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Codependency of H2B monoubiquitination and nucleosome reassembly on Chd1

机译:H2B单泛素化和核小体重组对Chd1的依赖性。

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摘要

Monoubiquitination of histone H2B on Lys 123 (H2BK123ub) is a transient histone modification considered to be essential for establishing H3K4 and H3K79 trimethylation by Set1/COMPASS and Dot1, respectively. Here, we identified Chd1 as a factor that is required for the maintenance of high levels of H2B monoubiquitination, but not for H3K4 and H3K79 trimethylation. Loss of Chd1 results in a substantial loss of H2BK123ub levels with little to no effect on the genome-wide pattern of H3K4 and H3K79 trimethylation. Our data show that nucleosomal occupancy is reduced in gene bodies in both chd1Δ and, as has been shown, K123A mutant backgrounds. We also demonstrated that Chd1's function in maintaining H2BK123ub levels is conserved from yeast to humans. Our study provides evidence that only small levels of H2BK123ub are necessary for full levels of H3K4 and H3K79 trimethylation in vivo and points to a possible role for Chd1 in positively regulating gene expression through promoting nucleosome reassembly coupled with H2B monoubiquitination.
机译:Lys 123(H2BK123ub)上组蛋白H2B的单泛素化是一种瞬时组蛋白修饰,被认为对于分别通过Set1 / COMPASS和Dot1建立H3K4和H3K79三甲基化至关重要。在这里,我们确定Chd1是维持高水平的H2B单泛素化所必需的因子,而对于H3K4和H3K79三甲基化则不是。 Chd1的损失导致H2BK123ub水平的大量损失,而对H3K4和H3K79三甲基化的全基因组模式几乎没有影响。我们的数据表明,在chd1Δ和K123A突变体背景下,基因体中核小体的占有率均降低。我们还证明了Chd1在维持H2BK123ub水平上的功能从酵母到人类都是保守的。我们的研究提供的证据表明,体内完整水平的H3K4和H3K79三甲基化仅需要少量的H2BK123ub,并指出Chd1在通过促进核小体重组与H2B单泛素化结合而积极调节基因表达中的可能作用。

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