Role of MINOS in mitochondrial membrane architecture and biogenesis
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Keywords:
MINOS
Organelle biogenesis
Background and Objectives
Mitochondrial biogenesis is a complex process involving the coordinated expression of mitochondrial and nuclear genes, the import of the products of the latter into the organelle and turnover of this process. Mitochondrial malfunction or defects in any of the many pathways involved in mitochondrial biogenesis can lead to degenerative diseases and possibly play an important part in aging.
Materials and Methods
Because of the mitochondrial relationship with some factors such as matrix proteins, cell cycle and evolution, in this review article we examined the mitochondrial relationship with these factors and mechanisms. The data were extracted from NCBI and SID databases.
Results
Changes and mutations in mitochondria are common in most of the molecular processes and important diseases including cancer, but these mutations do not result in mitochondria deactivation. Investigating these pathways helps us to identify and treat diseases such as cancer.
Conclusions
The mitochondria is the most important source of cellular energy supply, and mitochondrial damage can interfere with cellular activity and reduce the amount of energy produced and increase the production of free radicals. Mitochondria biogenesis is one of the protective methods of the cell against oxidative stress, which has a cell protective role.
Keywords:
Mitochondria , Organelle Biogenesis , DNA
Organelle
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Alternative oxidase
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Abstract Based on the observations suggesting that a digallate functionality might serve as a novel scaffold for inducers of mitochondrial biogenesis, we prepared a series of digallates and evaluated their activity in an in vitro model widely used in PD research (SH‐SY5Y cells). Flow cytometry‐based approach revealed stimulation of mitochondrial biogenesis by the gallates, particularly by those with the gallate substituted at the 1,2‐ or 1,3‐ positions. The relative mitochondrial mass calculated after taking cell sizes into account also confirmed the 1,2‐ or 1,3‐digallates as stimulators of mitochondrial biogenesis. Finally, energy sensing network including AMPK, SIRT1, and PGC‐1α was shown to be affected by 1,2‐ or 1,3‐digallates to stimulate mitochondrial biogenesis. Taken together, this study presents a 1,2‐ or 1,3‐ digallate as a novel scaffold for stimulators of mitochondrial biogenesis. As inducers of mitochondrial biogenesis remain scarce, the current findings provide a valuable tool in the battle against neurodegenerative diseases.
Organelle biogenesis
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Organelle biogenesis
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Abstract The sections in this article are Introduction Biogenesis of Prosthetic Groups Essential for Respiration Mitochondrial Respiratory Complexes Assembly Gene Expression for the Biogenesis of Mitochondrial Respiratory Complexes Mitochondria–Nucleus Cross Talk Concluding Remarks Acknowledgements
Organelle biogenesis
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Organelle biogenesis is regulated by transcriptional networks that modulate expression of specific genes encoding organellar proteins. Structural and functional specificity of organelles requires not only the transcription of specific genes and translation of resulting mRNAs, but also the transfer of encoded polypeptides to their site of function through signaling peptides. A defect in targeting of proteins to their subcellular site of function may not necessarily prevent biogenesis of the organelle, but would definitely lead to formation of a defective organelle with respect to that specific function. Several metabolic diseases are associated with dysfunction or defects in organelle biogenesis; among these, peroxisome biogenesis disorders, mitochondrial biogenesis defects and lysosomal storage disorders are an extensively studied group of genetic diseases where biogenesis of the organelle is compromised either due to a defect in assembly of the organelle itself or impaired import of matrix proteins into the organelle. Recent advances in biochemical and molecular aspects of biogenesis of subcellular organelles have not only unraveled the mechanisms for organization of cellular networks, but have also provided new insights into the development of metabolic diseases that are caused by disruption of organelle biogenesis. This article reviews the molecular mechanisms of biogenesis of mitochondria, lysosomes and peroxisomes in relation to the metabolic diseases of genetic or nongenetic origin.
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John E. Dominy and Pere Puigserver Department of Cancer Biology, Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02215 Correspondence: pere_puigserver{at}dfci.harvard.edu
Bioenergetics
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The induction of mitochondrial biogenesis could potentially alleviate mitochondrial and muscle disease. We show here that dimethyl fumarate (DMF) dose-dependently induces mitochondrial biogenesis and function dosed to cells in vitro, and also dosed in vivo to mice and humans. The induction of mitochondrial gene expression is more dependent on DMF's target Nrf2 than hydroxycarboxylic acid receptor 2 (HCAR2). Thus, DMF induces mitochondrial biogenesis primarily through its action on Nrf2, and is the first drug demonstrated to increase mitochondrial biogenesis with in vivo human dosing. This is the first demonstration that mitochondrial biogenesis is deficient in Multiple Sclerosis patients, which could have implications for MS pathophysiology and therapy. The observation that DMF stimulates mitochondrial biogenesis, gene expression and function suggests that it could be considered for mitochondrial disease therapy and/or therapy in muscle disease in which mitochondrial function is important.
Mitochondrial disease
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Branched-chain amino acids (BCAA) are essential in the diet and promote several vital cell responses which may have benefits for health and athletic performance, as well as disease prevention. While BCAA are well-known for their ability to stimulate muscle protein synthesis, their effects on cell energetics are also becoming well-documented, but these receive less attention. In this review, much of the current evidence demonstrating BCAA ability (as individual amino acids or as part of dietary mixtures) to alter regulators of cellular energetics with an emphasis on mitochondrial biogenesis and related signaling is highlighted. Several studies have shown, both in vitro and in vivo, that BCAA (either individual or as a mixture) may promote signaling associated with increased mitochondrial biogenesis including the upregulation of master regulator of mitochondrial biogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), as well as numerous downstream targets and related function. However, sparse data in humans and the difficulty of controlling variables associated with feeding studies leave the physiological relevance of these findings unclear. Future well-controlled diet studies will be needed to assess if BCAA consumption is associated with increased mitochondrial biogenesis and improved metabolic outcomes in healthy and/or diseased human populations.
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