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Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy
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Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 December 2019) | Viewed by 27116

Special Issue Editor

Dr. Dhanendra Tomar

E-Mail Website
Guest Editor
Center for Translational Medicine, Lewis Katz School of Medicine of Temple University, Philadelphia, PA 19140, USA
Interests: mitochondria; calcium; post-translational modifications; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are the central hub for cellular metabolism and provide energy to perform all cellular functions. Besides their critical role in bioenergetics, mitochondria are the site of cell death signaling events. Mitochondrial signaling is determined by the spatiotemporal regulation of mitochondrial shape, size, and location. The functional mitochondrial pool in the cell is maintained through the processes of biogenesis, fusion-fission, movement, and mitophagy, collectively known as mitochondrial dynamics. Mitochondrial homeostasis is regulated by various metabolic inputs like nutrient availability and hormonal regulation, which also regulate Ca2+ dynamics. In response to various pathophysiological signals, mitochondria exhibit early alterations in their shape and function, which, may be explained by mitochondrial fission, fusion, structural remodeling, and mitochondrial permeability transition pore (MPTP) regulated swelling. Upon physiological stimulation, cytosolic Ca2+ content is increased and taken up into the mitochondrial matrix via the Mitochondrial Calcium Uniporter Channel (mtCU). The mtCU mediated Ca2+ sequestration is essential to increase the activity of the TCA-cycle which fuels the electron transport chain to generate the ATP. Although Ca2+ signals shape mitochondrial bioenergetic output, sustained elevation of cytosolic Ca2+ drives excessive Ca2+ uptake which is a prerequisite for the opening of MPTP, mitochondrial swelling, and plasma membrane rupture and necrotic cell death.

The current Special Issue welcomes original research articles and reviews covering many aspects of mitochondrial biology. These include, but not limited to, mitochondrial biogenesis, fission/fusion, mitochondrial structural changes, mitochondrial trafficking, mitophagy, and mitochondrial Ca2+ signaling. We look forward to your contributions.

Dr. Dhanendra Tomar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Mitochondria
  • Mitochondrial Calcium
  • Mitochondrial dynamics
  • Mitochondrial biogenesis
  • Fission/fusion
  • Calcium
  • Mitochondrial trafficking
  • Mitophagy
  • MCU
  • MPTP
  • Bioenergetics

Published Papers (4 papers)

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Review

23 pages, 1278 KiB  
Review
Mitochondrial Protein Quality Control Mechanisms
by Pooja Jadiya and Dhanendra Tomar
Genes 2020, 11(5), 563; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11050563 - 18 May 2020
Cited by 47 | Viewed by 8418
Abstract
Mitochondria serve as a hub for many cellular processes, including bioenergetics, metabolism, cellular signaling, redox balance, calcium homeostasis, and cell death. The mitochondrial proteome includes over a thousand proteins, encoded by both the mitochondrial and nuclear genomes. The majority (~99%) of proteins are [...] Read more.
Mitochondria serve as a hub for many cellular processes, including bioenergetics, metabolism, cellular signaling, redox balance, calcium homeostasis, and cell death. The mitochondrial proteome includes over a thousand proteins, encoded by both the mitochondrial and nuclear genomes. The majority (~99%) of proteins are nuclear encoded that are synthesized in the cytosol and subsequently imported into the mitochondria. Within the mitochondria, polypeptides fold and assemble into their native functional form. Mitochondria health and integrity depend on correct protein import, folding, and regulated turnover termed as mitochondrial protein quality control (MPQC). Failure to maintain these processes can cause mitochondrial dysfunction that leads to various pathophysiological outcomes and the commencement of diseases. Here, we summarize the current knowledge about the role of different MPQC regulatory systems such as mitochondrial chaperones, proteases, the ubiquitin-proteasome system, mitochondrial unfolded protein response, mitophagy, and mitochondria-derived vesicles in the maintenance of mitochondrial proteome and health. The proper understanding of mitochondrial protein quality control mechanisms will provide relevant insights to treat multiple human diseases. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy)
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Graphical abstract

