scholarly journals Electron transport chain biogenesis activated by a JNK-insulin-Myc relay primes mitochondrial inheritance in Drosophila

2019 ◽  
Author(s):  
Zong-Heng Wang ◽  
Yi Liu ◽  
Vijender Chaitankar ◽  
Mehdi Pirooznia ◽  
Hong Xu
Keyword(s):  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Protein Import ◽  
Mitochondrial Protein ◽  
Mtdna Copy Number ◽  
Mtdna Mutation ◽  
Cellular Mechanisms ◽  
Transport Chain ◽  
Mtdna Replication

SUMMARYOogenesis features an enormous increase in mitochondrial mass and mtDNA copy number, which are required to furnish mature eggs with adequate mitochondria and to curb the transmission of deleterious mtDNA variants. Quiescent in dividing germ cells, mtDNA replication initiates upon oocyte determination in the Drosophila ovary, which necessitates active mitochondrial respiration. However, the underlying mechanism for this dynamic regulation remains unclear. Here, we show that an feedforward insulin-Myc loop promotes mitochondrial respiration and biogenesis by boosting the expression of electron transport chain subunits and factors essential for mtDNA replication and expression, and mitochondrial protein import. We further reveal that transient activation of JNK enhances the expression of insulin receptor and initiates the insulin-Myc signaling loop. Importantly, this signaling relay ensures sufficient mtDNA in eggs and limits the transmission of a deleterious mtDNA mutation. Our study demonstrates cellular mechanisms that couple mitochondrial biogenesis and inheritance with oocyte development.

scholarly journals Electron transport chain biogenesis activated by a JNK-insulin-Myc relay primes mitochondrial inheritance in Drosophila

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Zong-Heng Wang ◽  
Yi Liu ◽  
Vijender Chaitankar ◽  
Mehdi Pirooznia ◽  
Hong Xu
Keyword(s):  
Electron Transport ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Mtdna Copy Number ◽  
Cellular Mechanisms ◽  
Dynamic Regulation ◽  
Mtdna Mutations ◽  
Transport Chain ◽  
Mtdna Replication

Oogenesis features an enormous increase in mitochondrial mass and mtDNA copy number, which are required to furnish mature eggs with an adequate supply of mitochondria and to curb the transmission of deleterious mtDNA variants. Quiescent in dividing germ cells, mtDNA replication initiates upon oocyte determination in the Drosophila ovary, which necessitates active mitochondrial respiration. However, the underlying mechanism for this dynamic regulation remains unclear. Here, we show that an feedforward insulin-Myc loop promotes mitochondrial respiration and biogenesis by boosting the expression of electron transport chain subunits and of factors essential for mtDNA replication and expression, and for the import of mitochondrial proteins. We further reveal that transient activation of JNK enhances the expression of the insulin receptor and initiates the insulin-Myc signaling loop. This signaling relay promotes mitochondrial biogenesis in the ovary, and thereby plays a role in limiting the transmission of deleterious mtDNA mutations. Our study demonstrates cellular mechanisms that couple mitochondrial biogenesis and inheritance with oocyte development.

scholarly journals Age-Dependent Loss of Mitochondrial Function in Epithelial Tissue Can Be Reversed by Coenzyme Q10

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Daniel Schniertshauer ◽  
Daniel Gebhard ◽  
Jörg Bergemann
Keyword(s):  
Electron Transport ◽  
Coenzyme Q10 ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Epithelial Tissue ◽  
Atp Production ◽  
Transport Chain ◽  
Respiratory Parameters ◽  
Age Dependent ◽  
Theory Of Aging

The process of aging is characterized by the increase of age-associated disorders as well as severe diseases. Due to their role in the oxidative phosphorylation and thus the production of ATP which is crucial for many cellular processes, one reason for this could be found in the mitochondria. The accumulation of reactive oxygen species damaged mitochondrial DNA and proteins can induce mitochondrial dysfunction within the electron transport chain. According to the “mitochondrial theory of aging,” understanding the impact of harmful external influences on mitochondrial function is therefore essential for a better view on aging in general, but the measurement of mitochondrial respiration in skin cells from cell cultures cannot completely reflect the real situation in skin. Here, we describe a new method to measure the mitochondrial respiratory parameters in epithelial tissue derived from human skin biopsies using a XF24 extracellular flux analyzer to evaluate the effect of coenzyme Q10. We observed a decrease in mitochondrial respiration and ATP production with donor age corresponding to the “mitochondrial theory of aging.” For the first time ex vivo in human epidermis, we could show also a regeneration of mitochondrial respiratory parameters if the reduced form of coenzyme Q10, ubiquinol, was administered. In conclusion, an age-related decrease in mitochondrial respiration and ATP production was confirmed. Likewise, an increase in the respiratory parameters by the addition of coenzyme Q10 could also be shown. The fact that there is a significant effect of administered coenzyme Q10 on the respiratory parameters leads to the assumption that this is mainly caused by an increase in the electron transport chain. This method offers the possibility of testing age-dependent effects of various substances and their influence on the mitochondrial respiration parameters in human epithelial tissue.

