Diacylglycerol kinase β (DGKβ) is an enzyme converting DG to phosphatidic acid (PA) and is specifically expressed in neurons, especially those in the cerebral cortex, hippocampus and striatum. We previously reported that DGKβ induces neurite outgrowth and spinogenesis, contributing to higher brain function including emotion and memory, and plasma membrane localization of DGKβ via the C1 domain and a cluster of basic amino acids at the C-terminus is necessary for its function. To clarify the mechanisms involved in neuronal development by DGKβ, we investigated whether DGKβ activity induces neurite outgrowth using human neuroblastoma SH-SY5Y cells. DGKβ induced neurite outgrowth by activation of mammalian target of rapamycin complex 1 (mTORC1) through a kinase-dependent pathway. In addition, in primary cultured cortical and hippocampal neurons, inhibition of mTORC1 abolished DGKβ induced-neurite outgrowth, branching and spinogenesis. These results indicated that DGKβ induces neurite outgrowth and spinogenesis by activating mTORC1 in a kinase-dependent pathway.

中文翻译：

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mTORC1参与DGKβ诱导的神经突生长和自发发生。

二酰基甘油激酶β（DGKβ）是将DG转化为磷脂酸（PA）的酶，在神经元中特别是在大脑皮层，海马和纹状体中表达。我们之前曾报道过DGKβ诱导神经突向外生长和自旋发生，从而促进了包括情感和记忆在内的更高的大脑功能，并且通过C1域和DG端在C端的碱性氨基酸簇对DGKβ进行了质膜定位是其功能所必需的。为了阐明DGKβ参与神经元发育的机制，我们调查了DGKβ活性是否使用人类神经母细胞瘤SH-SY5Y细胞诱导神经突生长。DGKβ通过激酶依赖性途径激活哺乳动物雷帕霉素复合物1（mTORC1）靶标诱导神经突生长。此外，在原代培养的皮质和海马神经元中，抑制mTORC1消除了​​DGKβ诱导的神经突向外生长，分支和纺丝发生。这些结果表明，DGKβ通过激活激酶依赖性途径中的mTORC1来诱导神经突生长和自旋发生。