非侵入性力测量揭示了ARL-8调节轴突运输中突触囊泡前体上活性驱动蛋白的数量
Non-invasive force measurement reveals the number of active kinesins on a synaptic vesicle precursor in axonal transport regulated by ARL-8
摘要：
驱动蛋白超家族蛋白<$104是驱动蛋白3家族的一员，主要转运突触囊泡前体（SVP）。在这项研究中，有活性的α-104分子牵引一个单一的SVP在蠕虫秀丽隐杆线虫轴突的数量进行了计数，通过应用一种新开发的非侵入性的力测量技术。作用在由α-104运输的SVP上的力的分布分散在几个簇中，这意味着存在几个力产生单元（FPU）。然后，我们比较了野生型蠕虫与arl-8基因缺失突变体蠕虫中FPU的数量。ARL-8是一种SVP结合的arf样小鸟苷三磷酸酶，已知可促进马达自身抑制的解锁，这对于避免马达不与SVP结合时三磷酸腺苷的不必要消耗至关重要。在arl-8突变体蠕虫中存在较少的FPU。这一发现表明，缺乏ARL-8减少了活跃的ESTA-104马达的数量，从而导致负责SVP运输的马达数量减少。
英文摘要：
Kinesin superfamily protein UNC-104, a member of the kinesin-3 family, transports synaptic vesicle precursors (SVPs). In this study, the number of active UNC-104 molecules hauling a single SVP in axons in the worm Caenorhabditis elegans was counted by applying a newly developed non-invasive force measurement technique. The distribution of the force acting on a SVP transported by UNC-104 was spread out over several clusters, implying the presence of several force-producing units (FPUs). We then compared the number of FPUs in the wild-type worms with that in arl-8 gene-deletion mutant worms. ARL-8 is a SVP-bound arf-like small guanosine triphosphatase, and is known to promote unlocking of the autoinhibition of the motor, which is critical for avoiding unnecessary consumption of adenosine triphosphate when the motor does not bind to a SVP. There were fewer FPUs in the arl-8 mutant worms. This finding indicates that a lack of ARL-8 decreased the number of active UNC-104 motors, which then led to a decrease in the number of motors responsible for SVP transport.
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