Mains P E, Kemphues K J, Sprunger S A, Sulston I A, Wood W B
Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder 80309.
Genetics. 1990 Nov;126(3):593-605. doi: 10.1093/genetics/126.3.593.
We describe interactions between maternal-effect lethal mutations in four genes of Caenorhabditis elegans whose products appear to be involved in the meiotic and mitotic divisions of the one-cell embryo. Mitosis is disrupted by two dominant temperature-sensitive gain-of-function maternal-effect lethal mutations, mei-1(ct46) and mel-26(ct61), and by recessive loss-of-function maternal-effect lethal mutations of zyg-9. The phenotypic defects resulting from these mutations are similar. Doubly mutant combinations show a strong enhancement of the maternal-effect lethality under semipermissive conditions, suggesting that the mutant gene products interact. We isolated 15 dominant suppressors of the gain-of-function mutation mei-1(ct46). Thirteen of these suppressors are apparently intragenic, but 11 of them suppress in trans as well as cis. Two extragenic suppressors define a new gene, mei-2. The suppressor mutations in these two genes also result in recessive maternal-effect lethality, but with meiotic rather than mitotic defects. Surprisingly, most of these suppressors are also able to suppress mel-26(ct61) in addition to mei-1(ct46). The products of the four genes mei-1, mei-2, zyg-9 and mel-26 could be responsible for some of the specialized features that distinguish the meiotic from the mitotic divisions in the one-cell embryo.
我们描述了秀丽隐杆线虫四个基因中的母性效应致死突变之间的相互作用,这些基因的产物似乎参与了单细胞胚胎的减数分裂和有丝分裂。有丝分裂受到两个显性温度敏感型功能获得性母性效应致死突变mei-1(ct46)和mel-26(ct61)以及zyg-9的隐性功能丧失性母性效应致死突变的干扰。这些突变导致的表型缺陷相似。双突变组合在半允许条件下显示出母性效应致死性的强烈增强,表明突变基因产物相互作用。我们分离出了15个mei-1(ct46)功能获得性突变的显性抑制子。其中13个抑制子显然是基因内的,但其中11个在反式和顺式中都能发挥抑制作用。两个基因外抑制子定义了一个新基因mei-2。这两个基因中的抑制子突变也会导致隐性母性效应致死性,但具有减数分裂而非有丝分裂缺陷。令人惊讶的是,除了mei-1(ct46)之外,这些抑制子中的大多数还能够抑制mel-26(ct61)。mei-1、mei-2、zyg-9和mel-26这四个基因的产物可能是区分单细胞胚胎减数分裂和有丝分裂的一些特殊特征的原因。