The Complex Dance of Organelles during Mitochondrial Division

Tábara, Luis-Carlos; Morris, James B.; Prudent, Julien

doi:10.1016/j.tcb.2020.12.005

Cited by 47 publications

(33 citation statements)

References 101 publications

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“…These are essential for maintaining mitochondrial quality. Mitochondrial fusion provides placement for metabolic reactions, material synthesis, and content exchange, while fission is vital for mitochondrial autophagy and updates 17,18 . In the cell cycle, mitochondria fuse into a tubular formation at the G1‐S phase and induce cell cycle‐related protein changes via an unknown mechanism 19 .…”

Section: Introductionmentioning

confidence: 99%

“…Mitochondrial fusion provides placement for metabolic reactions, material synthesis, and content exchange, while fission is vital for mitochondrial autophagy and updates. 17 , 18 In the cell cycle, mitochondria fuse into a tubular formation at the G1‐S phase and induce cell cycle‐related protein changes via an unknown mechanism. 19 Therefore, we hypothesized the presence of some essential communication between the mitochondrial dynamics and the cell cycle.…”

Section: Introductionmentioning

confidence: 99%

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Non‐metabolic function of MTHFD2 activates CDK2 in bladder cancer

Liu

Piao

et al. 2021

Cancer Science

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Bladder cancer is a common tumor with a high recurrence rate and high fatality rate, and its mechanism of occurrence and development remains unclear. Many proteins and metabolites reprogram at different stages of tumor development to support tumor cell growth. The moonlighting effect happens when a protein performs multiple functions simultaneously in a cell. In this study, we identified a metabolic protein, MTHFD2, which participates in the cell cycle by binding to CDK2 in bladder cancer. MTHFD2 has been shown to affect bladder cancer cell growth, which is independent of its metabolic function. We found that MTHFD2 was involved in cell cycle regulation and could encourage cell cycle progression by activating CDK2 and sequentially affecting E2F1 activation. In addition, moonlighting MTHFD2 might be regulated by the dynamics of the mitochondria. In conclusion, MTHFD2 localizes in the nucleus to perform a distinct function of catalyzing metabolic reactions. Moreover, the nuclear MTHFD2 activates CDK2 and promotes bladder cancer cell growth by modulating the cell cycle.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Non‐metabolic function of MTHFD2 activates CDK2 in bladder cancer

Liu

Piao

et al. 2021

Cancer Science

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“…In contrast, mitochondrial fusion is the union of two mitochondria forming a large new mitochondrion. This is generally regulated by mitofusin‐1 (MFN1), mitofusin‐2 (MFN2), and optic atrophy 1 (OPA1), three GTPase‐dependent proteins in the dynamin superfamily 86,89,90 . The balance between fission and fusion is crucial to ensure a steady energy supply and cellular homeostasis.…”

Section: Melatonin: a Possible New Role In Mscs Communication?mentioning

confidence: 99%

Tunneling nanotubes and mesenchymal stem cells: New insights into the role of melatonin in neuronal recovery

Luchetti

Carloni

Nasoni

et al. 2022

Journal of Pineal Research

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Efficient cell-to-cell communication is essential for tissue development, homeostasis, and the maintenance of cellular functions after injury. Tunneling nanotubes (TNTs) have emerged as a new important method of cell-to-cell communication.TNTs are primarily established between stressed and unstressed cells and can transport a variety of cellular components. Mitochondria are important trafficked entities through TNTs. Transcellular mitochondria transfer permits the incorporation of healthy mitochondria into the endogenous network of recipient cells, changing the bioenergetic profile and other functional properties of the recipient and may allow the recipient cells to recuperate from apoptotic processes and return to a normal operating state. Mesenchymal cells (MSCs) can form TNTs and transfer mitochondria and other constituents to target cells. This occurs under both physiological and pathological conditions, leading to changes in cellular energy metabolism and functions. This review summarizes the newly described capacity of melatonin to improve mitochondrial fusion/fission dynamics and promote TNT formation. This new evidence suggests that melatonin's protective effects could be attributed to its ability to prevent mitochondrial damage in injured cells, reduce senescence, and promote anastasis, a natural cell recovery phenomenon that rescues cells from the brink of death. The modulation of these new routes of intercellular communication by melatonin could play a key role in increasing the therapeutic potential of MSCs.

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“…However, as we mentioned above, the mitochondrial fission sites are found at ER and also at multiple organelles, including lysosomes and trans-Golgi network (TNG) vesicles [ 161 , 162 ]. Examination of the interaction between mitochondrial fission and the TGN vesicles suggests that these vesicles drive the last step of mitochondrial division [ 163 ]. Another possibility is that the smaller organelles can locally change their position driven by thermal energy, without the involvement of cellular transport machinery, to facilitate fission or fusion.…”

Section: Role Of Cellular Cytoskeleton In Mitochondrial Fission/fusion Dynamicsmentioning

confidence: 99%

Acetylation in Mitochondria Dynamics and Neurodegeneration

Waddell

Banerjee

Kristián

2021

Cells

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Mitochondria are a unique intracellular organelle due to their evolutionary origin and multifunctional role in overall cellular physiology and pathophysiology. To meet the specific spatial metabolic demands within the cell, mitochondria are actively moving, dividing, or fusing. This process of mitochondrial dynamics is fine-tuned by a specific group of proteins and their complex post-translational modifications. In this review, we discuss the mitochondrial dynamics regulatory enzymes, their adaptor proteins, and the effect of acetylation on the activity of fusion and fission machinery as a ubiquitous response to metabolic stresses. Further, we discuss the role of intracellular cytoskeleton structures and their post-translational modifications in the modulation of mitochondrial fusion and fission. Finally, we review the role of mitochondrial dynamics dysregulation in the pathophysiology of acute brain injury and the treatment strategies based on modulation of NAD+-dependent deacetylation.

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The Complex Dance of Organelles during Mitochondrial Division

Abstract: TGN vesicles are recruited to mitochondria-ER contacts and mitochondrial fission sites.

Cited by 47 publications

References 101 publications

Non‐metabolic function of MTHFD2 activates CDK2 in bladder cancer

Non‐metabolic function of MTHFD2 activates CDK2 in bladder cancer

Tunneling nanotubes and mesenchymal stem cells: New insights into the role of melatonin in neuronal recovery

Acetylation in Mitochondria Dynamics and Neurodegeneration

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