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NO66，一种组蛋白去甲基化酶 Jumonji 家族，调控成骨细胞特异性转录因子 Osterix。

Regulation of the osteoblast-specific transcription factor Osterix by NO66, a Jumonji family histone demethylase.

机构信息

Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

EMBO J. 2010 Jan 6;29(1):68-79. doi: 10.1038/emboj.2009.332. Epub 2009 Nov 19.

DOI:10.1038/emboj.2009.332
PMID:19927124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2780536/
Abstract

Osterix (Osx) is an osteoblast-specific transcription factor required for osteoblast differentiation and bone formation. Osx null mice develop a normal cartilage skeleton but fail to form bone and to express osteoblast-specific marker genes. To better understand the control of transcriptional regulation by Osx, we identified Osx-interacting proteins using proteomics approaches. Here, we report that a Jumonji C (JmjC)-domain containing protein, called NO66, directly interacts with Osx and inhibits Osx-mediated promoter activation. The knockdown of NO66 in preosteoblast cells triggered accelerated osteoblast differentiation and mineralization, and markedly stimulated the expression of Osx target genes. A JmjC-dependent histone demethylase activity was exhibited by NO66, which was specific for both H3K4me and H3K36me in vitro and in vivo, and this activity was needed for the regulation of osteoblast-specific promoters. During BMP-2-induced differentiation of preosteoblasts, decreased NO66 occupancy correlates with increased Osx occupancy at Osx-target promoters. Our results indicate that interactions between NO66 and Osx regulate Osx-target genes in osteoblasts by modulating histone methylation states.

摘要

osterix(osx)是一种成骨细胞特异性转录因子，对于成骨细胞分化和骨形成是必需的。osx 敲除小鼠会形成正常的软骨骨骼，但无法形成骨组织，也无法表达成骨细胞特异性的标记基因。为了更好地理解 osx 对转录调控的控制，我们使用蛋白质组学方法鉴定了 osx 的相互作用蛋白。在这里，我们报告一种含有 jumonji c(jmjc)结构域的蛋白，称为 no66，可直接与 osx 相互作用，并抑制 osx 介导的启动子激活。在成骨前体细胞中敲低 no66 会触发成骨细胞的加速分化和矿化，并显著刺激 osx 靶基因的表达。no66 表现出 jmjc 依赖性组蛋白去甲基化酶活性，该活性在体外和体内均特异性针对 h3k4me 和 h3k36me，并且这种活性对于成骨细胞特异性启动子的调控是必需的。在 bmp-2 诱导的成骨前体细胞分化过程中，no66 的占有率降低与 osx 靶启动子上 osx 占有率的增加相关。我们的结果表明，no66 和 osx 之间的相互作用通过调节组蛋白甲基化状态来调节成骨细胞中的 osx 靶基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/6262155f397d/emboj2009332f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/e6617b38a0f3/emboj2009332f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/09ee7b847493/emboj2009332f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/2e1fdae02fc1/emboj2009332f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/192fda411745/emboj2009332f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/5dd9c2476343/emboj2009332f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/6262155f397d/emboj2009332f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/e6617b38a0f3/emboj2009332f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/09ee7b847493/emboj2009332f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/2e1fdae02fc1/emboj2009332f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/192fda411745/emboj2009332f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/5dd9c2476343/emboj2009332f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41af/2808379/6262155f397d/emboj2009332f6.jpg

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