VIB Center for Brain and Disease Research, Leuven, Belgium.
Institute of Molecular Life Sciences, University of Zurich, 8057 Zurich, Switzerland.
Science. 2019 May 3;364(6439). doi: 10.1126/science.aau9952.
Central nervous system (CNS) circuit development requires subcellular control of synapse formation and patterning of synapse abundance. We identified the membrane-anchored phosphatase of regenerating liver (Prl-1) as an axon-intrinsic factor that promotes synapse formation in a spatially restricted fashion. The loss of Prl-1 in mechanosensory neurons reduced the number of CNS presynapses localized on a single axon collateral and organized as a terminal arbor. Flies lacking all Prl-1 protein had locomotor defects. The overexpression of Prl-1 induced ectopic synapses. In mechanosensory neurons, Prl-1 modulates the insulin receptor (InR) signaling pathway within a single contralateral axon compartment, thereby affecting the number of synapses. The axon branch-specific localization and function of Prl-1 depend on untranslated regions of the messenger RNA (mRNA). Therefore, compartmentalized restriction of Prl-1 serves as a specificity factor for the subcellular control of axonal synaptogenesis.
中枢神经系统（CNS）的回路发育需要亚细胞控制突触形成和突触数量的模式化。我们发现再生肝脏的膜锚定磷酸酶（Prl-1）是一种轴突内在的因子，以空间限制的方式促进突触形成。机械感觉神经元中 Prl-1 的缺失减少了定位于单个轴突侧支上的 CNS 前突触的数量，并作为末端树突组织起来。缺乏所有 Prl-1 蛋白的果蝇表现出运动缺陷。Prl-1 的过表达诱导了异位突触。在机械感觉神经元中，Prl-1 在单个对侧轴突隔室内调节胰岛素受体（InR）信号通路，从而影响突触的数量。Prl-1 的轴突分支特异性定位和功能依赖于 mRNA 的非翻译区。因此，Prl-1 的隔室限制作为轴突突触发生的亚细胞控制的特异性因素。
