EMB30:: An APC4 homologue required for metaphase-to-anaphase transitions during meiosis and mitosis in Caenorhabditis elegans
EMB30:: An APC4 homologue required for metaphase-to-anaphase transitions during meiosis and mitosis in Caenorhabditis elegans
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DOI：
10.1091/mbc.11.4.1401
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发表时间：
2000-04-01
影响因子：
3.3
通讯作者：
Greenstein, D
中科院分区：
文献类型：
--
作者：
Furuta, T;Tuck, S;Greenstein, D
在这里，我们表明，emb-30是必需的中期到后期的转换过程中的减数分裂和有丝分裂在秀丽隐杆线虫。胚系特异的emb-30突变等位基因阻断减数分裂。突变的卵母细胞，与野生型精子受精，建立一个减数分裂纺锤体，但不进展到后期I。结果，极体不能产生，原核不能形成，胞质分裂不能发生。emb-30等位基因（I类等位基因）功能严重降低导致合子不育，并导致生殖系和体细胞缺陷，这与有丝分裂期间促进中期向后期转变的重要作用一致。对这些emb-30（I类）突变动物的外阴细胞谱系的分析表明，当母体贡献的emb-30变得受限时，有丝分裂延长并最终停止。通过进一步降低母体emb-30功能有助于I类突变动物，我们表明，emb-30是所需的中期到后期的过渡，在许多，如果不是所有的细胞。emb-30突变体的中期阻滞不是由于纺锤体组装检查点的激活，而是反映了emb-30对M期进展的基本要求。emb-30活性的降低可以抑制mdf-1（纺锤体组装检查点机制的一个组成部分）中的无效突变引起的致死性和不育性。这一结果表明，延迟后期开始可以绕过正常发育所需的纺锤体检查点。定位克隆确定，emb-30编码可能的秀丽隐杆线虫直向同源物APC 4/Lid 1，后期促进复合物/细胞周期体的组成部分，中期到后期的过渡所需的。因此，后期促进复合物/环体可能是多细胞生物体中所有中期到后期转换所必需的。
Here we show that emb-30 is required for metaphase-to-anaphase transitions during meiosis and mitosis in Caenorhabditis elegans. Germline-specific emb-30 mutant alleles block the meiotic divisions. Mutant oocytes, fertilized by wild-type sperm, set up a meiotic spindle but do not progress to anaphase I. As a result, polar bodies are not produced, pronuclei fail to form, and cytokinesis does not occur. Severe-reduction-of-function emb-30 alleles (class I alleles) result in zygotic sterility and lead to germline and somatic defects that are consistent with an essential role in promoting the metaphase-to-anaphase transition during mitosis. Analysis of the vulval cell lineages in these emb-30(class I) mutant animals suggests that mitosis is lengthened and eventually arrested when maternally contributed emb-30 becomes Limiting. By further reducing maternal emb-30 function contributed to class I mutant animals, we show that emb-30 is required for the metaphase-to-anaphase transition in many, if not all, cells. Metaphase arrest in emb-30 mutants is not due to activation of the spindle assembly checkpoint but rather reflects an essential emb-30 requirement for M-phase progression. A reduction in emb-30 activity can suppress the lethality and sterility caused by a null mutation in mdf-l, a component of the spindle assembly checkpoint machinery. This result suggests that delaying anaphase onset can bypass the spindle checkpoint requirement for normal development. Positional cloning established that emb-30 encodes the likely C, elegans orthologue of APC4/Lid1, a component of the anaphase-promoting complex/cyclosome, required for the metaphase-to-anaphase transition. Thus, the anaphase-promoting complex/cyclosome is likely to be required for all metaphase-to-anaphase transitions in a multicellular organism.