The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII.
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 poly...
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Format: | Article |
Language: | English |
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Public Library of Science (PLoS)
2022-01-01
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Series: | PLoS ONE |
Online Access: | https://doi.org/10.1371/journal.pone.0267615 |
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author | Barbara N Borsos Vasiliki Pantazi Zoltán G Páhi Hajnalka Majoros Zsuzsanna Ujfaludi Ivett Berzsenyi Tibor Pankotai |
author_facet | Barbara N Borsos Vasiliki Pantazi Zoltán G Páhi Hajnalka Majoros Zsuzsanna Ujfaludi Ivett Berzsenyi Tibor Pankotai |
author_sort | Barbara N Borsos |
collection | DOAJ |
description | 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. |
first_indexed | 2024-12-10T09:50:11Z |
format | Article |
id | doaj.art-4bf93282b3b648659a565bc9f9956c02 |
institution | Directory Open Access Journal |
issn | 1932-6203 |
language | English |
last_indexed | 2024-12-10T09:50:11Z |
publishDate | 2022-01-01 |
publisher | Public Library of Science (PLoS) |
record_format | Article |
series | PLoS ONE |
spelling | doaj.art-4bf93282b3b648659a565bc9f9956c022022-12-22T01:53:41ZengPublic Library of Science (PLoS)PLoS ONE1932-62032022-01-01175e026761510.1371/journal.pone.0267615The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII.Barbara N BorsosVasiliki PantaziZoltán G PáhiHajnalka MajorosZsuzsanna UjfaludiIvett BerzsenyiTibor PankotaiDNA 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.https://doi.org/10.1371/journal.pone.0267615 |
spellingShingle | Barbara N Borsos Vasiliki Pantazi Zoltán G Páhi Hajnalka Majoros Zsuzsanna Ujfaludi Ivett Berzsenyi Tibor Pankotai The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. PLoS ONE |
title | The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. |
title_full | The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. |
title_fullStr | The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. |
title_full_unstemmed | The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. |
title_short | The role of p53 in the DNA damage-related ubiquitylation of S2P RNAPII. |
title_sort | role of p53 in the dna damage related ubiquitylation of s2p rnapii |
url | https://doi.org/10.1371/journal.pone.0267615 |
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