Nature子刊：三篇文章鉴别可拓展“核染质编码”两种新变异
生物谷综合报道：核染质是构成染色体的DNA和蛋白质的一个组分。在12月在线出版的《自然—细胞生物学》期刊上，三篇论文对核染质进行了分析，鉴别出可拓展“核染质编码”的两种新变异。研究人员还发现，核染质的一种变异调控了“后生记忆”，这是克隆过程中一个非常关键的步骤。
人类的DNA分子总共有2米长。为了防止长长的DNA分子处于混乱状态，基因组紧紧地缠在一种名为组蛋白的蛋白质复合体上。最近的研究发现，组蛋白质也参与了基因活性的调控，这些蛋白质的大量可逆转化学修饰也被揭示出来，它们也能调控基因的表达。
在核染质密码的周期表中，Roland Schüle和同事鉴别出一种名为磷酸化组蛋白的新元素H3，并发现这种元素让包裹在磷酸化H3中的基因变得活跃。
Pax7是调控肌肉基因活性的一个关键因子。在一篇相关的论文中，Michael Rudnicki和同事揭示出Pax7的工作原理。通过将一种附加到甲基组团的酶与H3结合，它能调控某种控制干细胞分化成肌肉细胞的基因。
最后，John Gurdon和同事发现了一种基因在克隆过程中是如何保持自己的活跃状态。这种基因状态的记忆依赖于H3的特别变异H3.3。最令人吃惊的是，这种记忆可一直保持到受精卵细胞的第24次分裂增生。
生物谷推荐英文原文
英文原文一：
Nature Cell Biology
Published online: 9 December 2007; | doi:10.1038/ncb1668
Phosphorylation of histone H3 at threonine 11 establishes a novel chromatin mark for transcriptional regulation
Posttranslational modifications of histones such as methylation, acetylation and phosphorylation regulate chromatin structure and gene expression. Here we show that protein-kinase-C-related kinase 1 (PRK1) phosphorylates histone H3 at threonine 11 (H3T11) upon ligand-dependent recruitment to androgen receptor target genes. PRK1 is pivotal to androgen receptor function because PRK1 knockdown or inhibition impedes androgen receptor-dependent transcription. Blocking PRK1 function abrogates androgen-induced H3T11 phosphorylation and inhibits androgen-induced demethylation of histone H3. Moreover, serine-5-phosphorylated RNA polymerase II is no longer observed at androgen receptor target promoters. Phosphorylation of H3T11 by PRK1 accelerates demethylation by the Jumonji C (JmjC)-domain-containing protein JMJD2C. Thus, phosphorylation of H3T11 by PRK1 establishes a novel chromatin mark for gene activation, identifying PRK1 as a gatekeeper of androgen receptor-dependent transcription. Importantly, levels of PRK1 and phosphorylated H3T11 correlate with Gleason scores of prostate carcinomas. Finally, inhibition of PRK1 blocks proliferation of androgen receptor-induced tumour cell proliferation, making PRK1 a promising therapeutic target.
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