Expanding Our Understanding of mtDNA Deletions

Martin Picard; Amy E Vincent; Doug M Turnbull

doi:10.1016/j.cmet.2016.06.024

Expanding Our Understanding of mtDNA Deletions

Cell Metab. 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: [email protected].

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.

Publication types

Comment

MeSH terms

Aging / genetics
Animals
Caenorhabditis elegans / genetics*
DNA, Mitochondrial / genetics*
Humans
Mitochondria / genetics
Unfolded Protein Response

Substances

DNA, Mitochondrial

Abstract

Publication types

MeSH terms

Substances

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