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一种 alpha-catulin 同源物通过定位肌营养不良复合物和 BK 通道控制秀丽隐杆线虫的神经肌肉功能。

An alpha-catulin homologue controls neuromuscular function through localization of the dystrophin complex and BK channels in Caenorhabditis elegans.

机构信息

Department of Cell Biology and Anatomy, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, United States of America.

出版信息

PLoS Genet. 2010 Aug 26;6(8):e1001077. doi: 10.1371/journal.pgen.1001077.

DOI:10.1371/journal.pgen.1001077
PMID:20865173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2928805/
Abstract

The large conductance, voltage- and calcium-dependent potassium (BK) channel serves as a major negative feedback regulator of calcium-mediated physiological processes and has been implicated in muscle dysfunction and neurological disorders. In addition to membrane depolarization, activation of the BK channel requires a rise in cytosolic calcium. Localization of the BK channel near calcium channels is therefore critical for its function. In a genetic screen designed to isolate novel regulators of the Caenorhabditis elegans BK channel, SLO-1, we identified ctn-1, which encodes an α-catulin homologue with homology to the cytoskeletal proteins α-catenin and vinculin. ctn-1 Mutants resemble slo-1 loss-of-function mutants, as well as mutants with a compromised dystrophin complex. We determined that CTN-1 uses two distinct mechanisms to localize SLO-1 in muscles and neurons. In muscles, CTN-1 utilizes the dystrophin complex to localize SLO-1 channels near L-type calcium channels. In neurons, CTN-1 is involved in localizing SLO-1 to a specific domain independent of the dystrophin complex. Our results demonstrate that CTN-1 ensures the localization of SLO-1 within calcium nanodomains, thereby playing a crucial role in muscles and neurons.

摘要

大电导、电压和钙依赖性钾 (BK) 通道是钙介导的生理过程的主要负反馈调节剂，与肌肉功能障碍和神经紊乱有关。除了膜去极化外，BK 通道的激活还需要细胞浆钙离子的增加。因此，BK 通道在钙通道附近的定位对于其功能至关重要。在一个旨在分离新型调控线虫 BK 通道 SLO-1 的基因筛选中，我们发现了 ctn-1，它编码一种与细胞骨架蛋白 α-连环蛋白和 vinculin 同源的 α-微管蛋白同源物。ctn-1 突变体类似于 slo-1 功能丧失突变体，以及与营养不良复合物受损的突变体。我们确定 CTN-1 利用两种不同的机制将 SLO-1 定位于肌肉和神经元中。在肌肉中，CTN-1 利用营养不良复合物将 SLO-1 通道定位于 L 型钙通道附近。在神经元中，CTN-1 参与将 SLO-1 定位于一个独立于营养不良复合物的特定区域。我们的结果表明，CTN-1 确保了 SLO-1 在钙纳米域内的定位，从而在肌肉和神经元中发挥了关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/4b2dd7b20554/pgen.1001077.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/c4f29376516e/pgen.1001077.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/3168062765c7/pgen.1001077.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/bd64718b8b5a/pgen.1001077.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/65b38bc712ee/pgen.1001077.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/18d5b81110fb/pgen.1001077.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/4b2dd7b20554/pgen.1001077.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/c4f29376516e/pgen.1001077.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/3168062765c7/pgen.1001077.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/bd64718b8b5a/pgen.1001077.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/65b38bc712ee/pgen.1001077.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/18d5b81110fb/pgen.1001077.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d664/2928805/4b2dd7b20554/pgen.1001077.g006.jpg

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