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表观遗传调控。

Epigenetic control.

作者信息

Delcuve Geneviève P, Rastegar Mojgan, Davie James R

机构信息

Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Manitoba, Canada.

出版信息

J Cell Physiol. 2009 May;219(2):243-50. doi: 10.1002/jcp.21678.

Abstract

Epigenetics refers to mitotically and/or meiotically heritable variations in gene expression that are not caused by changes in DNA sequence. Epigenetic mechanisms regulate all biological processes from conception to death, including genome reprogramming during early embryogenesis and gametogenesis, cell differentiation and maintenance of a committed lineage. Key epigenetic players are DNA methylation and histone post-translational modifications, which interplay with each other, with regulatory proteins and with non-coding RNAs, to remodel chromatin into domains such as euchromatin, constitutive or facultative heterochromatin and to achieve nuclear compartmentalization. Besides epigenetic mechanisms such as imprinting, chromosome X inactivation or mitotic bookmarking which establish heritable states, other rapid and transient mechanisms, such as histone H3 phosphorylation, allow cells to respond and adapt to environmental stimuli. However, these epigenetic marks can also have long-term effects, for example in learning and memory formation or in cancer. Erroneous epigenetic marks are responsible for a whole gamut of diseases including diseases evident at birth or infancy or diseases becoming symptomatic later in life. Moreover, although epigenetic marks are deposited early in development, adaptations occurring through life can lead to diseases and cancer. With epigenetic marks being reversible, research has started to focus on epigenetic therapy which has had encouraging success. As we witness an explosion of knowledge in the field of epigenetics, we are forced to revisit our dogma. For example, recent studies challenge the idea that DNA methylation is irreversible. Further, research on Rett syndrome has revealed an unforeseen role for methyl-CpG-binding protein 2 (MeCP2) in neurons.

摘要

表观遗传学是指基因表达中可通过有丝分裂和/或减数分裂遗传的变异,这些变异并非由DNA序列的变化引起。表观遗传机制调控着从受孕到死亡的所有生物过程,包括早期胚胎发育和配子发生过程中的基因组重编程、细胞分化以及特定谱系的维持。关键的表观遗传作用因子包括DNA甲基化和组蛋白翻译后修饰,它们相互作用,并与调控蛋白和非编码RNA相互作用,将染色质重塑为常染色质、组成型或兼性异染色质等结构域,以实现细胞核的区室化。除了诸如印记、X染色体失活或有丝分裂标记等建立可遗传状态的表观遗传机制外,其他快速且短暂的机制,如组蛋白H3磷酸化,使细胞能够对环境刺激做出反应并适应。然而,这些表观遗传标记也可能产生长期影响,例如在学习和记忆形成或癌症发生过程中。错误的表观遗传标记会导致一系列疾病,包括出生时或婴儿期就明显的疾病,或在生命后期出现症状的疾病。此外,尽管表观遗传标记在发育早期就已沉积,但一生中发生的适应性变化可能导致疾病和癌症。由于表观遗传标记是可逆的,研究已开始聚焦于表观遗传治疗,并且取得了令人鼓舞的成功。随着我们见证表观遗传学领域知识的爆炸式增长,我们不得不重新审视我们的教条。例如,最近的研究对DNA甲基化是不可逆的这一观点提出了挑战。此外,对雷特综合征的研究揭示了甲基化CpG结合蛋白2(MeCP2)在神经元中具有意想不到的作用。

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