Semaphorin 3A-Neuropilin-1 signaling regulates peripheral axon fasciculation and pathfinding but not developmental cell death patterns
Semaphorin 3A-Neuropilin-1 signaling regulates peripheral axon fasciculation and pathfinding but not developmental cell death patterns
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DOI：
10.1111/j.1460-9568.2010.07154.x
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发表时间：
2010-04-01
影响因子：
3.4
通讯作者：
Huber, Andrea B.
中科院分区：
文献类型：
--
作者：
Haupt, Corinna;Kloos, Karina;Huber, Andrea B.
在早期发育中，产生了过量的神经元，其中约一半将由于各自目标区域的营养支持供应有限而通过细胞死亡而丢失。然而，一些神经元在其轴突尚未到达其目标时死亡，从而表明存在发育性细胞死亡的其他原因。Semaphorin 3A（Sema 3A）除了作为运动和感觉轴突生长的时间和成束的引导线索和介导剂的功能外，还可以在体外诱导感觉神经元的死亡。然而，它是未知的神经纤毛蛋白-1（Npn-1），其结合受体在轴突导向，是否也介导的死亡诱导活动。我们在这里表明，取消Sema 3A-Npn-1信号不影响细胞死亡模式的运动或感觉神经元在发育过程中的程序性细胞死亡。运动和感觉神经元的数量在胚胎第15.5天没有变化，当这个波结束时。有趣的是，在没有Sema 3A或Npn-1的情况下观察到的早期运动和感觉投射的解束持续到出生后阶段。因此，Sema 3A-Npn-1信号传导在运动和感觉轴突的引导和成束中起重要作用，但不有助于这些神经元的发育消除。
In early development, an excess of neurons is generated, of which later about half will be lost by cell death due to a limited supply of trophic support by their respective target areas. However, some of the neurons die when their axons have not yet reached their target, thus suggesting that additional causes of developmental cell death exist. Semaphorin 3A (Sema3A), in addition to its function as a guidance cue and mediator of timing and fasciculation of motor and sensory axon outgrowth, can also induce death of sensory neurons in vitro. However, it is unknown whether Neuropilin-1 (Npn-1), its binding receptor in axon guidance, also mediates the death-inducing activity. We show here that abolished Sema3A-Npn-1 signaling does not influence the cell death patterns of motor or sensory neurons in mouse during the developmental wave of programmed cell death. The number of motor and sensory neurons was unchanged at embryonic day 15.5 when this wave is concluded. Interestingly, the defasciculation of early motor and sensory projections that is observed in the absence of Sema3A or Npn-1 persists to postnatal stages. Thus, Sema3A-Npn-1 signaling plays an important role in the guidance and fasciculation of motor and sensory axons but does not contribute to the developmental elimination of these neurons.