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CDK-5 regulates the abundance of GLR-1 glutamate receptors in the ventral cord of Caenorhabditis elegans

机译:CDK-5调节秀丽隐杆线虫腹线中GLR-1谷氨酸受体的丰度

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摘要

The proline-directed kinase Cdk5 plays a role in several aspects of neuronal development. Here, we show that CDK-5 activity regulates the abundance of the glutamate receptor GLR-1 in the ventral cord of Caenorhabditis elegans and that it produces corresponding changes in GLR-1-dependent behaviors. Loss of CDK-5 activity results in decreased abundance of GLR-1 in the ventral cord, accompanied by accumulation of GLR-1 in neuronal cell bodies. Genetic analysis of cdk-5 and the clathrin adaptin unc-11 AP180 suggests that CDK-5 functions prior to endocytosis at the synapse. The scaffolding protein LIN-10/Mint-1 also regulates GLR-1 abundance in the nerve cord. CDK-5 phosphorylates LIN-10/Mint-1 in vitro and bidirectionally regulates the abundance of LIN-10/Mint-1 in the ventral cord. We propose that CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.
机译:脯氨酸指导的激酶Cdk5在神经元发育的多个方面发挥作用。在这里,我们显示CDK-5活性调节秀丽隐杆线虫腹侧谷氨酸受体GLR-1的丰度,并且它会在GLR-1依赖性行为中产生相应的变化。 CDK-5活性的丧失会导致腹侧GLR-1的丰度降低,并伴有神经元细胞体中GLR-1的积累。 cdk-5和网格蛋白adaptin unc-11 AP180的遗传分析表明,CDK-5在突触内吞之前起作用。脚手架蛋白LIN-10 / Mint-1还调节神经索中的GLR-1丰度。 CDK-5在体外使LIN-10 / Mint-1磷酸化,并双向调节腹帘线中LIN-10 / Mint-1的丰度。我们建议CDK-5促进GLR-1的顺行运输,而LIN-10的磷酸化可能在此过程中起作用。

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