Ghila Luiza, Gomez Marie
Department of Zoology and Animal Biology and NCCR Frontiers in Genetics, University of Geneva, Sciences III, 30 quai Ernest-Ansermet, 1211 Genève 4, Switzerland.
Eur J Neurosci. 2008 Feb;27(3):621-30. doi: 10.1111/j.1460-9568.2008.06049.x.
The control of vesicle-mediated transport in nerve cells is of great importance in the function, development and maintenance of synapse. In this paper, we characterize the new Caenorhabditis elegans gene, lnp-1. The lnp-1 gene is broadly distributed in many neuronal structures and its localization is dependent of the UNC-104/kinesin protein. Deletion mutations in lnp-1 result in increased resistance to aldicarb, an acetylcholinesterase inhibitor, and in locomotor defects. However, sensitivity to levamisole, a nicotinic agonist which, unlike aldicarb, only affects postsynaptic function, was similar to that of wild-type animals, suggesting a presynaptic function for LNP-1 in neurotransmission. The mislocalization of presynaptic proteins, such as synaptobrevin-1 or RAB-3, in lnp-1 mutants further supports this hypothesis. In summary, our studies suggest that LNP-1 plays a role in synaptogenesis by regulating vesicular transport or localization.
囊泡介导的神经细胞转运调控在突触的功能、发育和维持过程中具有重要意义。在本文中,我们对秀丽隐杆线虫的新基因lnp-1进行了表征。lnp-1基因广泛分布于许多神经元结构中,其定位依赖于UNC-104/驱动蛋白。lnp-1的缺失突变导致对乙酰胆碱酯酶抑制剂涕灭威的抗性增加以及运动缺陷。然而,对左旋咪唑(一种烟碱激动剂,与涕灭威不同,它仅影响突触后功能)的敏感性与野生型动物相似,这表明LNP-1在神经传递中具有突触前功能。lnp-1突变体中突触前蛋白(如突触小泡蛋白-1或RAB-3)的定位错误进一步支持了这一假设。总之,我们的研究表明LNP-1通过调节囊泡转运或定位在突触形成中发挥作用。