Kinesin light chains are essential for axonal transport in Drosophila.
Kinesin light chains are essential for axonal transport in Drosophila.
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DOI：
10.1083/jcb.141.2.443
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发表时间：
1998-04-20
期刊：
影响因子：
--
通讯作者：
Goldstein LS
中科院分区：
文献类型：
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作者：
Gindhart JG Jr;Desai CJ;Beushausen S;Zinn K;Goldstein LS
驱动蛋白是一种由两条115 - kD重链和两条58 - kD轻链组成的异源四聚体。驱动蛋白的微管运动活性由重链执行，但轻链的功能了解甚少。在果蝇驱动蛋白轻链（Klc）基因中产生了突变，并在行为和细胞水平上分析了Klc功能缺失的表型后果。Klc功能缺失导致渐进性嗜睡、爬行缺陷和麻痹，在二龄幼虫末期死亡。Klc突变的轴突在节段神经轴突中含有大量膜性细胞器聚集体。这些聚集体，或细胞器堵塞物（赫德，D.D.，和W.M.萨克斯顿，1996年，《遗传学》，144卷：1075 - 1085页），包含突触小泡前体以及可能由驱动蛋白、驱动蛋白样蛋白68D和细胞质动力蛋白运输的细胞器，从而提供了证据表明Klc功能缺失阻断了轴突运输的多种途径。Klc和Khc（《细胞》64卷：1093 - 1102页；赫德，D.D.，和W.M.萨克斯顿，1996年，《遗传学》144卷：1075 - 1085页）突变表型的相似性表明，KLC对驱动蛋白的功能至关重要，也许是通过将KHC连接到细胞内货物上或激活驱动蛋白运动来实现的。
Kinesin is a heterotetramer composed of two 115-kD heavy chains and two 58-kD light chains. The microtubule motor activity of kinesin is performed by the heavy chains, but the functions of the light chains are poorly understood. Mutations were generated in the Drosophila gene Kinesin light chain (Klc), and the phenotypic consequences of loss of Klc function were analyzed at the behavioral and cellular levels. Loss of Klc function results in progressive lethargy, crawling defects, and paralysis followed by death at the end of the second larval instar. Klc mutant axons contain large aggregates of membranous organelles in segmental nerve axons. These aggregates, or organelle jams (Hurd, D.D., and W.M. Saxton. 1996. Genetics. 144: 1075–1085), contain synaptic vesicle precursors as well as organelles that may be transported by kinesin, kinesin-like protein 68D, and cytoplasmic dynein, thus providing evidence that the loss of Klc function blocks multiple pathways of axonal transport. The similarity of the Klc and Khc (. Cell 64:1093–1102; Hurd, D.D., and W.M. Saxton. 1996. Genetics 144: 1075–1085) mutant phenotypes indicates that KLC is essential for kinesin function, perhaps by tethering KHC to intracellular cargos or by activating the kinesin motor.