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首页> 外文期刊>Epigenetics & Chromatin >Rbm10 facilitates heterochromatin assembly via the Clr6 HDAC complex
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Rbm10 facilitates heterochromatin assembly via the Clr6 HDAC complex

机译：RBM10通过CLR6 HDAC络合物促进异铬胺组件

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摘要

Splicing factors have recently been shown to be involved in heterochromatin formation, but their role in controlling heterochromatin structure and function remains poorly understood. In this study, we identified a fission yeast homologue of human splicing factor RBM10, which has been linked to TARP syndrome. Overexpression of Rbm10 in fission yeast leads to strong global intron retention. Rbm10 also interacts with splicing factors in a pattern resembling that of human RBM10, suggesting that the function of Rbm10 as a splicing regulator is conserved. Surprisingly, our deep-sequencing data showed that deletion of Rbm10 caused only minor effect on genome-wide gene expression and splicing. However, the mutant displays severe heterochromatin defects. Further analyses indicated that the heterochromatin defects in the mutant did not result from mis-splicing of heterochromatin factors. Our proteomic data revealed that Rbm10 associates with the histone deacetylase Clr6 complex and chromatin remodelers known to be important for heterochromatin silencing. Deletion of Rbm10 results in significant reduction of Clr6 in heterochromatin. Our work together with previous findings further suggests that different splicing subunits may play distinct roles in heterochromatin regulation.
机译：最近已被证明剪接因子参与异染色素形成，但它们在控制异粒子结构和功能方面的作用仍然是较差的。在这项研究中，我们鉴定了人剪接因子RBM10的裂变酵母同源物，其已与Tarp综合征有关。裂变酵母中RBM10的过度表达导致强大的全球内含子保留。 RBM10还在类似于人RBM10的模式中与拼接因子相互作用，表明RBM10作为拼接调节器的功能是保守的。令人惊讶的是，我们的深度测序数据显示RBM10的缺失仅对基因组基因表达和剪接引起了微小的影响。然而，突变体显示出严重的异铬胺缺陷。进一步分析表明突变体中的异铬胺缺陷未受异铬素因子的错误剪接。我们的蛋白质组学数据显示RBM10与组蛋白脱乙酰化酶CLR6复合物和染色质重塑者已知是对异铬胺沉默的重要性。 RBM10的缺失导致异铬胺中的CLR6显着减少。我们与先前发现的工作进一步表明，不同的剪接亚基可能在异铬胺调节中起不同的作用。

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