scholarly journals Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise

2007 ◽  
Vol 102 (5) ◽  
pp. 1844-1849 ◽  
Author(s):  
Maria Fernström ◽  
Linda Bakkman ◽  
Michail Tonkonogi ◽  
Irina G. Shabalina ◽  
Zinaida Rozhdestvenskaya ◽  
...  
Keyword(s):  
Electron Transport ◽  
Electron Transport Chain ◽  
Uncoupling Protein ◽  
Mitochondrial Protein ◽  
Oxygen Demand ◽  
Atp Synthesis ◽  
Whole Body ◽  
Palmitoyl Carnitine ◽  
Transport Chain ◽  
Mitochondrial Efficiency

The hypothesis that ultraendurance exercise influences muscle mitochondrial function has been investigated. Athletes in ultraendurance performance performed running, kayaking, and cycling at 60% of their peak O2 consumption for 24 h. Muscle biopsies were taken preexercise (Pre-Ex), postexercise (Post-Ex), and after 28 h of recovery (Rec). Respiration was analyzed in isolated mitochondria during state 3 (coupled to ATP synthesis) and state 4 (noncoupled respiration), with fatty acids alone [palmitoyl carnitine (PC)] or together with pyruvate (Pyr). Electron transport chain activity was measured with NADH in permeabilized mitochondria. State 3 respiration with PC increased Post-Ex by 39 and 41% ( P < 0.05) when related to mitochondrial protein and to electron transport chain activity, respectively. State 3 respiration with Pyr was not changed ( P > 0.05). State 4 respiration with PC increased Post-Ex but was lower than Pre-Ex at Rec ( P < 0.05 vs. Pre-Ex). Mitochondrial efficiency [amount of added ADP divided by oxygen consumed during state 3 (P/O ratio)] decreased Post-Ex by 9 and 6% ( P < 0.05) with PC and PC + Pyr, respectively. P/O ratio remained reduced at Rec. Muscle uncoupling protein 3, measured with Western blotting, was not changed Post-Ex but tended to decrease at Rec ( P = 0.07 vs. Pre-Ex). In conclusion, extreme endurance exercise decreases mitochondrial efficiency. This will increase oxygen demand and may partly explain the observed elevation in whole body oxygen consumption during standardized exercise (+13%). The increased mitochondrial capacity for PC oxidation indicates plasticity in substrate oxidation at the mitochondrial level, which may be of advantage during prolonged exercise.

Method for recovering ATP content and mitochondrial function after chemical anoxia in renal cell cultures

1994 ◽  
Vol 266 (6) ◽  
pp. C1803-C1811 ◽  
Author(s):  
R. B. Doctor ◽  
R. Bacallao ◽  
L. J. Mandel
Keyword(s):  
Electron Transport ◽  
Oxidative Metabolism ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Cultured Cells ◽  
Good Method ◽  
Complete Recovery ◽  
Specific Method ◽  
Cellular Effects ◽  
Transport Chain

Cultured renal cells provide a highly reproducible and malleable model to study cellular responses to metabolic perturbations. Nevertheless, there is currently no good method to achieve metabolic inhibition and complete recovery in cultured cells. This study describes a specific method for reversibly inhibiting both glycolytic and oxidative metabolism. Glycolysis was inhibited by removing all glycolytic substrates, and mitochondrial respiration was inhibited with rotenone, a site I inhibitor of the electron transport chain. Within 30 min, ATP values were decreased by 98%. Glycolysis was restored through the reintroduction of glucose. Oxidative metabolism was restored by the addition of heptanoate, a short odd-chain fatty acid, which supplies reducing equivalents to site II of the electron transport chain. Employing Madin-Darby canine kidney and LLC-PK1 cell lines, this protocol caused the immediate and complete recovery of mitochondrial respiration and, by 60 min, the complete recovery of cellular ATP levels. Application of this protocol should allow the investigation of the cellular effects and alterations that occur within cells recovering from sublethal energy depletion.

scholarly journals FOXM1 nuclear transcription factor translocates into mitochondria and inhibits oxidative phosphorylation

2020 ◽  
Vol 31 (13) ◽  
pp. 1411-1424
Author(s):  
Markaisa Black ◽  
Paritha Arumugam ◽  
Samriddhi Shukla ◽  
Arun Pradhan ◽  
Vladimir Ustiyan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Membrane Potential ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Nuclear Transcription Factor ◽  
Transport Chain

It was found that the transcription factor FOXM1 translocates into mitochondria and inhibits mitochondrial respiration and membrane potential, directly binds to mitochondrial PTCD1, and inhibits the electron transport chain by stabilizing PTCD1.

scholarly journals Higher Mitochondrial Respiration and Uncoupling with Reduced Electron Transport Chain Contentin Vivoin Muscle of Sedentary Versus Active Subjects

2013 ◽  
Vol 98 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Kevin E. Conley ◽  
Catherine E. Amara ◽  
Sudip Bajpeyi ◽  
Sheila R. Costford ◽  
Kori Murray ◽  
...  
Keyword(s):  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Transport Chain
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