title: Expanding Our Understanding of mtDNA Deletions.
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.
authors.affiliation: 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.
authors.forename: Martin
authors.initials: M
authors.lastname: Picard
authors.affiliation: Wellcome Trust Centre for Mitochondrial Research and Newcastle Centre for Ageing and Vitality, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne NE1 7RU, UK.
authors.forename: Amy E
authors.initials: AE
authors.lastname: Vincent
authors.affiliation: 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.
authors.forename: Doug M
authors.initials: DM
authors.lastname: Turnbull
mesh_terms: D000375:Aging / Q000235:genetics; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics*; D004272:DNA, Mitochondrial / Q000235:genetics*; D006801:Humans; D008928:Mitochondria / Q000235:genetics; D056811:Unfolded Protein Response
chemical_list: D004272:DNA, Mitochondrial