The SAD-1 kinase regulates presynaptic vesicle clustering and axon termination
The SAD-1 kinase regulates presynaptic vesicle clustering and axon termination
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DOI：
10.1016/s0896-6273(01)00184-2
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发表时间：
2001-01-01
期刊：
影响因子：
16.2
通讯作者：
Bargmann, CI
中科院分区：
文献类型：
--
作者：
Crump, JG;Zhen, M;Bargmann, CI
在突触形成过程中，突触前轴突生长终止，突触前囊泡簇与活性区蛋白相关，并且活性区与突触后神经递质受体对齐。我们在此报道了一种新的丝氨酸/苏氨酸激酶SAD-1的鉴定，SAD-1调节C.优美的在sad-1突变的动物中，感觉神经元和运动神经元中的突触前囊泡簇是弥漫性的和无序的。在SAD-1突变体中感觉轴突不能终止，而SAD-1的过表达导致感觉轴突过早终止。SAD-1蛋白在神经系统中表达，并定位于轴突的突触丰富区域。SAD-1与PAR-1相关，PAR-1是一种在不对称细胞分裂期间调节细胞极性的激酶。SAD-1的过度表达导致囊泡蛋白质错误定位到树突，表明SAD-1影响轴突-树突极性以及突触发育。
During synapse formation, presynaptic axon outgrowth is terminated, presynaptic clusters of vesicles are associated with active zone proteins, and active zones are aligned with postsynaptic neurotransmitter receptors. We report here the identification of a novel serine/threonine kinase, SAD-1,that regulates several aspects of presynaptic differentiation in C. elegans. In sad-1 mutant animals presynaptic vesicle clusters in sensory neurons and motor neurons are diffuse and disorganized. Sensory axons fail to terminate in sad-1 mutants, whereas overexpression of SAD-1 causes sensory axons to terminate prematurely. SAD-1 protein is expressed in the nervous system and localizes to synapse-rich regions of the axons. SAD-1 is related to PAR-1, a kinase that regulates cell polarity during asymmetric cell division. Overexpression of SAD-1 causes mislocalization of vesicle proteins to dendrites, suggesting that sad-1 affects axonal-dendritic polarity as well as synaptic development.