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首页> 外文期刊>Molecular and Cellular Biology >Rho family GTPases and neuronal growth cone remodelling: relationship between increased complexity induced by Cdc42Hs, Rac1, and acetylcholine and collapse induced by RhoA and lysophosphatidic acid.
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Rho family GTPases and neuronal growth cone remodelling: relationship between increased complexity induced by Cdc42Hs, Rac1, and acetylcholine and collapse induced by RhoA and lysophosphatidic acid.

机译：Rho家族GTPases和神经元生长锥重塑：Cdc42Hs，Rac1和乙酰胆碱引起的复杂性增加与RhoA和溶血磷脂酸引起的崩溃之间的关系。

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Rho family GTPases have been assigned important roles in the formation of actin-based morphologies in nonneuronal cells. Here we show that microinjection of Cdc42Hs and Rac1 promoted formation of filopodia and lamellipodia in N1E-115 neuroblastoma growth cones and along neurites. These actin-containing structures were also induced by injection of Clostridium botulinum C3 exoenzyme, which abolishes RhoA-mediated functions such as neurite retraction. The C3 response was inhibited by coinjection with the dominant negative mutant Cdc42Hs(T17N), while the Cdc42Hs response could be competed by coinjection with RhoA. We also demonstrate that the neurotransmitter acetylcholine (ACh) can induce filopodia and lamellipodia on neuroblastoma growth cones via muscarinic ACh receptor activation, but only when applied in a concentration gradient. ACh-induced formation of filopodia and lamellipodia was inhibited by preinjection with the dominant negative mutants Cdc42Hs(T17N) and Rac1(T17N), respectively. Lysophosphatidic acid (LPA)-induced neurite retraction, which is mediated by RhoA, was inhibited by ACh, while C3 exoenzyme-mediated neurite outgrowth was inhibited by injection with Cdc42Hs(T17N) or Rac1(T17N). Together these results suggest that there is competition between the ACh- and LPA-induced morphological pathways mediated by Cdc42Hs and/or Rac1 and by RhoA, leading to either neurite development or collapse.
机译：Rho家族GTPases在非神经元细胞中基于肌动蛋白的形态形成中被赋予重要作用。在这里，我们显示微注射Cdc42Hs和Rac1促进了N1E-115神经母细胞瘤生长锥和神经突中丝状伪足和片状脂蛋白的形成。这些含有肌动蛋白的结构也可以通过注射肉毒梭菌C3外酶来诱导，从而消除了RhoA介导的功能，例如神经突回缩。与显性负突变体Cdc42Hs（T17N）共注射可抑制C3反应，而Cdc42Hs反应可与RhoA共注射竞争。我们还证明了神经递质乙酰胆碱（ACh）可以通过毒蕈碱型ACh受体激活，在神经母细胞瘤生长锥上诱导丝状伪足和片状脂质体，但只有在浓度梯度下才能使用。 ACh诱导的丝状伪足和片状脂质体的形成分别通过预先注射显性负突变Cdc42Hs（T17N）和Rac1（T17N）来抑制。 RhoA介导的溶血磷脂酸（LPA）诱导的神经突退缩受ACh抑制，而C3外切酶介导的神经突生长受Cdc42Hs（T17N）或Rac1（T17N）注射抑制。这些结果共同表明，由Cdc42Hs和/或Rac1和RhoA介导的ACh和LPA诱导的形态学途径之间存在竞争，从而导致神经突发展或崩溃。

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