Maryon E B, Saari B, Anderson P
Department of Genetics, University of Wisconsin, Madison, Wisconsin 53706, USA.
J Cell Sci. 1998 Oct;111 ( Pt 19):2885-95. doi: 10.1242/jcs.111.19.2885.
Ryanodine receptor channels regulate contraction of striated muscle by gating the release of calcium ions from the sarcoplasmic reticulum. Ryanodine receptors are expressed in excitable and non-excitable cells of numerous species, including the nematode C. elegans. Unlike vertebrates, which have at least three ryanodine receptor genes, C. elegans has a single gene encoded by the unc-68 locus. We show that unc-68 is expressed in most muscle cells, and that the phenotypic defects exhibited by unc-68 null mutants result from the loss of unc-68 function in pharyngeal and body-wall muscle cells. The loss of unc-68 function in the isthmus and terminal bulb muscles of the pharynx causes a reduction in growth rate and brood size. unc-68 null mutants exhibit defective pharyngeal pumping (feeding) and have abnormal vacuoles in the terminal bulb of the pharynx. unc-68 is required in body-wall muscle cells for normal motility. We show that UNC-68 is localized in body-wall muscle cells to flattened vesicular sacs positioned between the apical plasma membrane and the myofilament lattice. In unc-68 mutants, the vesicles are enlarged and densely stained. The flattened vesicles in body-wall muscle cells thus represent the C. elegans sarcoplasmic reticulum. Morphological and behavioral phenotypes of unc-68 mutants suggest that intracellular calcium release is not essential for excitation-contraction coupling in C. elegans.
兰尼碱受体通道通过控制肌浆网中钙离子的释放来调节横纹肌的收缩。兰尼碱受体在包括线虫秀丽隐杆线虫在内的众多物种的可兴奋和不可兴奋细胞中均有表达。与至少有三个兰尼碱受体基因的脊椎动物不同,秀丽隐杆线虫有一个由unc-68位点编码的单一基因。我们发现unc-68在大多数肌肉细胞中表达,并且unc-68基因敲除突变体所表现出的表型缺陷是由于咽和体壁肌肉细胞中unc-68功能的丧失所致。咽峡部和咽终球肌肉中unc-68功能的丧失会导致生长速率和产卵量降低。unc-68基因敲除突变体表现出有缺陷的咽泵吸(进食),并且在咽终球中有异常液泡。体壁肌肉细胞中正常运动需要unc-68。我们发现UNC-68定位于体壁肌肉细胞中位于顶端质膜和肌丝晶格之间的扁平囊泡。在unc-68突变体中,囊泡增大且染色浓密。因此,体壁肌肉细胞中的扁平囊泡代表了秀丽隐杆线虫的肌浆网。unc-68突变体的形态和行为表型表明,细胞内钙释放对于秀丽隐杆线虫的兴奋-收缩偶联并非必不可少。