PSD-95 mediates membrane clustering of the human plasma membrane Ca2+ pump isoform 4b.
PSD-95 mediates membrane clustering of the human plasma membrane Ca2+ pump isoform 4b.
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DOI：
10.1016/j.bbamcr.2008.11.007
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发表时间：
2009-06
期刊：
影响因子：
--
通讯作者：
Enyedi A
中科院分区：
文献类型：
--
作者：
Padányi R;Pászty K;Strehler EE;Enyedi A
除了控制整体钙变化外，特定的质膜钙ATP酶（PMCA）亚型还参与局部钙信号的调节。虽然局部钙信号传导需要将信号分子限制在微区中，但对质膜内PMCA分子的具体组织知之甚少。在这里，我们表明，与突触后密度-95（PSD-95）支架蛋白的共表达增加了PMCA 4 b的质膜表达，并将泵重新分配成簇。PMCA 4 b的聚集完全依赖于其PDZ结合序列的存在。使用荧光恢复后的光漂白（FRAP）技术，我们表明，侧膜迁移率的聚PMCA 4 b是显着低于非聚簇分子。细胞松弛素D破坏肌动蛋白为基础的细胞骨架，导致集群大小增加。我们的研究结果表明，PSD-95促进高密度PMCA 4 b微区的形成在质膜和膜细胞骨架在这一过程中起着重要的调节作用。
Besides the control of global calcium changes, specific plasma membrane calcium ATPase (PMCA) isoforms are involved in the regulation of local calcium signals. Although local calcium signaling requires the confinement of signaling molecules into microdomains, little is known about the specific organization of PMCA molecules within the plasma membrane. Here we show that co-expression with the postsynaptic–density-95 (PSD-95) scaffolding protein increased the plasma membrane expression of PMCA4b and redistributed the pump into clusters. The clustering of PMCA4b was fully dependent on the presence of its PDZ-binding sequence. Using the fluorescence recovery after photobleaching (FRAP) technique, we show that the lateral membrane mobility of the clustered PMCA4b is significantly lower than that of the non-clustered molecules. Disruption of the actin-based cytoskeleton by cytochalasin D resulted in increased cluster size. Our results suggest that PSD-95 promotes the formation of high-density PMCA4b microdomains in the plasma membrane and that the membrane cytoskeleton plays an important role in the regulation of this process.
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