The Drosophila mei-S332 gene promotes sister-chromatid cohesion in meiosis following kinetochore differentiation.
The Drosophila mei-S332 gene promotes sister-chromatid cohesion in meiosis following kinetochore differentiation.
复制标题
果蝇 mei-S332 基因在着丝粒分化后的减数分裂中促进姐妹染色单体的凝聚。
DOI：
10.1093/genetics/130.4.827
复制
发表时间：
1992
期刊：
影响因子：
3.3
通讯作者：
Orr-Weaver,TL
中科院分区：
文献类型：
--
作者：
Kerrebrock,AW;Miyazaki,WY;Birnby,D;Orr-Weaver,TL
果蝇mei-S332基因在雄性和雌性减数分裂后期II之前起维持姐妹染色单体凝聚力的作用。通过分离和分析7个新的等位基因和一个发现mei-S332基因缺陷的基因，我们证明了对mei-S332的需要直到后期I才开始。我们所有的等位基因主要导致等性（减数分裂II）不分离和少量的减数分裂（减数分裂I）不分离。细胞学分析表明，姐妹染色单体经常分离后期I在这些突变体。由于姐妹染色单体在第一次分裂后期仍保持联合，因此在减数分裂I期间染色体正常分离，而过早姐妹染色单体分离的遗传后果被视为减数分裂II中的不分离。由突变证明的mei-S332作用的迟发性不是残余基因功能的结果，因为两个强的，并且可能是无效的等位基因作为纯合子和反式缺陷都提供了主要的等式不分离。mei-S332是不需要的，直到中期I之后，当动粒从由姐妹染色单体共同组织成两个不同的姐妹动粒的单个半球形动粒分化时。因此，我们认为mei-S322产物的作用是将加倍的动粒保持在一起，直到后期II。所有的等位基因都是完全可行的，当在反式缺陷，因此mei-S332是不必要的有丝分裂。其中四个等位基因显示出意想不到的性别特异性。
The Drosophila mei-S332 gene acts to maintain sister-chromatid cohesion before anaphase II of meiosis in both males and females. By isolating and analyzing seven new alleles and a deficiency uncovering the mei-S332 gene we have demonstrated that the onset of the requirement for mei-S332 is not until late anaphase I. All of our alleles result primarily in equational (meiosis II) nondisjunction with low amounts of reductional (meiosis I) nondisjunction. Cytological analysis revealed that sister chromatids frequently separate in late anaphase I in these mutants. Since the sister chromatids remain associated until late in the first division, chromosomes segregate normally during meiosis I, and the genetic consequences of premature sister-chromatid dissociation are seen as nondisjunction in meiosis II. The late onset of mei-S332 action demonstrated by the mutations was not a consequence of residual gene function because two strong, and possibly null, alleles give predominantly equational nondisjunction both as homozygotes and in trans to a deficiency. mei-S332 is not required until after metaphase I, when the kinetochore differentiates from a single hemispherical kinetochore jointly organized by the sister chromatids into two distinct sister kinetochores. Therefore, we propose that the mei-S322 product acts to hold the doubled kinetochore together until anaphase II. All of the alleles are fully viable when in trans to a deficiency, thus mei-S332 is not essential for mitosis. Four of the alleles show an unexpected sex specificity.