Suppr超能文献

姐妹染色单体端粒黏连是不可替代的,并且能抵抗纺锤体作用力和端粒运动。

Sister-chromatid telomere cohesion is nonredundant and resists both spindle forces and telomere motility.

作者信息

Antoniacci Lisa M, Skibbens Robert V

机构信息

Department of Biological Sciences, Lehigh University, Bethlehem, Pennsylvania 18015, USA.

出版信息

Curr Biol. 2006 May 9;16(9):902-6. doi: 10.1016/j.cub.2006.03.060.

Abstract

It is well documented that inactivation of essential cohesion proteins results in precocious sister-chromatid separation. On average, however, only approximately 55% of cohesin-deficient budding yeast cells arrested prior to anaphase contain separated sister chromatids , suggesting that cohesin-independent factors also contribute to sister-chromatid pairing. Recently, redundant pairing mechanisms were found to occur at both rDNA and centromeres . Here, we tested whether redundant mechanisms also function to pair telomeres or whether cohesins provide sole pairing activity. Results from both mcd1 and ctf7 mutant cells show that nearly 100% of telomeres separate prior to anaphase, twice the cohesion defect reported for centromeres. Such complete loci separation reveals that cohesins are singularly responsible for maintaining telomere cohesion, in contrast to other loci. We also found that sister telomeres moved 141% farther apart than centromeres. Telomere separation occurred in the absence of spindle microtubules and an actin cytoskeleton and persisted in cells abrogated for Mps3p function-an integral nuclear envelope protein previously shown to function in cohesion . These findings are consistent with numerous studies that telomeres translocate along the nuclear periphery and provide new evidence that telomere dynamics can contribute to sister-chromatid separation, independent of centromere motility.

摘要

有充分的文献记载,必需的黏连蛋白失活会导致姐妹染色单体过早分离。然而,平均而言,在后期之前停滞的黏连蛋白缺陷型芽殖酵母细胞中,只有约55%含有分离的姐妹染色单体,这表明不依赖黏连蛋白的因素也有助于姐妹染色单体配对。最近发现,冗余配对机制在核糖体DNA(rDNA)和着丝粒处均有发生。在此,我们测试了冗余机制是否也在端粒配对中起作用,或者黏连蛋白是否提供唯一的配对活性。mcd1和ctf7突变细胞的结果均表明,近100%的端粒在后期之前分离,这是报道的着丝粒黏连缺陷的两倍。这种完全的位点分离表明,与其他位点不同,黏连蛋白是维持端粒黏连的唯一原因。我们还发现,姐妹端粒分开的距离比着丝粒远141%。端粒分离在没有纺锤体微管和肌动蛋白细胞骨架的情况下发生,并且在缺失Mps3p功能的细胞中持续存在——Mps3p是一种先前已证明在黏连中起作用的完整核膜蛋白。这些发现与众多关于端粒沿核周移位的研究一致,并提供了新的证据,即端粒动态变化可导致姐妹染色单体分离,而与着丝粒运动无关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验