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首页> 外文期刊>Journal of cell biology >unc-68 encodes a ryanodine receptor involved in regulating C. elegans body-wall muscle contraction.
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unc-68 encodes a ryanodine receptor involved in regulating C. elegans body-wall muscle contraction.

机译:unc-68编码参与调节秀丽隐杆线虫体壁肌肉收缩的瑞丹碱受体。

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Striated muscle contraction is elicited by the release of stored calcium ions through ryanodine receptor channels in the sarcoplasmic reticulum. ryr-1 is a C. elegans ryanodine receptor homologue that is expressed in body-wall muscle cells used for locomotion. Using genetic methods, we show that ryr-1 is the previously identified locus unc-68. First, transposon-induced deletions within ryr-1 are alleles of unc-68. Second, transformation of unc-68 mutants with ryr-1 genomic DNA results in rescue of the Unc phenotype. unc-68 mutants move poorly, exhibiting an incomplete flaccid paralysis, yet have normal muscle ultrastructure. The mutants are insensitive to the paralytic effects of ryanodine, and lack detectable ryanodine-binding activity. The Unc-68 phenotype suggests that ryanodine receptors are not essential for excitation-contraction coupling in nematodes, but act to amplify a (calcium) signal that is sufficient for contraction.
机译:横纹肌的收缩是由肌浆网中的ryanodine受体通道释放储存的钙离子引起的。 ryr-1是秀丽隐杆线虫ryanodine受体的同源物,在用于运动的体壁肌肉细胞中表达。使用遗传方法,我们表明ryr-1是先前确定的unc-68基因座。首先,转座子诱导的ryr-1缺失是unc-68的等位基因。其次,用ryr-1基因组DNA转化unc-68突变体可拯救Unc表型。 unc-68突变体移动不良,表现出不完全的松弛性麻痹,但具有正常的肌肉超微结构。突变体对雷诺定的麻痹作用不敏感,并且缺乏可检测的雷诺定结合活性。 Unc-68表型表明,对于线虫中的激发-收缩偶联而言,雷诺丁受体并不是必不可少的,但其作用是放大足以收缩的(钙)信号。

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