Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.
Mol Cell Neurosci. 2012 Apr;49(4):475-86. doi: 10.1016/j.mcn.2011.12.007. Epub 2011 Dec 23.
Efficient synaptic transmission at the neuromuscular junction (NMJ) requires the topological maturation of the postsynaptic apparatus from an oval acetylcholine receptor (AChR)-rich plaque into a complex pretzel-shaped array of branches. However, compared to NMJ formation very little is known about the mechanisms that regulate NMJ maturation. Recently the process of in vivo transformation from plaque into pretzel has been reproduced in vitro by culturing myotubes aneurally on laminin-coated substrate. It was proposed that the formation of complex AChR clusters is regulated by a MuSK-dependent muscle intrinsic program. To elucidate the structure-function role of MuSK in the aneural maturation of AChR pretzels, we used muscle cell lines expressing MuSK mutant and chimeric proteins. Here we report, that besides its role during agrin-induced AChR clustering, MuSK kinase activity is also necessary for substrate-dependent cluster formation. Constitutive-active MuSK induces larger AChR clusters, a faster cluster maturation on laminin and increases the anchorage of AChRs to the cytoskeleton compared to MuSK wild-type. In addition, we find that the juxtamembrane region of MuSK, which has previously been shown to regulate agrin-induced AChR clustering, is unable to induce complex AChR clusters on laminin substrate. Most interestingly, MuSK kinase activity is not sufficient for laminin-dependent AChR cluster formation since the MuSK ectodomain is also required suggesting a so far undiscovered instructive role for the extracellular domain of MuSK.
在神经肌肉接头(NMJ)处的有效突触传递需要在后突触装置从椭圆形乙酰胆碱受体(AChR)丰富斑块到复杂的椒盐卷饼状分支的拓扑成熟。然而,与 NMJ 形成相比,调节 NMJ 成熟的机制知之甚少。最近,通过在层粘连蛋白涂层基底上无神经培养肌管,在体外再现了从斑块到椒盐卷饼的体内转化过程。有人提出,复杂 AChR 簇的形成受 MuSK 依赖性肌肉内在程序调节。为了阐明 MuSK 在 AChR 椒盐卷饼无神经成熟中的结构 - 功能作用,我们使用表达 MuSK 突变体和嵌合蛋白的肌细胞系。在这里,我们报告除了在神经递质乙酰胆碱受体(AChR)聚集过程中的作用外,MuSK 激酶活性对于基底依赖性簇形成也是必需的。组成型激活的 MuSK 诱导更大的 AChR 簇,在层粘连蛋白上更快的簇成熟,并与 MuSK 野生型相比增加 AChR 与细胞骨架的锚定。此外,我们发现 MuSK 的跨膜区先前被证明可以调节神经递质乙酰胆碱受体(AChR)诱导的聚集,不能在层粘连蛋白基质上诱导复杂的 AChR 簇。最有趣的是,MuSK 激酶活性不足以进行层粘连蛋白依赖性 AChR 簇形成,因为 MuSK 细胞外结构域也是必需的,这表明 MuSK 细胞外结构域具有迄今为止尚未发现的指导作用。