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由与Gfi1相互作用的肿瘤抑制因子PRDM5对蛋白质编码基因和微小RNA基因进行的表观遗传调控。

Epigenetic regulation of protein-coding and microRNA genes by the Gfi1-interacting tumor suppressor PRDM5.

作者信息

Duan Zhijun, Person Richard E, Lee Hu-Hui, Huang Shi, Donadieu Jean, Badolato Raffaele, Grimes H Leighton, Papayannopoulou Thalia, Horwitz Marshall S

机构信息

Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA.

出版信息

Mol Cell Biol. 2007 Oct;27(19):6889-902. doi: 10.1128/MCB.00762-07. Epub 2007 Jul 16.

Abstract

Gfi1 transcriptionally governs hematopoiesis, and its mutations produce neutropenia. In an effort to identify Gfi1-interacting proteins and also to generate new candidate genes causing neutropenia, we performed a yeast two-hybrid screen with Gfi1. Among other Gfi1-interacting proteins, we identified a previously uncharacterized member of the PR domain-containing family of tumor suppressors, PRDM5. PRDM5 has 16 zinc fingers, and we show that it acts as a sequence-specific, DNA binding transcription factor that targets hematopoiesis-associated protein-coding and microRNA genes, including many that are also targets of Gfi1. PRDM5 epigenetically regulates transcription similarly to Gfi1: it recruits the histone methyltransferase G9a and class I histone deacetylases to its target gene promoters and demonstrates repressor activity on synthetic reporters; on endogenous target genes, however, it functions as an activator, in addition to a repressor. Interestingly, genes that PRDM5 activates, as opposed to those it represses, are also targets of Gfi1, suggesting a competitive mechanism through which two repressors could cooperate in order to become transcriptional activators. In neutropenic patients, we identified PRDM5 protein sequence variants perturbing transcriptional function, suggesting a potentially important role in hematopoiesis.

摘要

Gfi1在转录水平上调控造血过程,其突变会导致中性粒细胞减少。为了鉴定与Gfi1相互作用的蛋白质,并发现导致中性粒细胞减少的新候选基因,我们用Gfi1进行了酵母双杂交筛选。在其他与Gfi1相互作用的蛋白质中,我们鉴定出一种先前未被表征的含PR结构域的肿瘤抑制因子家族成员PRDM5。PRDM5有16个锌指结构,我们发现它作为一种序列特异性的DNA结合转录因子,作用于造血相关的蛋白质编码基因和微小RNA基因,其中许多也是Gfi1的作用靶点。PRDM5与Gfi1类似,通过表观遗传调控转录:它将组蛋白甲基转移酶G9a和I类组蛋白去乙酰化酶招募到其靶基因启动子上,并在合成报告基因上表现出抑制活性;然而,在内源靶基因上,它除了作为抑制因子外,还起到激活因子的作用。有趣的是,PRDM5激活的基因,与其抑制的基因相反,也是Gfi1的作用靶点,这表明存在一种竞争机制,通过该机制两个抑制因子可以协同作用从而成为转录激活因子。在中性粒细胞减少症患者中,我们鉴定出了扰乱转录功能的PRDM5蛋白质序列变异体,这表明其在造血过程中可能发挥重要作用。

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