THE MINOR MYOSIN HEAVY-CHAIN, MHCA, OF CAENORHABDITIS-ELEGANS IS NECESSARY FOR THE INITIATION OF THICK FILAMENT ASSEMBLY
THE MINOR MYOSIN HEAVY-CHAIN, MHCA, OF CAENORHABDITIS-ELEGANS IS NECESSARY FOR THE INITIATION OF THICK FILAMENT ASSEMBLY
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DOI：
10.1002/j.1460-2075.1989.tb08507.x
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发表时间：
1989-11-01
期刊：
影响因子：
11.4
通讯作者：
WATERSTON, RH
中科院分区：
文献类型：
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作者：
WATERSTON, RH
秀丽隐杆线虫体壁肌有两种不同的肌球蛋白重链异构体mhcA和mhcB。先前的研究表明，消除主要亚型mhcB的突变会导致瘫痪的存活动物。在本文中，我们证明了次要异构体mhcA对生存能力至关重要。我们利用已知的mhcA编码基因的物理图谱位置，获得了两个隐性致死突变，几乎消除了mhcA的积累。这些突变是等位基因，这些等位基因与影响其他粗丝成分的突变的相互作用与新突变位于mhcA结构基因的假设一致。纯合子突变体运动很少，形态学分析表明粗丝组装严重受损。再加上mhcA位于粗细丝的中心（Miller et al., 1983），结果表明mhcA在启动细丝组装方面具有独特的作用。纯合突变对形态发生有意想不到的影响，这表明在发育过程中肌肉细胞和皮下组织之间存在相互作用。由此产生的表型可能有助于寻找额外的必需肌肉基因。
Caenorhabditis elegans body wall muscle has two distinct myosin heavy chain isoforms, mhcA and mhcB. Mutations eliminating the major isoform, mhcB, have previously been shown to yield paralyzed, viable animals. In this paper we show that the minor isoform, mhcA, is essential for viability. We have utilized the known physical map position of the gene encoding mhcA to obtain two recessive lethal mutations that virtually eliminate accumulation of mhcA. The mutations are allelic, and the interactions of these alleles with mutations affecting other thick filament components are consistent with the hypothesis that the new mutations lie in the structural gene for mhcA. The homozygous mutant animals move very little and morphological analysis shows that thick filament assembly is severely impaired. Together with the location of mhcA in the center of the thick filament (Miller et al., 1983), the results suggest that mhcA has a unique role in initiating filament assembly. The homozygous mutations have an unexpected effect on morphogenesis that indicates an interaction between the muscle cells and the hypodermis during development. The resultant phenotype may be useful in the search for additional essential muscle genes.