The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII

Barbara N Borsos; Vasiliki Pantazi; Zoltán G Páhi; Hajnalka Majoros; Zsuzsanna Ujfaludi; Ivett Berzsenyi; Tibor Pankotai

doi:10.1371/journal.pone.0267615

The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII

PLoS One. 2022 May 5;17(5):e0267615. doi: 10.1371/journal.pone.0267615. eCollection 2022.

Authors

Barbara N Borsos¹, Vasiliki Pantazi¹, Zoltán G Páhi¹, Hajnalka Majoros¹, Zsuzsanna Ujfaludi¹, Ivett Berzsenyi¹, Tibor Pankotai¹

Affiliation

¹ Institute of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.

Abstract

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

DNA Damage
DNA Repair
RNA Polymerase II* / metabolism
Transcription, Genetic
Tumor Suppressor Protein p53* / genetics
Ubiquitination

Substances

Tumor Suppressor Protein p53
RNA Polymerase II

Grants and funding

This research was funded by National Research, Development and Innovation Office grant GINOP-2.2.1-15-2017-00052, and NKFI-FK 132080. I.B. was funded by EFOP 3.6.3-VEKOP-16-2017-00009. T.P. was funded by National Research, Development and Innovation Office grant GINOP-2.2.1-15-2017-00052, the János Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/27/20, EMMI UNKP-20-5-SZTE-265 and UNKP-21-5-SZTE-563. B.N.B. was funded by NKFI-FK 132080, NTP-NFTÖ-21-B-0043, and EMBO short-term fellowship 8513. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.