EFFECTS OF KINESIN MUTATIONS ON NEURONAL FUNCTIONS
EFFECTS OF KINESIN MUTATIONS ON NEURONAL FUNCTIONS
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DOI：
10.1126/science.1384131
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发表时间：
1992-10-09
期刊：
影响因子：
56.9
通讯作者：
SAXTON, WM
中科院分区：
文献类型：
--
作者：
GHO, M;MCDONALD, K;SAXTON, WM
驱动蛋白被认为在轴突顺行运输中产生细胞器运动的力。编码驱动蛋白样蛋白的基因的鉴定表明，其他电机可能提供顺行力，而不是或除了驱动蛋白。为了深入了解驱动蛋白的特殊功能，研究了驱动蛋白重链基因（khc）突变对果蝇幼虫神经元生理和超微结构的影响。khc的突变损害轴突中动作电位的传播和神经末梢中神经递质的释放，但对神经末梢细胞质中突触囊泡的浓度没有明显影响。因此，驱动蛋白在体内是正常神经元功能所必需的，并且可以在将离子通道和突触释放机制的组分转运到其适当的细胞位置中具有活性。驱动蛋白似乎不需要突触囊泡或其组分的顺行运输。
Kinesin is believed to generate force for the movement of organelles in anterograde axonal transport. The identification of genes that encode kinesin-like proteins suggests that other motors may provide anterograde force instead of or in addition to kinesin. To gain insight into the specific functions of kinesin, the effects of mutations in the kinesin heavy chain gene (khc) on the physiology and ultrastructure of Drosophila larval neurons were studied. Mutations in khc impair both action potential propagation in axons and neurotransmitter release at nerve terminals but have no apparent effect on the concentration of synaptic vesicles in nerve terminal cytoplasm. Thus kinesin is required in vivo for normal neuronal function and may be active in the transport of ion channels and components of the synaptic release machinery to their appropriate cellular locations. Kinesin appears not to be required for the anterograde transport of synaptic vesicles or their components.