UNC-16是一种JNK信号支架蛋白，可调节秀丽隐杆线虫中的囊泡运输。

UNC-16, a JNK-signaling scaffold protein, regulates vesicle transport in C. elegans.

作者信息

Byrd D T, Kawasaki M, Walcoff M, Hisamoto N, Matsumoto K, Jin Y

机构信息

Department of MCD Biology, Sinsheimer Laboratories, University of California, Santa Cruz, Santa Cruz, CA 95064, USA.

出版信息

Neuron. 2001 Dec 6;32(5):787-800. doi: 10.1016/s0896-6273(01)00532-3.

DOI:10.1016/s0896-6273(01)00532-3

PMID:11738026

Abstract

Transport of synaptic components is a regulated process. Loss-of-function mutations in the C. elegans unc-16 gene result in the mislocalization of synaptic vesicle and glutamate receptor markers. unc-16 encodes a homolog of mouse JSAP1/JIP3 and Drosophila Sunday Driver. Like JSAP1/JIP3, UNC-16 physically interacts with JNK and JNK kinases. Deletion mutations in Caenorhabditis elegans JNK and JNK kinases result in similar mislocalization of synaptic vesicle markers and enhance weak unc-16 mutant phenotypes. unc-116 kinesin heavy chain mutants also mislocalize synaptic vesicle markers, as well as a functional UNC-16::GFP. Intriguingly, unc-16 mutations partially suppress the vesicle retention defect in unc-104 KIF1A kinesin mutants. Our results suggest that UNC-16 may regulate the localization of vesicular cargo by integrating JNK signaling and kinesin-1 transport.

摘要

突触成分的运输是一个受调控的过程。秀丽隐杆线虫unc-16基因的功能丧失突变会导致突触小泡和谷氨酸受体标志物的定位错误。unc-16编码小鼠JSAP1/JIP3和果蝇Sunday Driver的同源物。与JSAP1/JIP3一样，UNC-16与JNK和JNK激酶发生物理相互作用。秀丽隐杆线虫JNK和JNK激酶的缺失突变会导致突触小泡标志物出现类似的定位错误，并增强弱unc-16突变体表型。unc-116驱动蛋白重链突变体也会使突触小泡标志物以及功能性UNC-16::GFP发生定位错误。有趣的是，unc-16突变部分抑制了unc-104 KIF1A驱动蛋白突变体中的小泡滞留缺陷。我们的结果表明，UNC-16可能通过整合JNK信号传导和驱动蛋白-1运输来调节囊泡货物的定位。