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果蝇中酵母Sup35p同源物的缺失会破坏雄性减数分裂过程中的纺锤体组装、染色体分离和胞质分裂。

Depletion of a Drosophila homolog of yeast Sup35p disrupts spindle assembly, chromosome segregation, and cytokinesis during male meiosis.

作者信息

Basu J, Williams B C, Li Z, Williams E V, Goldberg M L

机构信息

Section of Genetics and Development, Cornell University, Ithaca, New York 14853-2703, USA.

出版信息

Cell Motil Cytoskeleton. 1998;39(4):286-302. doi: 10.1002/(SICI)1097-0169(1998)39:4<286::AID-CM4>3.0.CO;2-1.

DOI:10.1002/(SICI)1097-0169(1998)39:4<286::AID-CM4>3.0.CO;2-1
PMID:9556329
Abstract

In the course of a genetic screen for male-sterile mutations in Drosophila affecting chromosome segregation during the meiotic divisions in spermatocytes, we identified the mutation dsup35(63D). Examination of mutant testes showed that chromosome misbehavior was a consequence of major disruptions in meiotic spindle assembly. These perturbations included problems in aster formation, separation, and migration around the nuclear envelope; aberrations in spindle organization and integrity; and disappearance of the ana/telophase central spindle, which in turn disrupts cytokinesis. The dsup35(63D) mutation is caused by a P element insertion that affects, specifically in the testis, the expression of a gene (dsup35) encoding the Drosophila homolog of the yeast Sup35p and Xenopus eRF3 proteins. These proteins are involved in the termination of polypeptide synthesis on ribosomes, but previous studies have suggested that Sup35p and closely related proteins of the same family also interact directly with microtubules. An affinity-purified antibody directed against the product of the dsup35 gene was prepared; interestingly, this antibody specifically labels primary spermatocytes in one or two discrete foci of unknown structure within the nucleoplasm. We discuss how depletion of the dsup35 gene product in spermatocytes might lead to the global disruptions in meiotic spindle assembly seen in mutant spermatocytes.

摘要

在对果蝇中影响精母细胞减数分裂过程中染色体分离的雄性不育突变进行遗传筛选的过程中,我们鉴定出了突变体dsup35(63D)。对突变体睾丸的检查表明,染色体行为异常是减数分裂纺锤体组装严重破坏的结果。这些干扰包括星体形成、分离以及围绕核膜迁移方面的问题;纺锤体组织和完整性的畸变;以及后期/末期中央纺锤体的消失,进而破坏胞质分裂。dsup35(63D)突变是由一个P因子插入引起的,该插入特异性地影响睾丸中一个基因(dsup35)的表达,该基因编码酵母Sup35p和非洲爪蟾eRF3蛋白的果蝇同源物。这些蛋白质参与核糖体上多肽合成的终止,但先前的研究表明,Sup35p以及同一家族中密切相关的蛋白质也直接与微管相互作用。制备了一种针对dsup35基因产物的亲和纯化抗体;有趣的是,这种抗体特异性地标记核质中一个或两个结构未知的离散位点内的初级精母细胞。我们讨论了精母细胞中dsup35基因产物的缺失可能如何导致突变体精母细胞中所见的减数分裂纺锤体组装的整体破坏。

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