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Selective transcriptional regulation by Myc in cellular growth control and lymphomagenesis

机译：Myc在细胞生长控制和淋巴瘤发生中的选择性转录调控

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摘要

哺乳动物Myc致癌蛋白是与数千个启动子相结合的一种转录因子。关于Myc功能的两个当前模型提出,它要么是转录的一个基因特异性调控因子,要么是所有活性基因的一个普遍性放大因子。在本期Nature上发表文章的两个小组提供了支持以下观点的证据：Myc调控特定基因。Arianna Sabo等人分析了在小鼠的B-细胞淋巴瘤发生过程中Myc的基因组分布及RNA表达特征；Susanne Walz等人对正常细胞和被Myc改变的肿瘤细胞做了对比。虽然这两个小组都发现Myc的表达能导致基因表达的普遍增加,但该效应是间接的。受其他各种转录因子所调制,Myc似乎主要是通过调控特定类别的基因来发挥作用的。%The c-myc proto-oncogene product, Myc, is a transcription tactor that binds thousands of genomic loci. Recent work suggested that rather than up-and downregulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed 'invasion') and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunopre-cipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or messenger RNA copies per cell (hereby termed 'amplification') when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, although having the potential to interact with all active or poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results indicate that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover.
机译：哺乳动物Myc致癌蛋白是与数千个启动子相结合的一种转录因子。关于Myc功能的两个当前模型提出,它要么是转录的一个基因特异性调控因子,要么是所有活性基因的一个普遍性放大因子。在本期Nature上发表文章的两个小组提供了支持以下观点的证据：Myc调控特定基因。Arianna Sabo等人分析了在小鼠的B-细胞淋巴瘤发生过程中Myc的基因组分布及RNA表达特征；Susanne Walz等人对正常细胞和被Myc改变的肿瘤细胞做了对比。虽然这两个小组都发现Myc的表达能导致基因表达的普遍增加,但该效应是间接的。受其他各种转录因子所调制,Myc似乎主要是通过调控特定类别的基因来发挥作用的。%The c-myc proto-oncogene product, Myc, is a transcription tactor that binds thousands of genomic loci. Recent work suggested that rather than up-and downregulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed 'invasion') and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunopre-cipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or messenger RNA copies per cell (hereby termed 'amplification') when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, although having the potential to interact with all active or poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results indicate that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover.

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  • 来源
    《Nature》 |2014年第7510期|488-492b2|共6页
  • 作者

    Arianna Sabo; Theresia R. Kress; Mattia Pelizzola; Stefano de Pretis; Marcin M. Gorski; Alessandra Tesi; Marco J. Morelli; Pranami Bora; Mirko Doni; Alessandro Verrecchia; Claudia Tonelli; Giovanni Faga; Valerio Bianchi; Alberto Ronchi; Diana Low; Heiko Mueller; Ernesto Guccione; Stefano Campaner; Bruno Amati;

  • 作者单位

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty,Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty,Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Institute of Molecular and Cell Biology, Singapore 138673, Singapore;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Institute of Molecular and Cell Biology, Singapore 138673, Singapore;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty;

    Centerfor Genomic Science of IIT@SEMM,Fondazionelstituto ltaliano di Tecnologia (IIT),Via Adamello 16,20139 Milan, Itaty,Departmentof Expert mental Oncology, European Institute of Oncology (IEO),Via Adamello 16,20139 Milan,Italy;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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