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A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress

The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved stress response pathway that is activated by vari...

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Autores principales: Demirbag-Sarikaya, Sinem, Akkoc, Yunus, Turgut, Sıla, Erbil-Bilir, Secil, Kocaturk, Nur Mehpare, Dengjel, Joern, Gozuacik, Devrim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9114114/
https://www.ncbi.nlm.nih.gov/pubmed/35581289
http://dx.doi.org/10.1038/s41598-022-11704-9
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author Demirbag-Sarikaya, Sinem
Akkoc, Yunus
Turgut, Sıla
Erbil-Bilir, Secil
Kocaturk, Nur Mehpare
Dengjel, Joern
Gozuacik, Devrim
author_facet Demirbag-Sarikaya, Sinem
Akkoc, Yunus
Turgut, Sıla
Erbil-Bilir, Secil
Kocaturk, Nur Mehpare
Dengjel, Joern
Gozuacik, Devrim
author_sort Demirbag-Sarikaya, Sinem
collection PubMed
description The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved stress response pathway that is activated by various insults including DNA damage. All sorts of damage to DNA potentially cause loss of genetic information and trigger genomic instability. Most of these lesions are repaired by the activation of DNA damage response following DNA repair mechanisms. Here we describe, a novel protein complex containing the autophagy protein ATG5 and the non-homologous end-joining repair system proteins. We discovered for the first time that ATG5 interacted with both Ku80 (XRCC5) and Ku70 (XRCC6). This novel interaction is facilitated mainly via Ku70. Our results suggest that this interaction is dynamic and enhanced upon genotoxic stresses. Strikingly, we identified that ATG5-Ku70 interaction is necessary for DNA repair and effective recovery from genotoxic stress. Therefore, our results are demonstrating a novel, direct, dynamic, and functional interaction between ATG5 and Ku70 proteins that plays a crucial role in DNA repair under genotoxic stress conditions.
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spelling pubmed-91141142022-05-19 A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress Demirbag-Sarikaya, Sinem Akkoc, Yunus Turgut, Sıla Erbil-Bilir, Secil Kocaturk, Nur Mehpare Dengjel, Joern Gozuacik, Devrim Sci Rep Article The maintenance of cellular homeostasis in living organisms requires a balance between anabolic and catabolic reactions. Macroautophagy (autophagy herein) is determined as one of the major catabolic reactions. Autophagy is an evolutionarily conserved stress response pathway that is activated by various insults including DNA damage. All sorts of damage to DNA potentially cause loss of genetic information and trigger genomic instability. Most of these lesions are repaired by the activation of DNA damage response following DNA repair mechanisms. Here we describe, a novel protein complex containing the autophagy protein ATG5 and the non-homologous end-joining repair system proteins. We discovered for the first time that ATG5 interacted with both Ku80 (XRCC5) and Ku70 (XRCC6). This novel interaction is facilitated mainly via Ku70. Our results suggest that this interaction is dynamic and enhanced upon genotoxic stresses. Strikingly, we identified that ATG5-Ku70 interaction is necessary for DNA repair and effective recovery from genotoxic stress. Therefore, our results are demonstrating a novel, direct, dynamic, and functional interaction between ATG5 and Ku70 proteins that plays a crucial role in DNA repair under genotoxic stress conditions. Nature Publishing Group UK 2022-05-17 /pmc/articles/PMC9114114/ /pubmed/35581289 http://dx.doi.org/10.1038/s41598-022-11704-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Demirbag-Sarikaya, Sinem
Akkoc, Yunus
Turgut, Sıla
Erbil-Bilir, Secil
Kocaturk, Nur Mehpare
Dengjel, Joern
Gozuacik, Devrim
A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title_full A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title_fullStr A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title_full_unstemmed A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title_short A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress
title_sort novel atg5 interaction with ku70 potentiates dna repair upon genotoxic stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9114114/
https://www.ncbi.nlm.nih.gov/pubmed/35581289
http://dx.doi.org/10.1038/s41598-022-11704-9
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