Expanding Our Understanding of mtDNA Deletions

Martin Picard¹, Amy E Vincent², Doug M Turnbull³

Affiliations

¹ Department of Psychiatry, Division of Behavioral Medicine, Columbia University Medical Center, New York, NY 10032, USA; Department of Neurology and Columbia Translational Neuroscience Initiative, H. Houston Merritt Center, Columbia University Medical Center, New York, NY 10032, USA; Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
² Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
³ Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK. Electronic address: doug.turnbull@newcastle.ac.uk.

PMID: 27411002
DOI: 10.1016/j.cmet.2016.06.024

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Expanding Our Understanding of mtDNA Deletions

Martin Picard et al. Cell Metab. 2016.

Free article

. 2016 Jul 12;24(1):3-4.

doi: 10.1016/j.cmet.2016.06.024.

Authors

Martin Picard¹, Amy E Vincent², Doug M Turnbull³

Affiliations

¹ Department of Psychiatry, Division of Behavioral Medicine, Columbia University Medical Center, New York, NY 10032, USA; Department of Neurology and Columbia Translational Neuroscience Initiative, H. Houston Merritt Center, Columbia University Medical Center, New York, NY 10032, USA; Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
² Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
³ Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK. Electronic address: doug.turnbull@newcastle.ac.uk.

PMID: 27411002
DOI: 10.1016/j.cmet.2016.06.024

Abstract

Clonal expansion of mtDNA deletions compromises mitochondrial function in human disease and aging, but how deleterious mtDNA genomes propagate has remained unclear. In this issue (Gitschlag et al., 2016) and in a recent Nature publication, C. elegans studies implicate the mitochondrial unfolded protein response (UPR(mt)) and offer mechanistic insights into this process.

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Homeostatic Responses Regulate Selfish Mitochondrial Genome Dynamics in C. elegans.
Gitschlag BL, Kirby CS, Samuels DC, Gangula RD, Mallal SA, Patel MR. Gitschlag BL, et al. Cell Metab. 2016 Jul 12;24(1):91-103. doi: 10.1016/j.cmet.2016.06.008. Cell Metab. 2016. PMID: 27411011 Free PMC article.

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Expanding Our Understanding of mtDNA Deletions

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