Clark-Maguire S, Mains P E
Department of Medical Biochemistry, University of Calgary, Alberta, Canada.
J Cell Biol. 1994 Jul;126(1):199-209. doi: 10.1083/jcb.126.1.199.
Genetic evidence suggests that the product of the mei-1 gene of Caenorhabditis elegans is specifically required for meiosis in the female germline. Loss-of-function mei-1 mutations block meiotic spindle formation while a gain-of-function allele instead results in spindle defects during the early mitotic cleavages. In this report, we use immunocytochemistry to examine the localization of the mei-1 product in wild-type and mutant embryos. During metaphase of meiosis I in wild-type embryos, mei-1 protein was found throughout the spindle but was more concentrated toward the poles. At telophase I, mei-1 product colocalized with the chromatin at the spindle poles. The pattern was repeated during meiosis II but no mei-1 product was visible during the subsequent mitotic cleavages. The mei-1 gain-of-function allele resulted in ectopic mei-1 staining in the centers of the microtubule-organizing centers during interphase and in the spindles during the early cleavages. This aberrant localization is probably responsible for the poorly formed and misoriented cleavage spindles characteristic of the mutation. We also examined the localization of mei-1(+) product in the presence of mutations of genes that genetically interact with mei-1 alleles. mei-2 is apparently required to localize mei-1 product to the spindle during meiosis while mel-26 acts as a postmeiotic inhibitor. We conclude that mei-1 encodes a novel spindle component, one that is specialized for the acentriolar meiotic spindles unique to female meiosis. The genes mei-2 and mel-26 are part of a regulatory network that confines mei-1 activity to meiosis.
遗传学证据表明,秀丽隐杆线虫的mei-1基因产物是雌性生殖系减数分裂所特需的。功能丧失型mei-1突变会阻断减数分裂纺锤体的形成,而功能获得型等位基因则会在有丝分裂早期分裂过程中导致纺锤体缺陷。在本报告中,我们使用免疫细胞化学方法来检测野生型和突变型胚胎中mei-1产物的定位。在野生型胚胎减数分裂I的中期,mei-1蛋白在整个纺锤体中都有发现,但在两极更为集中。在减数分裂I的末期,mei-1产物与纺锤体两极的染色质共定位。这种模式在减数分裂II期间重复出现,但在随后的有丝分裂分裂过程中没有可见的mei-1产物。mei-1功能获得型等位基因导致在间期微管组织中心的中心以及早期分裂期间的纺锤体中出现异位的mei-1染色。这种异常定位可能是该突变特征性的形成不良和方向错误的分裂纺锤体的原因。我们还检测了在与mei-1等位基因发生遗传相互作用的基因突变存在的情况下mei-1(+)产物的定位。mei-2显然是在减数分裂期间将mei-1产物定位到纺锤体所必需的,而mel-26则作为减数分裂后的抑制剂。我们得出结论,mei-1编码一种新型纺锤体成分,一种专门用于雌性减数分裂特有的无中心粒减数分裂纺锤体的成分。基因mei-2和mel-26是将mei-1活性限制在减数分裂的调控网络的一部分。