一种与突触小泡相关的钙离子通道促进内吞作用，并将外排作用与内吞作用相偶联。
A synaptic vesicle-associated Ca2+ channel promotes endocytosis and couples exocytosis to endocytosis.
作者信息
Yao Chi-Kuang, Lin Yong Qi, Ly Cindy V, Ohyama Tomoko, Haueter Claire M, Moiseenkova-Bell Vera Y, Wensel Theodore G, Bellen Hugo J
机构信息
Howard Hughes Medical Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
出版信息
Cell. 2009 Sep 4;138(5):947-60. doi: 10.1016/j.cell.2009.06.033.
Synaptic vesicle (SV) exo- and endocytosis are tightly coupled to sustain neurotransmission in presynaptic terminals, and both are regulated by Ca(2+). Ca(2+) influx triggered by voltage-gated Ca(2+) channels is necessary for SV fusion. However, extracellular Ca(2+) has also been shown to be required for endocytosis. The intracellular Ca(2+) levels (<1 microM) that trigger endocytosis are typically much lower than those (>10 microM) needed to induce exocytosis, and endocytosis is inhibited when the Ca(2+) level exceeds 1 microM. Here, we identify and characterize a transmembrane protein associated with SVs that, upon SV fusion, localizes at periactive zones. Loss of Flower results in impaired intracellular resting Ca(2+) levels and impaired endocytosis. Flower multimerizes and is able to form a channel to control Ca(2+) influx. We propose that Flower functions as a Ca(2+) channel to regulate synaptic endocytosis and hence couples exo- with endocytosis.
突触小泡（SV）的胞吐和胞吞作用紧密偶联，以维持突触前终末的神经传递，二者均受Ca(2+)调控。电压门控Ca(2+)通道触发的Ca(2+)内流是SV融合所必需的。然而，细胞外Ca(2+)也被证明是胞吞作用所必需的。触发胞吞作用的细胞内Ca(2+)水平（<1 microM）通常远低于诱导胞吐作用所需的水平（>10 microM），当Ca(2+)水平超过1 microM时，胞吞作用受到抑制。在这里，我们鉴定并表征了一种与SV相关的跨膜蛋白，在SV融合时，它定位于活性区周围。Flower缺失导致细胞内静息Ca(2+)水平受损和胞吞作用受损。Flower多聚化并能够形成一个通道来控制Ca(2+)内流。我们提出，Flower作为一个Ca(2+)通道来调节突触胞吞作用，从而将胞吐作用与胞吞作用偶联起来。
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