Sir2和Fun30通过MCM基酶定位和核细胞占用率来调节核细胞DNA复制时间
Carmina Lichauco1, Eric J Foss1, Tonibelle Gatbonton-Schwager1
1Translational Science and Therapeutics Division, Human Biology Division, Fred Hutchinson Cancer Center, Seattle, WA.
bioRxiv : the preprint server for biology
|April 8, 2024
概括
Sir2蛋白通过重新定位MCM旋酶来延迟DNA复制时间. 染色体重塑器FUN30对于这种重新定位至关重要,并影响酵母核糖体DNA的原始点火.
科学领域:
- * 分子生物学 * 分子生物学
- * 表观遗传学 是一种表观遗传学.
- * 酵母遗传学公司
背景情况:
- * 晚期复制时间和低转录在异色素蛋白中相关,但机制尚不清楚.
- * Sir2 (希斯脱乙酶) 对于静止和晚期复制酵母核糖体DNA (rDNA) 阵列至关重要.
- * SIR2的损失导致RNA聚合酶II重新定位MCM螺旋体,远离rDNA来源.
研究的目的:
- *阐明Sir2在rDNA起源时延迟复制时间的机制.
- * 调查染色体重塑在MCM酶重新定位和原始激活中的作用.
- * 为了确定影响复制原始点火的因素,以响应染色体环境.
主要方法:
- * 开发了一种新的方法来区分密切距离的MCM复合体的激活.
- *分析了Saccharomyces cerevisiae中rDNA起源的MCM旋酶定位和激活.
- *研究了MCM重新定位和起源激活对染色体重塑剂FUN30的依赖性.
主要成果:
- * 在rDNA起源处移位的MCM旋酶与非移位的MCM旋酶相比,具有更高的发射倾向.
- *重新定位的MCM的激活和相邻区域的低核细胞占用量取决于FUN30的染色体重塑活性.
- * Sir2在延迟复制时间方面的作用与受FUN30影响的MCM重新定位有机学的联系.
结论:
- * Sir2通过促进MCM酶重新定位来延迟复制时间,这一过程依赖于FUN30.
- *原始活化在体内受到由染色体重塑器FUN30建立的核细胞背景的直接影响.
- *这项研究提供了第一个 in vivo 证据,将单个染色体重塑剂与特定的复制起源激活联系起来.
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