Repair of ribosomal DNA (rDNA) is a very important nuclear process due to the most active transcription of ribosomal genes. Proper repair of rDNA is required for physiological biogenesis of ribosomes. Here, we analyzed the epigenetics of the DNA damage response in a nucleolar compartment, thus in the ribosomal genes studied in nonirradiated and UVA-irradiated mouse embryonic fibroblasts (MEFs). We found that the promoter of ribosomal genes is not abundant on H4K20me2, but it is densely occupied by H4K20me3. Ribosomal genes, regulated via UBF1/2 proteins, were characterized by an interaction between UBF1/2 and H4K20me2/me3. This interaction was strengthened by UVA irradiation that additionally causes a focal accumulation of H4K20me3 in the nucleolus. No interaction has been found between UBF1/2 and H3K9me3. Interestingly, UVA irradiation decreases the levels of H3K9me3 and H4K20me3 at 28S rDNA. Altogether, the UVA light affects the epigenetic status of ribosomal genes at 28S rDNA and strengthens an interaction between UBF1/2 proteins and H4K20me2/me3.

中文翻译：

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UVA辐射增强了UBF1 / 2蛋白与H4K20二甲基/三甲基化之间的相互作用。

由于核糖体基因的最活跃转录，核糖体DNA（rDNA）的修复是一个非常重要的核过程。核糖体的生理生物发生需要正确修复rDNA。在这里，我们分析了在核仁区室中DNA损伤反应的表观遗传学，因此在非辐照和UVA辐照的小鼠胚胎成纤维细胞（MEF）中研究了核糖体基因。我们发现核糖体基因的启动子在H4K20me2上并不丰富，但被H4K20me3密集地占据。通过UBF1 / 2蛋白调节的核糖体基因的特征在于UBF1 / 2与H4K20me2 / me3之间的相互作用。UVA辐照增强了这种相互作用，UVA辐照另外引起了H4K20me3在核仁中的聚集。在UBF1 / 2和H3K9me3之间未发现相互作用。有趣的是 UVA辐照降低28S rDNA时H3K9me3和H4K20me3的水平。总之，UVA光线会影响28S rDNA上核糖体基因的表观遗传状态，并增强UBF1 / 2蛋白与H4K20me2 / me3之间的相互作用。