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ATM controls DNA repair and mitochondria transfer between neighboring cells

Intercellular communication is essential for multicellular tissue vitality and homeostasis. We show that healthy cells message protective signals through direct cell–cell connections to adjacent DNA–damaged cells in a microtubule–dependent manner. In DNA–damaged cells, mitochondria restoration is fa...

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Detalles Bibliográficos
Autores principales: Jin, Sha, Cordes, Nils
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842230/
https://www.ncbi.nlm.nih.gov/pubmed/31703695
http://dx.doi.org/10.1186/s12964-019-0472-x
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author Jin, Sha
Cordes, Nils
author_facet Jin, Sha
Cordes, Nils
author_sort Jin, Sha
collection PubMed
description Intercellular communication is essential for multicellular tissue vitality and homeostasis. We show that healthy cells message protective signals through direct cell–cell connections to adjacent DNA–damaged cells in a microtubule–dependent manner. In DNA–damaged cells, mitochondria restoration is facilitated by fusion with undamaged mitochondria from healthy cells and their DNA damage repair is optimized in presence of healthy cells. Both, mitochondria transfer and intercellular signaling for an enhanced DNA damage response are critically regulated by the activity of the DNA repair protein ataxia telangiectasia mutated (ATM). These healthy–to–damaged prosurvival processes sustain normal tissue integrity and may be exploitable for overcoming resistance to therapy in diseases such as cancer.
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spelling pubmed-68422302019-11-14 ATM controls DNA repair and mitochondria transfer between neighboring cells Jin, Sha Cordes, Nils Cell Commun Signal Short Report Intercellular communication is essential for multicellular tissue vitality and homeostasis. We show that healthy cells message protective signals through direct cell–cell connections to adjacent DNA–damaged cells in a microtubule–dependent manner. In DNA–damaged cells, mitochondria restoration is facilitated by fusion with undamaged mitochondria from healthy cells and their DNA damage repair is optimized in presence of healthy cells. Both, mitochondria transfer and intercellular signaling for an enhanced DNA damage response are critically regulated by the activity of the DNA repair protein ataxia telangiectasia mutated (ATM). These healthy–to–damaged prosurvival processes sustain normal tissue integrity and may be exploitable for overcoming resistance to therapy in diseases such as cancer. BioMed Central 2019-11-08 /pmc/articles/PMC6842230/ /pubmed/31703695 http://dx.doi.org/10.1186/s12964-019-0472-x Text en © The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Jin, Sha
Cordes, Nils
ATM controls DNA repair and mitochondria transfer between neighboring cells
title ATM controls DNA repair and mitochondria transfer between neighboring cells
title_full ATM controls DNA repair and mitochondria transfer between neighboring cells
title_fullStr ATM controls DNA repair and mitochondria transfer between neighboring cells
title_full_unstemmed ATM controls DNA repair and mitochondria transfer between neighboring cells
title_short ATM controls DNA repair and mitochondria transfer between neighboring cells
title_sort atm controls dna repair and mitochondria transfer between neighboring cells
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842230/
https://www.ncbi.nlm.nih.gov/pubmed/31703695
http://dx.doi.org/10.1186/s12964-019-0472-x
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