Dscam expression levels determine presynaptic arbor sizes in Drosophila sensory neurons.
Dscam expression levels determine presynaptic arbor sizes in Drosophila sensory neurons.
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DOI：
10.1016/j.neuron.2013.05.020
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发表时间：
2013-06-05
期刊：
影响因子：
16.2
通讯作者：
Ye B
中科院分区：
文献类型：
--
作者：
Kim JH;Wang X;Coolon R;Ye B
唐氏综合征细胞粘附分子（Dscam）的表达在几种神经系统疾病患者的大脑中增加。尽管Dscam在神经元发育的许多方面都有重要作用，但对其表达的调控机制或Dscam表达失调的功能后果知之甚少。在这里，我们表明，Dscam表达水平作为一个指导性的代码突触前乔木的大小控制。Dscam的表达受两条会聚通路的调控，即双亮氨酸拉链激酶（DLK）和脆性X智力低下蛋白（FMRP）。Dscam翻译的这种调节缺陷导致果蝇体觉神经元突触前乔木生长旺盛。我们的研究结果证明了Dscam功能的一个以前未知的方面，并提供了Dscam失调如何有助于神经系统疾病的发病机制的见解。
Expression of the Down syndrome cell-adhesion molecule (Dscam) is increased in the brains of patients with several neurological disorders. Although Dscam is critically involved in many aspects of neuronal development, little is known about either the mechanism that regulates its expression or the functional consequences of dysregulated Dscam expression. Here, we show that Dscam expression levels serve as an instructive code for the size control of presynaptic arbor. Two convergent pathways, involving dual leucine zipper kinase (DLK) and fragile X mental retardation protein (FMRP), control Dscam expression through protein translation. Defects in this regulation of Dscam translation lead to exuberant presynaptic arbor growth in Drosophila somatosensory neurons. Our findings demonstrate a previously unknown aspect of Dscam function and provide insights into how dysregulated Dscam may contribute to the pathogenesis of neurological disorders.
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