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首页> 外文期刊>Cell cycle >Involvement of matrin 3 and SFPQ/NONO in the DNA damage response.
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Involvement of matrin 3 and SFPQ/NONO in the DNA damage response.

机译：Matrin 3和SFPQ / NONO参与DNA损伤反应。

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The DNA damage response (DDR) is a complex signaling network that is induced by DNA lesions and vigorously activated by double strand breaks (DSBs). The DSB response is mobilized by the nuclear protein kinase ATM, which phosphorylates key players in its various branches. SFPQ (PSF) and NONO (p54) are nuclear proteins that interact with each other and have diverse roles in nucleic acids metabolism. The SFPQ/NONO heterodimer was previously found to enhance DNA strand break rejoining in vitro. Our attention was drawn to these two proteins as they interact with the nuclear matrix protein Matrin 3 (MATR3), which we found to be a novel ATM target. We asked whether SFPQ and NONO too are involved in the DSB response. Proteins that function at the early phase of this response are often recruited to the damaged sites. We observed rapid recruitment of SFPQ/NONO to sites of DNA damage induced by laser microbeam. In MATR3 knockdown cells SFPQ/NONO retention at DNA damage sites was prolonged. SFPQ and MATR3 depletion led to abnormal accumulation of cells at the S-phase of the cell cycle following treatment with the radiomimetic chemical neocarzinostatin. Notably, proteins involved in DSB repair via nonhomologous end-joining co-immunoprecipitated with NONO; SFPQ depletion delayed DSB repair. Collectively the data suggest that SFPQ, NONO and MATR3 are involved in the early stage of the DSB response, setting the scene for DSB repair.
机译：DNA损伤反应（DDR）是一个复杂的信号网络，由DNA损伤诱导并由双链断裂（DSB）强烈激活。 DSB反应由核蛋白激酶ATM动员，该蛋白磷酸化其各个分支中的关键分子。 SFPQ（PSF）和NONO（p54）是相互相互作用的核蛋白，在核酸代谢中具有多种作用。先前发现SFPQ / NONO异二聚体可增强DNA链断裂在体外的重新结合。我们注意到这两种蛋白质与核基质蛋白Matrin 3（MATR3）相互作用，我们发现这是一种新型的ATM靶标。我们询问了DSB响应中是否也涉及SFPQ和NONO。在此反应早期阶段起作用的蛋白质通常被募集到受损部位。我们观察到SFPQ / NONO快速募集到激光微束诱导的DNA损伤部位。在MATR3组合式细胞中，SFPQ / NONO在DNA损伤部位的保留时间延长。 SFPQ和MATR3耗竭导致在用放射模拟化学新碳素抑制素处理后，在细胞周期的S期细胞异常蓄积。值得注意的是，通过与NONO共免疫沉淀的非同源末端连接参与DSB修复的蛋白质; SFPQ耗尽会延迟DSB修复。总体而言，数据表明SFPQ，NONO和MATR3参与了DSB响应的早期阶段，从而为DSB修复奠定了基础。

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