Distribution of the SynDIG4/Proline-Rich Transmembrane Protein 1 in Rat Brain
Distribution of the SynDIG4/Proline-Rich Transmembrane Protein 1 in Rat Brain
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DOI：
10.1002/cne.23945
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发表时间：
2016-08-01
影响因子：
2.5
通讯作者：
Diaz, Elva
中科院分区：
文献类型：
--
作者：
Kirk, Lyndsey M.;Ti, Shu W.;Diaz, Elva
突触中AMPA受体（AMPAR）含量的调节被认为是记忆和学习的基本分子机制。突触时的AMPAR含量是高度塑性的，并且受众多AMPAR辅助跨膜蛋白（例如防水布，玉米片和Ckamps）的调节。 Syndig（突触分化诱导的基因）定义了四个基因（Syndig1-4）的家族，该家族在大脑中以不同的重叠模式表达。 Syndig1先前被鉴定为一种调节突触强度的新型跨膜AMPAR相关蛋白。相关蛋白syndig4 [也称为PRRT1（富含脯氨酸的跨膜蛋白1）]最近已被鉴定为AMPAR复合物的组成部分。在这项研究中，我们表明syndig1和syndig4在中枢神经系统中具有不同但重叠的表达模式，而syndig4在海马，尤其是在CA1中特别突出。与Syndig1和其他传统的AMPAR辅助亚基相反，Syndig4以突触后密度偏移，并与原发性解离神经元培养中的外鼻glua1点共定位。这些结果表明，尽管Syndig4共享与Syndig1的序列相似性，但它可能通过独特的机制作为辅助抗肌外glua1的辅助因子的作用。 （c）2015 Wiley Wercenials，Inc。
The modulation of AMPA receptor (AMPAR) content at synapses is thought to be an underlying molecular mechanism of memory and learning. AMPAR content at synapses is highly plastic and is regulated by numerous AMPAR accessory transmembrane proteins such as TARPs, cornichons, and CKAMPs. SynDIG (synapse differentiation-induced gene) defines a family of four genes (SynDIG1-4) expressed in distinct and overlapping patterns in the brain. SynDIG1 was previously identified as a novel transmembrane AMPAR-associated protein that regulates synaptic strength. The related protein SynDIG4 [also known as Prrt1 (proline-rich transmembrane protein 1)] has recently been identified as a component of AMPAR complexes. In this study, we show that SynDIG1 and SynDIG4 have distinct yet overlapping patterns of expression in the central nervous system, with SynDIG4 having especially prominent expression in the hippocampus and particularly within CA1. In contrast to SynDIG1 and other traditional AMPAR auxiliary subunits, SynDIG4 is de-enriched at the postsynaptic density and colocalizes with extrasynaptic GluA1 puncta in primary dissociated neuron culture. These results indicate that, although SynDIG4 shares sequence similarity with SynDIG1, it might act through a unique mechanism as an auxiliary factor for extrasynaptic GluA1-containing AMPARs. (C) 2015 Wiley Periodicals, Inc.