Ura K, Wolffe A P, Hayes J J
Laboratory of Molecular Embryology, NICHD, National Institutes of Health, Bethesda, Maryland 20892.
J Biol Chem. 1994 Nov 4;269(44):27171-4.
We demonstrate that acetylation of core histone tails does not significantly impair the ability of linker histones to bind preferentially and asymmetrically to a defined sequence mononucleosome core reconstituted in vitro. Thus a simple inhibition mechanism cannot explain models whereby acetylation is causal for the observed reduction in the linker histone content in chromatin. Other models to explain this correlation are discussed.
我们证明,核心组蛋白尾部的乙酰化不会显著损害连接组蛋白优先且不对称地结合到体外重构的特定序列单核小体核心上的能力。因此,一种简单的抑制机制无法解释这样的模型,即乙酰化是染色质中连接组蛋白含量降低的原因。文中还讨论了解释这种相关性的其他模型。