Edit Abstract: Trudeau 2014 Abstract MiP2014

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Abstract:	Mitochondrial fusion and fission have been shown to allow for the equilibration of protein across the mitochondrial population as well as coordinate autophagy-mediated removal of defective mitochondria [1]. We hypothesized that mitochondrial fusion is serving a role in shuttling newly synthesized proteins from a subset of mitochondria that import them to the rest of the mitochondrial population, thereby determining distribution of young and old protein within the network. We assessed mitochondrial protein age by targeting a time-sensitive fluorescent protein, MitoTimer, to the mitochondrial matrix. Emitted fluorescence of a newly translated timer is green and over time the emission shifts to red [2]. We fused the fluorescent timer to the mitochondrial targeting sequence of the Cox8a subunit, to form the MitoTimer construct. Mitochondrial protein age, a result of equilibrated young and old proteins, was dependent on turnover rates as pulsed synthesis or autophagic inhibition increased the proportion of old MitoTimer protein. Mitochondrial fusion promotes the distribution of young mitochondrial protein across the mitochondrial network as cells lacking essential fusion genes Mfn1 and Mfn2, or down-regulated Opa1, displayed increased heterogeneity in mitochondrial protein age and accumulation of mitochondria with old protein. Experiments in hippocampal neurons illustrate that intracellular spatial organization also impairs distribution of young mitochondrial material and this effect was reduced by over-expression of mitochondrial transport protein, Miro1. Collectively our data show that equilibration of young and old protein in the mitochondrial network is dependent on mitochondrial turnover, fusion, and transport.
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MiP areas:	Gender Respiration Instruments;methods mt-Biogenesis;mt-density mt-Structure;fission;fusion mt-Membrane mtDNA;mt-genetics nDNA;cell genetics Genetic knockout;overexpression Comparative MiP;environmental MiP Developmental biology Exercise physiology;nutrition;life style mt-Medicine Patients Pharmacology;toxicology mt-Awareness
Pathological states:	COPD Aging;senescence Alzheimer's Autism Cancer Cardiovascular Diabetes Inherited Infectious Myopathy Neurodegenerative Obesity Parkinson's Sepsis Other
Stress conditions:	Hypoxia Cell death Cryopreservation Ischemia-reperfusion Permeability transition Oxidative stress;RONS Temperature Mitochondrial disease
Organism:	Pig Human Mouse Rat Guinea pig Bovines Horse Dog Rabbit Cat Other mammals Chicken Zebrafish Drosophila Artemia Caenorhabditis elegans Saccharomyces cerevisiae Birds Reptiles Amphibians Fishes Chelicerates Crustaceans Hexapods Myriapods Annelids Molluscs Nematodes Other invertebrates Fungi Plants Protists Eubacteria Archea Algae
Tissues;cells:	Fat Heart Skeletal muscle Nervous system Liver Kidney Lung;gill Islet cell;pancreas;thymus Endothelial;epithelial;mesothelial cell Blood cells Genital Other cell lines CHO HEK HeLa Neuroblastoma Fibroblast HUVEC Macrophage-derived Lymphocyte Platelet Stem cells
Preparations:	SMP Intact organism Intact organ Permeabilized cells Permeabilized tissue Homogenate Isolated mitochondria Chloroplasts Enzyme Oxidase;biochemical oxidation Intact cells
Enzymes:	Complex I Adenine nucleotide translocase Complex II;succinate dehydrogenase Complex III Complex IV;cytochrome c oxidase Complex V;ATP synthase Inner mt-membrane transporter Marker enzyme Supercomplex TCA cycle and matrix dehydrogenases Uncoupling protein
Regulation:	pH Aerobic glycolysis ADP ATP ATP production AMP Calcium Coupling efficiency;uncoupling Cyt c Flux control Inhibitor Ion;substrate transport mt-Membrane potential Oxygen kinetics PCr;Cr Phosphate Redox state Substrate Temperature Threshold;excess capacity Uncoupler Fatty acid Amino acid Q-junction effect
Coupling:	ET LEAK ROUTINE OXPHOS
Pathways:	F N S Gp DQ CIV NS Other combinations ROX
High-resolution respirometry:	pH Oxygraph-2k TIP2k O2k-Fluorometer NO TPP Ca O2k-Spectrophotometer O2k-Manual O2k-Protocol Theory NextGen-O2k
Event:	A1 A2 A3 A4 B1 B2 B3 B4 C1 C2 C3 C4 D1 D2 D3 D4 E1 E2 Oral Poster P-flash Review
Additional labels:	(separate values by colon)

Free text: Any additional information (e.g. affiliations of authors). == Affiliation == 1-Dep Medicine, Obesity Nutrition Section, Evans Biomed Research Center, Boston Univ School Med, MA, USA; 2-Donald P. Shiley Biosc Center, San Diego State Univ, CA, USA. - kmtru@bu.edu == References and acknowledgements == Supported by: National Science Foundation Graduate Research Fellowship. # Twig G, Elorza A, Molina AJ, Mohamed H, Wikstrom JD, Walzer G, Stiles L, Haigh SE, Katz S, Las G, Alroy J, Wu M, Py BF, Yuan J, Deeney JT, Corkey BE, Shirihai OS (2008) Fission and selective fusion govern mitochondrial segregation and elimination by autophagy. EMBO J 27: 433-46. # Terskikh A, Fradkov A, Ermakova G, Zaraisky A, Tan P, Kajava AV, Zhao X, Lukyanov S, Matz M, Kim S, Weissman I, Siebert P (2000) 'Fluorescent timer': protein that changes color with time. Science 290: 1585-8.

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