EAT-4, a homolog of a mammalian sodium-dependent inorganic phosphate cotransporter, is necessary for glutamatergic neurotransmission in Caenorhabditis elegans
EAT-4, a homolog of a mammalian sodium-dependent inorganic phosphate cotransporter, is necessary for glutamatergic neurotransmission in Caenorhabditis elegans
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DOI：
10.1523/jneurosci.19-01-00159.1999
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发表时间：
1999-01-01
影响因子：
5.3
通讯作者：
Avery, L
中科院分区：
文献类型：
--
作者：
Lee, RYN;Sawin, ER;Avery, L
秀丽线虫Eat-4基因影响多种谷氨酸能神经传递途径。我们发现EAT-4编码的蛋白质序列类似于哺乳动物大脑特异的钠依赖的无机磷酸共转运蛋白I(BNPI)。像大鼠中枢神经系统中的BNPI一样，EAT-4主要在特定的神经元亚群中表达，包括几个被认为是谷氨酸能的神经元。EAT-4功能缺失突变会导致谷氨酸能化学传递缺陷，但似乎对神经元的其他功能影响不大。我们的数据表明，磷酸离子通过转运蛋白如EAT-4和BNPI进入谷氨酸能神经元是谷氨酸能神经传递所特需的。
The Caenorhabditis elegans gene eat-4 affects multiple glutamatergic neurotransmission pathways. We find that eat-4 encodes a protein similar in sequence to a mammalian brain-specific sodium-dependent inorganic phosphate cotransporter I (BNPI). Like BNPI in the rat CNS, eat-4 is expressed predominantly in a specific subset of neurons, including several proposed to be glutamatergic. Loss-of-function mutations in eat-4 cause defective glutamatergic chemical transmission but appear to have little effect on other functions of neurons. Our data suggest that phosphate ions imported into glutamatergic neurons through transporters such as EAT-4 and BNPI are required specifically for glutamatergic neurotransmission.