Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109, USA.
Nat Commun. 2013;4:1952. doi: 10.1038/ncomms2952.
Excitation-contraction coupling, the process that regulates contractions by skeletal muscles, transduces changes in membrane voltage by activating release of Ca(2+) from internal stores to initiate muscle contraction. Defects in excitation-contraction coupling are associated with muscle diseases. Here we identify Stac3 as a novel component of the excitation-contraction coupling machinery. Using a zebrafish genetic screen, we generate a locomotor mutation that is mapped to stac3. We provide electrophysiological, Ca(2+) imaging, immunocytochemical and biochemical evidence that Stac3 participates in excitation-contraction coupling in muscles. Furthermore, we reveal that a mutation in human STAC3 is the genetic basis of the debilitating Native American myopathy (NAM). Analysis of NAM stac3 in zebrafish shows that the NAM mutation decreases excitation-contraction coupling. These findings enhance our understanding of both excitation-contraction coupling and the pathology of myopathies.
兴奋-收缩偶联是调节骨骼肌收缩的过程,通过激活内质网释放 Ca(2+)来引发肌肉收缩,从而将膜电压的变化转化为信号。兴奋-收缩偶联的缺陷与肌肉疾病有关。在这里,我们鉴定出 Stac3 是兴奋-收缩偶联机制的一个新组件。我们利用斑马鱼基因筛选,产生了一个运动突变,该突变被映射到 stac3。我们提供了电生理学、Ca(2+)成像、免疫细胞化学和生化证据,表明 Stac3 参与肌肉的兴奋-收缩偶联。此外,我们揭示了人类 STAC3 的突变是导致使人衰弱的美洲原住民肌病(NAM)的遗传基础。对斑马鱼中 NAM stac3 的分析表明,NAM 突变降低了兴奋-收缩偶联。这些发现增强了我们对兴奋-收缩偶联和肌病病理的理解。