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首页> 外文期刊>Epigenetics & Chromatin >SUMOylated non-canonical polycomb PRC1.6 complex as a prerequisite for recruitment of transcription factor RBPJ
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SUMOylated non-canonical polycomb PRC1.6 complex as a prerequisite for recruitment of transcription factor RBPJ

机译：雄性为非规范的polycomb prc1.6复合体作为转录因子RBPJ募集的先决条件

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摘要

Notch signaling controls cell fate decisions in many contexts during development and adult stem cell homeostasis and, when dysregulated, leads to carcinogenesis. The central transcription factor RBPJ assembles the Notch coactivator complex in the presence of Notch signaling, and represses Notch target gene expression in its absence. We identified L3MBTL2 and additional members of the non-canonical polycomb repressive PRC1.6 complex in DNA-bound RBPJ associated complexes and demonstrate that L3MBTL2 directly interacts with RBPJ. Depletion of RBPJ does not affect occupancy of PRC1.6 components at Notch target genes. Conversely, absence of L3MBTL2 reduces RBPJ occupancy at enhancers of Notch target genes. Since L3MBTL2 and additional members of the PRC1.6 are known to be SUMOylated, we investigated whether RBPJ uses SUMO-moieties as contact points. Indeed, we found that RBPJ binds to SUMO2/3 and that this interaction depends on a defined SUMO-interaction motif. Furthermore, we show that pharmacological inhibition of SUMOylation reduces RBPJ occupancy at Notch target genes. We propose that the PRC1.6 complex and its conjugated SUMO-modifications provide a favorable environment for binding of RBPJ to Notch target genes.
机译：Notch信号传导控制在发育和成人干细胞稳态期间的许多背景下的细胞命运决策，并且在疑虑的情况下导致致癌作用。中央转录因子RBPJ在陷波信号传导的存在下组装Notch CaCtivator综合体，并在不存在中抑制缺口靶基因表达。我们在DNA结合的RBPJ相关复合物中鉴定了L3MBTL2和非规范多元粒压抑PRC1.6复合物的附加成员，并证明L3MBTL2直接与RBPJ相互作用。 RBPJ的耗竭不会影响Notch靶基因的PRC1.6组分的占用。相反，没有L3MBT12减少了Notch靶基因增强剂的RBPJ占用。由于L3MBTL2和PRC1.6的其他成员尤其是友好的，因此我们调查了RBPJ是否使用Sumo-Moieties作为接触点。实际上，我们发现RBPJ绑定到SUMO2 / 3，并且该交互取决于定义的SUMO-Interaction主题。此外，我们表明Suboylation的药理学抑制在陷波靶基因下降低了RBPJ占用。我们提出了PRC1.6复合物及其共轭的SUMO-修饰为RBPJ结合到Notch靶基因提供了有利的环境。

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