Institute of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.
PLoS One. 2022 May 5;17(5):e0267615. doi: 10.1371/journal.pone.0267615. eCollection 2022.
DNA double-strand breaks are one of the most deleterious lesions for the cells, therefore understanding the macromolecular interactions of the DNA repair-related mechanisms is essential. DNA damage triggers transcription silencing at the damage site, leading to the removal of the elongating RNA polymerase II (S2P RNAPII) from this locus, which provides accessibility for the repair factors to the lesion. We previously demonstrated that following transcription block, p53 plays a pivotal role in transcription elongation by interacting with S2P RNAPII. In the current study, we reveal that p53 is involved in the fine-tune regulation of S2P RNAPII ubiquitylation. Furthermore, we emphasize the potential role of p53 in delaying the premature ubiquitylation and the subsequent chromatin removal of S2P RNAPII as a response to transcription block.
DNA 双链断裂是细胞中最具危害性的损伤之一，因此理解与 DNA 修复相关机制的大分子相互作用至关重要。DNA 损伤会在损伤部位触发转录沉默，导致延伸中的 RNA 聚合酶 II（S2P RNAPII）从该基因座上脱离，从而为修复因子接近损伤部位提供了便利。我们之前的研究表明，在转录受阻后，p53 通过与 S2P RNAPII 相互作用，在转录延伸中发挥关键作用。在本研究中，我们揭示了 p53 参与了 S2P RNAPII 泛素化的精细调控。此外，我们强调了 p53 在延迟 S2P RNAPII 的过早泛素化和随后的染色质去除方面的潜在作用，这是对转录受阻的一种响应。