24 pages, 1348 KiB  
Review
Imaging Mitochondrial Functions: From Fluorescent Dyes to Genetically-Encoded Sensors
by Elif Begüm Gökerküçük, Marc Tramier and Giulia Bertolin
Genes 2020, 11(2), 125; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11020125 - 23 Jan 2020
Cited by 25 | Viewed by 9765
Abstract
Mitochondria are multifunctional organelles that are crucial to cell homeostasis. They constitute the major site of energy production for the cell, they are key players in signalling pathways using secondary messengers such as calcium, and they are involved in cell death and redox [...] Read more.
Mitochondria are multifunctional organelles that are crucial to cell homeostasis. They constitute the major site of energy production for the cell, they are key players in signalling pathways using secondary messengers such as calcium, and they are involved in cell death and redox balance paradigms. Mitochondria quickly adapt their dynamics and biogenesis rates to meet the varying energy demands of the cells, both in normal and in pathological conditions. Therefore, understanding simultaneous changes in mitochondrial functions is crucial in developing mitochondria-based therapy options for complex pathological conditions such as cancer, neurological disorders, and metabolic syndromes. To this end, fluorescence microscopy coupled to live imaging represents a promising strategy to track these changes in real time. In this review, we will first describe the commonly available tools to follow three key mitochondrial functions using fluorescence microscopy: Calcium signalling, mitochondrial dynamics, and mitophagy. Then, we will focus on how the development of genetically-encoded fluorescent sensors became a milestone for the understanding of these mitochondrial functions. In particular, we will show how these tools allowed researchers to address several biochemical activities in living cells, and with high spatiotemporal resolution. With the ultimate goal of tracking multiple mitochondrial functions simultaneously, we will conclude by presenting future perspectives for the development of novel genetically-encoded fluorescent biosensors. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy)
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11 pages, 2342 KiB  
Review
Transmission of Functional, Wild-Type Mitochondria and the Fittest mtDNA to the Next Generation: Bottleneck Phenomenon, Balbiani Body, and Mitophagy
by Waclaw Tworzydlo, Malgorzata Sekula and Szczepan M. Bilinski
Genes 2020, 11(1), 104; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11010104 - 16 Jan 2020
Cited by 12 | Viewed by 3355
Abstract
The most important role of mitochondria is to supply cells with metabolic energy in the form of adenosine triphosphate (ATP). As synthesis of ATP molecules is accompanied by the generation of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) is highly vulnerable to impairment [...] Read more.
The most important role of mitochondria is to supply cells with metabolic energy in the form of adenosine triphosphate (ATP). As synthesis of ATP molecules is accompanied by the generation of reactive oxygen species (ROS), mitochondrial DNA (mtDNA) is highly vulnerable to impairment and, consequently, accumulation of deleterious mutations. In most animals, mitochondria are transmitted to the next generation maternally, i.e., exclusively from female germline cells (oocytes and eggs). It has been suggested, in this context, that a specialized mechanism must operate in the developing oocytes enabling escape from the impairment and subsequent transmission of accurate (devoid of mutations) mtDNA from one generation to the next. Literature survey suggest that two distinct and irreplaceable pathways of mitochondria transmission may be operational in various animal lineages. In some taxa, the mitochondria are apparently selected: functional mitochondria with high inner membrane potential are transferred to the cells of the embryo, whereas those with low membrane potential (overloaded with mutations in mtDNA) are eliminated by mitophagy. In other species, the respiratory activity of germline mitochondria is suppressed and ROS production alleviated leading to the same final effect, i.e., transmission of undamaged mitochondria to offspring, via an entirely different route. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy)
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22 pages, 870 KiB  
Review
Mitochondrial DNA: A Key Regulator of Anti-Microbial Innate Immunity
by Saima Kausar, Liqun Yang, Muhammad Nadeem Abbas, Xin Hu, Yongju Zhao, Yong Zhu and Hongjuan Cui
Genes 2020, 11(1), 86; https://0-doi-org.brum.beds.ac.uk/10.3390/genes11010086 - 11 Jan 2020
Cited by 18 | Viewed by 5109
Abstract
During the last few years, mitochondrial DNA has attained much attention as a modulator of immune responses. Due to common evolutionary origin, mitochondrial DNA shares various characteristic features with DNA of bacteria, as it consists of a remarkable number of unmethylated DNA as [...] Read more.
During the last few years, mitochondrial DNA has attained much attention as a modulator of immune responses. Due to common evolutionary origin, mitochondrial DNA shares various characteristic features with DNA of bacteria, as it consists of a remarkable number of unmethylated DNA as 2′-deoxyribose cytidine-phosphate-guanosine (CpG) islands. Due to this particular feature, mitochondrial DNA seems to be recognized as a pathogen-associated molecular pattern by the innate immune system. Under the normal physiological situation, mitochondrial DNA is enclosed in the double membrane structure of mitochondria. However, upon pathological conditions, it is usually released into the cytoplasm. Growing evidence suggests that this cytosolic mitochondrial DNA induces various innate immune signaling pathways involving NLRP3, toll-like receptor 9, and stimulator of interferon genes (STING) signaling, which participate in triggering downstream cascade and stimulating to produce effector molecules. Mitochondrial DNA is responsible for inflammatory diseases after stress and cellular damage. In addition, it is also involved in the anti-viral and anti-bacterial innate immunity. Thus, instead of entire mitochondrial importance in cellular metabolism and energy production, mitochondrial DNA seems to be essential in triggering innate anti-microbial immunity. Here, we describe existing knowledge on the involvement of mitochondrial DNA in the anti-microbial immunity by modulating the various immune signaling pathways. Full article
(This article belongs to the Special Issue Mitochondrial Calcium Signaling, Mitochondrial Dynamics, and Mitophagy)
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