Loss of G2 subunit of vacuolar-type proton transporting ATPase leads to G1 subunit upregulation in the brain.
Loss of G2 subunit of vacuolar-type proton transporting ATPase leads to G1 subunit upregulation in the brain.
复制标题
液泡质子转运ATPase的G2亚基的损失导致大脑中的G1亚基上调。
DOI：
10.1038/srep14027
复制
发表时间：
2015-09-10
影响因子：
4.6
通讯作者：
Wada Y
中科院分区：
文献类型：
--
作者：
Kawamura N;Sun-Wada GH;Wada Y
液泡型atp酶（v - atp酶）是一种主要的质子泵，在各种组织中具有多种功能。在神经细胞中，v - atp酶是神经递质积聚到分泌囊泡并随后在突触释放所必需的。神经元表达v - atp酶G亚基的特定亚型（G2），构成酶复合物的催化部分。利用基因靶向技术，我们培育了一只缺乏功能G2 （G2 null）的小鼠，该小鼠在结构和行为上没有明显的紊乱。在g2缺失的小鼠大脑中，G1亚基异构体在神经元和非神经元组织中普遍表达，比野生型动物积累更丰富。这种G1上调不伴有mRNA的增加。这些结果表明，神经元特异性G2异构体的功能丧失可以通过G1异构体水平的增加来补偿，而G1 mRNA没有明显上调。
Vacuolar-type ATPase (V-ATPase) is a primary proton pump with versatile functions in various tissues. In nerve cells, V-ATPase is required for accumulation of neurotransmitters into secretory vesicles and subsequent release at the synapse. Neurons express a specific isoform (G2) of the G subunit of V-ATPase constituting the catalytic sector of the enzyme complex. Using gene targeting, we generated a mouse lacking functional G2 (G2 null), which showed no apparent disorders in architecture and behavior. In the G2-null mouse brain, a G1 subunit isoform, which is ubiquitously expressed in neuronal and non-neuronal tissues, accumulated more abundantly than in wild-type animals. This G1 upregulation was not accompanied by an increase in mRNA. These results indicate that loss of function of neuron-specific G2 isoform was compensated by an increase in levels of the G1 isoform without apparent upregulation of the G1 mRNA.