Plexin A3 and plexin A4 convey semaphorin signals during facial nerve development.
Plexin A3 and plexin A4 convey semaphorin signals during facial nerve development.
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DOI：
10.1016/j.ydbio.2008.08.020
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发表时间：
2008-12-01
影响因子：
2.7
通讯作者：
Ruhrberg, Christiana
中科院分区：
文献类型：
--
作者：
Schwarz, Quenten;Waimey, Kathryn E.;Golding, Matthew;Takamatsu, Hyota;Kumanogoh, Atsushi;Fujisawa, Hajime;Cheng, Hwai-Jong;Ruhrberg, Christiana
关键词：
在脊椎动物中，3类信号蛋白（SEMA3）通过与神经元细胞表面受体结合来控制轴突行为，所述神经元细胞表面受体由称为神经纤毛蛋白（NRP）的配体结合亚基和A型丛蛋白家族（PLXNA）的信号转导亚基组成。我们已经确定了SEMA3/NRP/PLXN信号在面神经的发育中的需求，面神经包含来自两个运动神经元群体，鳃神经元和内脏神经元的轴突。SEMA3A/NRP1或SEMA3F/NRP2的缺失引起面鳃纤维轴突的去束和异位投射。相反，面部内脏神经轴突选择性地需要SEMA3A/NRP1。因此，当SEMA 3A或NRP1丢失时，岩大浅神经被去束，形成异位投射，并且不能在其靶区域内形成分支。为了研究A型丛蛋白在面神经发育过程中传递SEMA3/neuropilin信号，我们将表达分析与功能丧失研究相结合。尽管所有四种A型丛蛋白都在胚胎运动神经元中表达，但PLXNA 1和PLXNA 2对于面神经发育不是必需的。相反，PLXNA4的缺失表型模仿SEMA3A和NRP1突变体的缺陷，PLXNA3的缺失表型模仿SEMA3F和NRP2突变体的缺陷。PLXNA3和PLXNA4的合并损失损害面鳃纤维轴突的指导更严重的损失比任何单独的丛蛋白，这表明这两种途径通常合作，相比之下，损失的两个丛蛋白并没有损害面部内脏缺损任何损失的PLXNA4。我们的结论是，PLXNA3和PLXNA4协同图案的面神经，其中都需要在鳃神经元，但只有PLXNA4是必不可少的内脏神经元。
In vertebrates, class 3 semaphorins (SEMA3) control axon behaviour by binding to neuronal cell surface receptors composed of a ligand binding subunit termed neuropilin (NRP) and a signal transduction subunit of the A-type plexin family (PLXNA). We have determined the requirement for SEMA3/NRP/PLXN signalling in the development of the facial nerve, which contains axons from two motor neuron populations, branchiomotor and visceromotor neurons. Loss of either SEMA3A/NRP1 or SEMA3F/NRP2 caused defasciculation and ectopic projection of facial branchiomotor axons. In contrast, facial visceromotor axons selectively required SEMA3A/NRP1. Thus, the greater superficial petrosal nerve was defasciculated, formed ectopic projections and failed to branch in its target area when either SEMA3A or NRP1 were lost. To examine which A-type plexin conveyed SEMA3/neuropilin signals during facial nerve development, we combined an expression analysis with loss of function studies. Even though all four A-type plexins were expressed in embryonic motor neurons, PLXNA1 and PLXNA2 were not essential for facial nerve development. In contrast, loss of PLXNA4 phenocopied the defects of SEMA3A and NRP1 mutants, and loss of PLXNA3 phenocopied the defects of SEMA3F and NRP2 mutants. The combined loss of PLXNA3 and PLXNA4 impaired facial branchiomotor axon guidance more severely than loss of either plexin alone, suggesting that both pathways normally cooperate; in contrast, loss of both plexins did not impair facial visceromotor defects any worse than loss of PLXNA4. We conclude that PLXNA3 and PLXNA4 synergise to pattern the facial nerve, whereby both are required in branchiomotor neurons, but only PLXNA4 is essential for visceromotor neurons.
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