Dominant mutations affecting muscle structure in Caenorhabditis elegans that map near the actin gene cluster.
Dominant mutations affecting muscle structure in Caenorhabditis elegans that map near the actin gene cluster.
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影响秀丽隐杆线虫肌肉结构的显性突变位于肌动蛋白基因簇附近。
DOI：
10.1016/0022-2836(84)90023-8
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发表时间：
1984
影响因子：
5.6
通讯作者：
Lane,TR
中科院分区：
文献类型：
--
作者：
Waterston,RH;Hirsh,D;Lane,TR
通过检测诱变秀丽隐杆线虫的F1后代，我们发现了几个影响肌肉结构的显性突变。这些新突变中的5个导致了不同于先前识别的unc-54和unc-15显性等位基因的表型。图谱研究将所有五个突变都定位在同一连锁群v的小区域。偏振光、荧光和电子显微镜研究表明，肌丝晶格紊乱的一个突出特征是在体壁肌细胞内异常放置薄丝。咽部肌肉组织在纯合时也受其中三种突变的影响。在这五个突变中，只有三个是纯合的。所有这三种基因都有异常高的基因内逆转率，要么是自发的（~10−6），要么是在甲磺酸乙酯诱变后（2 × 10−5），这表明逆转是通过功能突变的丧失发生的。未发现非连锁抑制基因突变。这些突变的显性、对细丝的影响和逆转特性表明，这些新的显性突变存在于一个或多个基因中，这些基因指定了细丝的结构成分。三组肌动蛋白序列在同一区域的定位（Fileset al., 1983）使我们推测这些突变存在于肌动蛋白基因中。
By examining F1 progeny of mutagenizedCaenorhabditis eleganslarvae, we recovered several dominant mutations which affect muscle structure. Five of these new mutations resulted in phenotypes unlike the previously recognizedunc-54 andunc-15 dominant alleles. Mapping studies placed all five mutations in the same small region of linkage group V. Polarized light, fluorescence and electron microscopic studies showed that a prominent feature of the disorganized myofilament lattice is the abnormal placement of thin filaments within the body wall muscle cells. Pharyngeal musculature is also affected by three of the mutations when homozygous. Of the five mutations only three are homozygous viable. All three of these have unusually high intragenic reversion rates either spontaneously (~10−6) or after ethyl methanesulfonate mutagenesis (2 × 10−5), suggesting that reversion occurs through loss of function mutations. No unlinked suppressor mutations were found. The dominance of the mutations, the effect on thin filaments and the reversion properties suggested that these new dominant mutations lie in a gene or genes specifying a structural component of the thin filament. The positioning of a set of three actin sequences in the same region (Fileset al., 1983) led us to speculate that these mutations lie in actin genes.