculation. To address the biological functions of the Eph family member Nuk, two mutations in the mouse germline have been generated: a protein null allele (Nuk(1)) and an allele that encodes a Nuk-beta gal fusion receptor lacking the tyrosine kinase and C-terminal domains (Nuk(lacZ)). In Nuk(1) homozygous brains, the majority of axons forming the posterior tract of the anterior commissure migrate aberrantly to the floor of the brain, resulting in a failure of cortical neurons to link the two temporal lobes. These results indicate that Nuk, a receptor that binds transmembrane ligands, plays a critical and unique role in the pathfinding of specific axons in the mammalian central nervous system.