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秀丽隐杆线虫粗肌丝组装需要肌球蛋白ATP结合位点和肌动蛋白结合位点的功能。

Functions of the myosin ATP and actin binding sites are required for C. elegans thick filament assembly.

作者信息

Bejsovec A, Anderson P

机构信息

Department of Genetics, University of Wisconsin, Madison 53706.

出版信息

Cell. 1990 Jan 12;60(1):133-40. doi: 10.1016/0092-8674(90)90723-r.

Abstract

We have determined the positions and sequences of 31 dominant mutations affecting a C. elegans muscle myosin heavy chain gene. These mutations alter thick filament structure in heterozygotes by interfering with the ability of wild-type myosin to assemble into stable thick filaments. These assembly-disruptive mutations are missense alleles affecting the globular head of myosin. The most strongly dominant alleles alter highly conserved residues of the myosin ATP binding site, indicating that functions of the myosin ATPase are important for thick filament assembly. Other alleles alter the site at which myosin binds actin.

摘要

我们已经确定了影响秀丽隐杆线虫肌肉肌球蛋白重链基因的31个显性突变的位置和序列。这些突变通过干扰野生型肌球蛋白组装成稳定粗肌丝的能力,改变了杂合子中的粗肌丝结构。这些破坏组装的突变是影响肌球蛋白球状头部的错义等位基因。最具显性的等位基因改变了肌球蛋白ATP结合位点的高度保守残基,表明肌球蛋白ATP酶的功能对粗肌丝组装很重要。其他等位基因改变了肌球蛋白与肌动蛋白结合的位点。

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