b型细胞周期蛋白Clb4阻止出芽酵母减数分裂I姐妹着丝粒分离。

IF 2.1 3区 生物学 Q3 GENETICS & HEREDITY
Gal Lumbroso, Gisela Cairo, Soni Lacefield, Andrew W Murray
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引用次数: 0

摘要

在减数分裂中,一轮DNA复制之后是两轮染色体分离,原细胞的倍性减半。减数分裂I中染色体的准确分离依赖于同源染色体之间的重组。姐妹着丝粒在此分裂中附着在同一纺锤杆上,仅在减数分裂II中分离。我们使用出芽酵母来选择在没有重组的情况下产生活孢子的突变。最常见的突变使CLB4失活,它编码四种b型细胞周期蛋白中的一种。在两个野生酵母菌分离株Y55和SK1中,而不是W303实验室菌株中,删除CLB4会导致减数分裂I中姐妹着丝粒过早分离和分离,并在单次分裂后频繁终止减数分裂,这表明CLB4在减数分裂染色体动力学和减数分裂过程中起着新的作用。这种作用取决于遗传背景,因为W303的减数分裂在很大程度上独立于CLB4。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The B-type cyclin Clb4 prevents meiosis I sister centromere separation in budding yeast.

In meiosis, one round of DNA replication followed by two rounds of chromosome segregation halves the ploidy of the original cell. Accurate chromosome segregation in meiosis I depends on recombination between homologous chromosomes. Sister centromeres attach to the same spindle pole in this division and only segregate in meiosis II. We used budding yeast to select for mutations that produced viable spores in the absence of recombination. The most frequent mutations inactivated CLB4, which encodes one of four B-type cyclins. In two wild yeast isolates, Y55 and SK1, but not the W303 laboratory strain, deleting CLB4 causes premature sister centromere separation and segregation in meiosis I and frequent termination of meiosis after a single division, demonstrating a novel role for Clb4 in meiotic chromosome dynamics and meiotic progression. This role depends on the genetic background since meiosis in W303 is largely independent of CLB4.

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来源期刊
G3: Genes|Genomes|Genetics
G3: Genes|Genomes|Genetics GENETICS & HEREDITY-
CiteScore
5.10
自引率
3.80%
发文量
305
审稿时长
3-8 weeks
期刊介绍: G3: Genes, Genomes, Genetics provides a forum for the publication of high‐quality foundational research, particularly research that generates useful genetic and genomic information such as genome maps, single gene studies, genome‐wide association and QTL studies, as well as genome reports, mutant screens, and advances in methods and technology. The Editorial Board of G3 believes that rapid dissemination of these data is the necessary foundation for analysis that leads to mechanistic insights. G3, published by the Genetics Society of America, meets the critical and growing need of the genetics community for rapid review and publication of important results in all areas of genetics. G3 offers the opportunity to publish the puzzling finding or to present unpublished results that may not have been submitted for review and publication due to a perceived lack of a potential high-impact finding. G3 has earned the DOAJ Seal, which is a mark of certification for open access journals, awarded by DOAJ to journals that achieve a high level of openness, adhere to Best Practice and high publishing standards.
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