DNA damage invokes mitophagy through a pathway involving Spata18

Abstract Mitochondria are vital for cellular energy supply and intracellular signaling after stress. Here, we aimed to investigate how mitochondria respond to acute DNA damage with respect to mitophagy, which is an important mitochondrial quality control process. Our results show that mitophagy incr...

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Bibliographic Details
Published in:Nucleic acids research 2020-07, Vol.48 (12), p.6611-6623
Main Authors: Dan, Xiuli, Babbar, Mansi, Moore, Anthony, Wechter, Noah, Tian, Jingyan, Mohanty, Joy G, Croteau, Deborah L, Bohr, Vilhelm A
Format: Article
Language:English
Subjects:
Animals
Caenorhabditis elegans - genetics
Calcium - metabolism
Cell Line
Cell Proliferation - genetics
DNA Damage - genetics
DNA Repair - genetics
Fibroblasts - metabolism
Genome Integrity, Repair and
Humans
Mice
Mitochondria - genetics
Mitochondrial Proteins - genetics
Mitophagy - genetics
Neurons - metabolism
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Summary:Abstract Mitochondria are vital for cellular energy supply and intracellular signaling after stress. Here, we aimed to investigate how mitochondria respond to acute DNA damage with respect to mitophagy, which is an important mitochondrial quality control process. Our results show that mitophagy increases after DNA damage in primary fibroblasts, murine neurons and Caenorhabditis elegans neurons. Our results indicate that modulation of mitophagy after DNA damage is independent of the type of DNA damage stimuli used and that the protein Spata18 is an important player in this process. Knockdown of Spata18 suppresses mitophagy, disturbs mitochondrial Ca2+ homeostasis, affects ATP production, and attenuates DNA repair. Importantly, mitophagy after DNA damage is a vital cellular response to maintain mitochondrial functions and DNA repair.
ISSN:0305-1048
1362-4962
DOI:10.1093/nar/gkaa393