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首页> 外文期刊>Cell cycle >Tumor suppressor genes are larger than apoptosis-effector genes and have more regions of active chromatin: Connection to a stochastic paradigm for sequential gene expression programs
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Tumor suppressor genes are larger than apoptosis-effector genes and have more regions of active chromatin: Connection to a stochastic paradigm for sequential gene expression programs

机译：肿瘤抑制基因比凋亡抑制基因大，并且具有更多的活性染色质区域：与随机范式的连接用于顺序基因表达程序

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Apoptosis- and proliferation-effector genes are substantially regulated by the same transactivators, with E2F-1 and Oct-1 being notable examples. The larger proliferation-effector genes have more binding sites for the transactivators that regulate both sets of genes, and proliferation-effector genes have more regions of active chromatin, i.e, DNase I hypersensitive and histone 3, lysine-4 trimethylation sites. Thus, the size differences between the 2 classes of genes suggest a transcriptional regulation paradigm whereby the accumulation of transcription factors that regulate both sets of genes, merely as an aspect of stochastic behavior, accumulate first on the larger proliferation-effector gene traps, and then accumulate on the apoptosis effector genes, thereby effecting sequential activation of the 2 different gene sets. As IRF-1 and p53 levels increase, tumor suppressor proteins are first activated, followed by the activation of apoptosis-effector genes, for example during S-phase pausing for DNA repair. Tumor suppressor genes are larger than apoptosis-effector genes and have more IRF-1 and p53 binding sites, thereby likewise suggesting a paradigm for transcription sequencing based on stochastic interactions of transcription factors with different gene classes. In this report, using the ENCODE database, we determined that tumor suppressor genes have a greater number of open chromatin regions and histone 3 lysine-4 trimethylation sites, consistent with the idea that a larger gene size can facilitate earlier transcriptional activation via the inclusion of more transactivator binding sites.
机译：凋亡和增殖效应基因基本上由相同的反式激活因子调控，E2F-1和Oct-1是著名的例子。较大的增殖效应基因具有调节这两组基因的反式激活因子的更多结合位点，并且增殖效应基因具有更多的活性染色质区域，即DNase I超敏和组蛋白3赖氨酸4三甲基化位点。因此，两类基因之间的大小差异表明存在转录调节范式，即调节这两组基因的转录因子的积累（仅作为随机行为的一个方面）首先积累在较大的增殖效应基因陷阱上，然后积累在细胞凋亡效应基因上积累，从而实现2种不同基因集的顺序激活。随着IRF-1和p53水平的升高，首先激活抑癌蛋白，然后激活凋亡效应基因，例如在S期暂停进行DNA修复的过程中。肿瘤抑制基因要比凋亡抑制基因大，并具有更多的IRF-1和p53结合位点，因此同样提出了基于转录因子与不同基因类别的随机相互作用进行转录测序的范例。在此报告中，我们使用ENCODE数据库确定了肿瘤抑制基因具有更多的开放染色质区域和组蛋白3赖氨酸4三甲基化位点，这与更大的基因大小可以通过包含更多的基因来促进早期转录激活的想法一致。更多的反式激活子结合位点。

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