The HSPGs syndecan and dallylike bind the receptor phosphatase LAR and exert distinct effects on synaptic development
The HSPGs syndecan and dallylike bind the receptor phosphatase LAR and exert distinct effects on synaptic development
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DOI：
10.1016/j.neuron.2006.01.026
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发表时间：
2006-02-16
期刊：
影响因子：
16.2
通讯作者：
Van Vactor, D
中科院分区：
文献类型：
--
作者：
Johnson, KG;Tenney, AP;Van Vactor, D
突触连接的形成和可塑性依赖于突触前和突触后细胞之间的调节相互作用。我们表明，果蝇硫酸乙酰肝素蛋白聚糖（HSPGs）Syndecan（Sdc）和Dallylike（Dlp）是控制突触生物学不同方面所必需的突触蛋白。Sdc促进突触前末梢的生长，而Dip调节活动区的形式和功能。Sdc和Dlp都以高亲和力结合蛋白酪氨酸磷酸酶LAR，这是一种控制NMJ生长和活性区形态发生的保守受体。这些数据和双突变体试验表明，LAR的行动的两个HSPGs的要求导致一个模型，其中突触前LAR是在复杂的控制下，与Sdc促进和Dip抑制LAR，以控制突触形态发生和功能。
The formation and plasticity of synaptic connections rely on regulatory interactions between pre- and postsynaptic cells. We show that the Drosophila heparan sulfate proteoglycans (HSPGs) Syndecan (Sdc) and Dallylike (Dlp) are synaptic proteins necessary to control distinct aspects of synaptic biology. Sdc promotes the growth of presynaptic terminals, whereas Dip regulates active zone form and function. Both Sdc and Dlp bind at high affinity to the protein tyrosine phosphatase LAR, a conserved receptor that controls both NMJ growth and active zone morphogenesis. These data and double mutant assays showing a requirement of LAR for actions of both HSPGs lead to a model in which presynaptic LAR is under complex control, with Sdc promoting and Dip inhibiting LAR in order to control synapse morphogenesis and function.