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首页> 外文期刊>Journal of Cellular Physiology >Mitotic Inheritance of mRNA Facilitates Translational Activation of the Osteogenic-Lineage Commitment Factor Runx2 in Progeny of Osteoblastic Cells
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Mitotic Inheritance of mRNA Facilitates Translational Activation of the Osteogenic-Lineage Commitment Factor Runx2 in Progeny of Osteoblastic Cells

机译:有丝分裂继承mRNA的促进平移的激活Osteogenic-Lineage因素Runx2的承诺后代的成骨细胞的细胞

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摘要

Epigenetic mechanisms mediate the acquisition of specialized cellular phenotypes during tissue development, maintenance and repair. When phenotype-committed cells transit through mitosis, chromosomal condensation counteracts epigenetic activation of gene expression. Subsequent post-mitotic re-activation of transcription depends on epigenetic DNA and histone modifications, as well as other architecturally bound proteins that bookmark the genome. Osteogenic lineage commitment, differentiation and progenitor proliferation require the bone-related runt-related transcription factor Runx2. Here, we characterized a non-genomic mRNA mediated mechanism by which osteoblast precursors retain their phenotype during self-renewal. We show that osteoblasts produce maximal levels of Runx2 mRNA, but not protein, prior to mitotic cell division. Runx2 mRNA partitions symmetrically between daughter cells in a non-chromosomal tubulin-containing compartment. Subsequently, transcription-independent de novo synthesis of Runx2 protein in early G(1) phase results in increased functional interactions of Runx2 with a representative osteoblast-specific target gene (osteocalcin/BGLAP2) in chromatin. Somatic transmission of Runx2 mRNAs in osteoblasts and osteosarcoma cells represents a versatile mechanism for translational rather than transcriptional induction of this principal gene regulator to maintain osteoblast phenotype identity after mitosis. J. Cell. Physiol. 231: 1001-1014, 2016. (c) 2015 Wiley Periodicals, Inc.
机译:表观遗传机制调解收购在组织专门的细胞表型开发、维护和维修。phenotype-committed细胞运输通过有丝分裂,染色体缩合抵消表观遗传基因表达的激活。随后post-mitotic再活跃的转录取决于DNA和表观遗传组蛋白修饰,以及其他架构上蛋白质,书签基因组。分化和祖细胞增殖需要骨runt-related转录因子Runx2。特征non-genomic信使rna介导成骨细胞前体保留机制在自我更新他们的表型。成骨细胞产生最大的Runx2 mRNA水平,但不是蛋白质,有丝分裂细胞分裂之前。Runx2 mRNA分区之间的对称non-chromosomal子细胞tubulin-containing隔间。transcription-independent从头合成的Runx2蛋白质在G(1)阶段的早期结果增加功能的Runx2的交互代表osteoblast-specific目标基因(骨钙素/ BGLAP2)在染色质。Runx2 mrna在成骨细胞和的传播骨肉瘤细胞代表一个多才多艺转化的机制,而不是这主要基因的转录诱导监管机构保持成骨细胞表型有丝分裂后的身份。1001 - 1014年,2016年。

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