Circadian control of oscillations in mitochondrial rate-limiting enzymes and nutrient utilization by PERIOD proteins
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Circadian control of oscillations in mitochondrial rate-limiting enzymes and nutrient utilization by PERIOD proteins. / Neufeld-Cohen, Adi; Robles, Maria S; Aviram, Rona; Manella, Gal; Adamovich, Yaarit; Ladeuix, Benjamin; Nir, Dana; Rousso-Noori, Liat; Kuperman, Yael; Golik, Marina; Mann, Matthias; Asher, Gad.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 113, No. 12, 22.03.2016, p. E1673-82.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Circadian control of oscillations in mitochondrial rate-limiting enzymes and nutrient utilization by PERIOD proteins
AU - Neufeld-Cohen, Adi
AU - Robles, Maria S
AU - Aviram, Rona
AU - Manella, Gal
AU - Adamovich, Yaarit
AU - Ladeuix, Benjamin
AU - Nir, Dana
AU - Rousso-Noori, Liat
AU - Kuperman, Yael
AU - Golik, Marina
AU - Mann, Matthias
AU - Asher, Gad
PY - 2016/3/22
Y1 - 2016/3/22
N2 - Mitochondria are major suppliers of cellular energy through nutrients oxidation. Little is known about the mechanisms that enable mitochondria to cope with changes in nutrient supply and energy demand that naturally occur throughout the day. To address this question, we applied MS-based quantitative proteomics on isolated mitochondria from mice killed throughout the day and identified extensive oscillations in the mitochondrial proteome. Remarkably, the majority of cycling mitochondrial proteins peaked during the early light phase. We found that rate-limiting mitochondrial enzymes that process lipids and carbohydrates accumulate in a diurnal manner and are dependent on the clock proteins PER1/2. In this conjuncture, we uncovered daily oscillations in mitochondrial respiration that peak during different times of the day in response to different nutrients. Notably, the diurnal regulation of mitochondrial respiration was blunted in mice lacking PER1/2 or on a high-fat diet. We propose that PERIOD proteins optimize mitochondrial metabolism to daily changes in energy supply/demand and thereby, serve as a rheostat for mitochondrial nutrient utilization.
AB - Mitochondria are major suppliers of cellular energy through nutrients oxidation. Little is known about the mechanisms that enable mitochondria to cope with changes in nutrient supply and energy demand that naturally occur throughout the day. To address this question, we applied MS-based quantitative proteomics on isolated mitochondria from mice killed throughout the day and identified extensive oscillations in the mitochondrial proteome. Remarkably, the majority of cycling mitochondrial proteins peaked during the early light phase. We found that rate-limiting mitochondrial enzymes that process lipids and carbohydrates accumulate in a diurnal manner and are dependent on the clock proteins PER1/2. In this conjuncture, we uncovered daily oscillations in mitochondrial respiration that peak during different times of the day in response to different nutrients. Notably, the diurnal regulation of mitochondrial respiration was blunted in mice lacking PER1/2 or on a high-fat diet. We propose that PERIOD proteins optimize mitochondrial metabolism to daily changes in energy supply/demand and thereby, serve as a rheostat for mitochondrial nutrient utilization.
KW - Animals
KW - Circadian Rhythm
KW - Citric Acid Cycle
KW - Diet, High-Fat
KW - Dietary Fats
KW - Electron Transport
KW - Fatty Acids
KW - Feeding Behavior
KW - Gene Expression Profiling
KW - Male
KW - Mice
KW - Mice, Knockout
KW - Mitochondria, Liver
KW - Mitochondrial Proteins
KW - Motor Activity
KW - Period Circadian Proteins
KW - Proteome
KW - RNA, Messenger
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1073/pnas.1519650113
DO - 10.1073/pnas.1519650113
M3 - Journal article
C2 - 26862173
VL - 113
SP - E1673-82
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 12
ER -
ID: 186877445