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首页> 外文期刊>Neuron >Ubiquitin and AP180 Regulate the Abundance of GLR-1 Glutamate Receptors at Postsynaptic Elements in C. elegans.
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Ubiquitin and AP180 Regulate the Abundance of GLR-1 Glutamate Receptors at Postsynaptic Elements in C. elegans.

机译：泛素和AP180调节线虫中突触后元件上GLR-1谷氨酸受体的丰度。

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Regulated delivery and removal of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors (GluRs) from postsynaptic elements has been proposed as a mechanism for regulating synaptic strength. Here we test the role of ubiquitin in regulating synapses that contain a C. elegans GluR, GLR-1. GLR-1 receptors were ubiquitinated in vivo. Mutations that decreased ubiquitination of GLR-1 increased the abundance of GLR-1 at synapses and altered locomotion behavior in a manner that is consistent with increased synaptic strength. By contrast, overexpression of ubiquitin decreased the abundance of GLR-1 at synapses and decreased the density of GLR-1-containing synapses, and these effects were prevented by mutations in the unc-11 gene, which encodes a clathrin adaptin protein (AP180). These results suggest that ubiquitination of GLR-1 receptors regulates synaptic strength and the formation or stability of GLR-1-containing synapses.
机译：已提出从突触后元件中调节递送和去除α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）谷氨酸受体（GluRs）作为调节突触强度的机制。在这里，我们测试了泛素在调节包含秀丽隐杆线虫GluR，GLR-1的突触中的作用。 GLR-1受体在体内被泛素化。减少GLR-1泛素化的突变会增加突触中GLR-1的丰度，并以与增加突触强度一致的方式改变运动行为。相比之下，泛素的过表达降低了突触中GLR-1的丰度，并降低了含有GLR-1的突触的密度，而编码clathrrin Adaptin蛋白（AP180）的unc-11基因突变则阻止了这些作用。 。这些结果表明，GLR-1受体的泛素化调节突触强度和含有GLR-1的突触的形成或稳定性。

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