BCL6 对 Notch 依赖性转录进行调控，在左右模式形成过程中，将 Mastermind-like1 排除在某些靶基因之外。
BCL6 canalizes Notch-dependent transcription, excluding Mastermind-like1 from selected target genes during left-right patterning.
机构信息
Department of Biomedical Sciences, Florida State University, College of Medicine, Tallahassee, FL 32306, USA.
出版信息
Dev Cell. 2010 Mar 16;18(3):450-62. doi: 10.1016/j.devcel.2009.12.023.
Abstract
Although the Notch signaling pathway is one of the most intensely studied intracellular signaling pathways, the mechanisms by which Notch signaling regulates transcription remain incompletely understood. Here, we report that B cell leukemia/lymphoma 6 (BCL6), a transcriptional repressor, is a Notch-associated factor. BCL6 is necessary to maintain the expression of Pitx2 in the left lateral plate mesoderm during the patterning of left-right asymmetry in Xenopus embryos. For this process, BCL6 forms a complex with BCL6 corepressor (BCoR) on the promoters of selected Notch target genes such as enhancer of split related 1. BCL6 also inhibits the transcription of these genes by competing for the Notch1 intracellular domain, preventing the coactivator Mastermind-like1 (MAM1) from binding. These results define a mechanism restricting Notch-activated transcription to cell-type-appropriate subsets of target genes, and elucidate its relevance in vivo during left-right asymmetric development.
摘要
尽管 Notch 信号通路是研究最深入的细胞内信号通路之一，但 Notch 信号调节转录的机制仍不完全清楚。在这里，我们报告 B 细胞白血病/淋巴瘤 6（BCL6），一种转录抑制因子，是 Notch 相关因子。BCL6 对于在非洲爪蟾胚胎左右不对称模式形成过程中维持 Pitx2 在左侧侧板中胚层中的表达是必需的。对于这个过程，BCL6 在 Notch 靶基因如 Spl 相关增强子 1 的启动子上与 BCL6 核心抑制因子（BCoR）形成复合物。BCL6 还通过竞争 Notch1 细胞内结构域来抑制这些基因的转录，从而阻止辅激活因子 Mastermind 样蛋白 1（MAM1）结合。这些结果定义了一种限制 Notch 激活转录到细胞类型适当的靶基因子集的机制，并阐明了其在体内左右不对称发育过程中的相关性。
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