BCL6 canalizes Notch-dependent transcription, excluding Mastermind-like1 from selected target genes during left-right patterning.
BCL6 canalizes Notch-dependent transcription, excluding Mastermind-like1 from selected target genes during left-right patterning.
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DOI：
10.1016/j.devcel.2009.12.023
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发表时间：
2010-03-16
影响因子：
11.8
通讯作者：
Kato Y
中科院分区：
文献类型：
--
作者：
Sakano D;Kato A;Parikh N;McKnight K;Terry D;Stefanovic B;Kato Y
虽然Notch信号传导途径是研究最深入的细胞内信号传导途径之一，但Notch信号传导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（BCL 6），转录抑制因子，是一个Notch相关因子。BCL 6是维持Pitx 2在非洲爪蟾胚胎左右不对称模式形成过程中在左侧板中胚层中表达所必需的。对于该过程，BCL 6与选定的Notch靶基因（例如分裂相关增强子1）的启动子上的BCL 6共阻遏物（BCoR）形成复合物。BCL 6还通过竞争Notch 1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-like 1（MAM 1）的结合。这些结果定义了一种机制，限制刻缺蛋白激活转录的细胞类型适当的子集的靶基因，并阐明其在体内的相关性，在左右不对称的发展。
While 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 co-repressor (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 co-activator 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.
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