转录中组蛋白标记的阴阳。

IF 7.7 2区 生物学 Q1 GENETICS & HEREDITY Annual review of genomics and human genetics Pub Date : 2021-08-31 Epub Date: 2021-03-29 DOI:10.1146/annurev-genom-120220-085159
Paul B Talbert, Steven Henikoff
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引用次数: 33

摘要

核小体包裹DNA,阻碍转录机制的进入。构成核小体的核心组蛋白受到多种翻译后修饰或标记的影响,从而影响基因的转录。它们的功能有时很难推断,因为编写和读取它们的酶是复杂的、多功能的蛋白质。在这里,我们研究了标记功能的证据,并认为主要标记在促进转录或阻止转录方面发挥了相当小的作用。组蛋白核心的乙酰化和磷酸化破坏组蛋白与dna的接触和/或破坏核小体的稳定以促进转录。泛素化刺激甲基化,为沉默复合物的形成或对这些复合物的抗性提供支架,并携带转录状态的记忆。尾巴磷酸化在特定环境中解构沉默复合物。我们推测,这些相当简单的作用形成了组蛋白标记转录调控的基础。
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The Yin and Yang of Histone Marks in Transcription.

Nucleosomes wrap DNA and impede access for the machinery of transcription. The core histones that constitute nucleosomes are subject to a diversity of posttranslational modifications, or marks, that impact the transcription of genes. Their functions have sometimes been difficult to infer because the enzymes that write and read them are complex, multifunctional proteins. Here, we examine the evidence for the functions of marks and argue that the major marks perform a fairly small number of roles in either promoting transcription or preventing it. Acetylations and phosphorylations on the histone core disrupt histone-DNA contacts and/or destabilize nucleosomes to promote transcription. Ubiquitylations stimulate methylations that provide a scaffold for either the formation of silencing complexes or resistance to those complexes, and carry a memory of the transcriptional state. Tail phosphorylations deconstruct silencing complexes in particular contexts. We speculate that these fairly simple roles form the basis of transcriptional regulation by histone marks.

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来源期刊
CiteScore
14.90
自引率
1.10%
发文量
29
期刊介绍: Since its inception in 2000, the Annual Review of Genomics and Human Genetics has been dedicated to showcasing significant developments in genomics as they pertain to human genetics and the human genome. The journal emphasizes genomic technology, genome structure and function, genetic modification, human variation and population genetics, human evolution, and various aspects of human genetic diseases, including individualized medicine.
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