在神经系统发育过程中,神经元发出轴突,它必须导航很长的距离才能到达突触目标。轴突依次生长。早期生长的轴突,先驱,必须整合来自环境中各种指导线索的信息,以确定正确的生长方向。后来成长的追随者轴突可以至少部分地通过粘附先驱轴突来导航。在秀丽隐杆线虫中,最大纵向轴突束的右侧,腹神经索,由AVG轴突开创。AVG轴突如何导航只能部分理解。在这项研究中,我们描述了IgCAM家族的两个成员的作用,wrk-1和rig-5,在AVG轴突导航中。虽然wrk-1和rig-5单突变体没有显示AVG导航缺陷,两种突变体在nid-1突变体背景下都具有高度渗透的先驱和跟随导航缺陷。两种突变都会增加跟随错误的先驱轴突的比例。我们发现wrk-1和rig-5在不同的遗传途径中起作用,这表明我们确定了跟随轴突使用的两个与先驱无关的引导途径。我们评估了一般的运动能力,机械感觉反应,和习惯来确定轴突导航缺陷是否影响神经系统功能。在rig-5nid-1双突变体中,我们发现自由运动行为没有显著缺陷;然而,动物亚群在机械感觉刺激后,反应持续时间习惯发生了微小变化。这些结果表明,运动电路中轴突的引导缺陷不一定会导致主要的运动或行为缺陷,但会影响更复杂的行为调制。
During nervous system development, neurons send out axons, which must navigate large distances to reach synaptic targets. Axons grow out sequentially. The early outgrowing axons, pioneers, must integrate information from various guidance cues in their environment to determine the correct direction of outgrowth. Later outgrowing follower axons can at least in part navigate by adhering to pioneer axons. In Caenorhabditis elegans, the right side of the largest longitudinal axon tract, the ventral nerve cord, is pioneered by the AVG axon. How the AVG axon navigates is only partially understood. In this study, we describe the role of two members of the
IgCAM family, wrk-1 and rig-5, in AVG axon navigation. While wrk-1 and rig-5 single mutants do not show AVG navigation defects, both mutants have highly penetrant pioneer and follower navigation defects in a nid-1 mutant background. Both mutations increase the fraction of follower axons following the misguided pioneer axon. We found that wrk-1 and rig-5 act in different genetic pathways, suggesting that we identified two pioneer-independent guidance pathways used by follower axons. We assessed general locomotion, mechanosensory responsiveness, and habituation to determine whether axonal navigation defects impact nervous system function. In rig-5 nid-1 double mutants, we found no significant defects in free movement behavior; however, a subpopulation of animals shows minor changes in response duration habituation after mechanosensory stimulation. These results suggest that guidance defects of axons in the motor circuit do not necessarily lead to major movement or behavioral defects but impact more complex behavioral modulation.