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Mitochondria as a Core of Cell Signals

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (15 March 2024) | Viewed by 8880

Special Issue Editor


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Guest Editor
Institute for Chemical Research (IIQ), University of Seville - CSIC, Avda. Américo Vespucio 49, 41092 Sevilla, Spain
Interests: biochemistry and biophysics; protein chemistry; biomolecular interactions

Special Issue Information

Dear Colleagues,

Mitochondria are highly dynamic organelles that serve as a metabolic core wherein catabolic pathways converge upon fuel cells and building blocks for the synthesis of essential cell components. A plethora of regulatory and signalling pathways govern the dynamics and functionality of this organelle and the biochemical routes within. Conversely, many mitochondrial components participate in the control of cell homeostasis and fate. Reactive oxygen species and lipid peroxidation products function as powerful signalling molecules. Cytochrome c and other proapoptotic factors can activate cell death. Mitochondrial DNA mediates inflammatory responses. Further, tricarboxylic acid cycle metabolites released from mitochondria play a broad variety of nonmetabolic roles.

In this collection, we will present an updated view of the role of mitochondria as a core for signalling routes involved in distinct pathological processes including cancer, neurodegenerative syndromes, and diseases. How accumulated knowledge on these processes is aiding the creation of novel therapeutic approaches will be also discussed.

Dr. Antonio Díaz-Quintana
Guest Editor

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Keywords

  • mitochondrial signalling factors

  • metabolic reprogramming
  • metabolite-driven signals
  • oxidative stress response
  • mitochondrial diseases

Published Papers (4 papers)

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Research

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11 pages, 1427 KiB  
Communication
Assessing the Role of Post-Translational Modifications of Mitochondrial RNA Polymerase
by Karlie R. Platz, Emma J. Rudisel, Katelynn V. Paluch, Taylor R. Laurin and Kristin E. Dittenhafer-Reed
Int. J. Mol. Sci. 2023, 24(22), 16050; https://doi.org/10.3390/ijms242216050 - 07 Nov 2023
Viewed by 747
Abstract
The mitochondrial proteome is subject to abundant post-translational modifications, including lysine acetylation and phosphorylation of serine, threonine, and tyrosine. The biological function of the majority of these protein modifications is unknown. Proteins required for the transcription and translation of mitochondrial DNA (mtDNA) are [...] Read more.
The mitochondrial proteome is subject to abundant post-translational modifications, including lysine acetylation and phosphorylation of serine, threonine, and tyrosine. The biological function of the majority of these protein modifications is unknown. Proteins required for the transcription and translation of mitochondrial DNA (mtDNA) are subject to modification. This suggests that reversible post-translational modifications may serve as a regulatory mechanism for mitochondrial gene transcription, akin to mechanisms controlling nuclear gene expression. We set out to determine whether acetylation or phosphorylation controls the function of mitochondrial RNA polymerase (POLRMT). Mass spectrometry was used to identify post-translational modifications on POLRMT. We analyzed three POLRMT modification sites (lysine 402, threonine 315, threonine 993) found in distinct structural regions. Amino acid point mutants that mimic the modified and unmodified forms of POLRMT were employed to measure the effect of acetylation or phosphorylation on the promoter binding ability of POLRMT in vitro. We found a slight decrease in binding affinity for the phosphomimic at threonine 315. We did not identify large changes in viability, mtDNA content, or mitochondrial transcript level upon overexpression of POLRMT modification mimics in HeLa cells. Our results suggest minimal biological impact of the POLRMT post-translational modifications studied in our system. Full article
(This article belongs to the Special Issue Mitochondria as a Core of Cell Signals)
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Review

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38 pages, 2648 KiB  
Review
Mitochondrial Factors in the Cell Nucleus
by Katiuska González-Arzola and Antonio Díaz-Quintana
Int. J. Mol. Sci. 2023, 24(17), 13656; https://doi.org/10.3390/ijms241713656 - 04 Sep 2023
Cited by 1 | Viewed by 1623
Abstract
The origin of eukaryotic organisms involved the integration of mitochondria into the ancestor cell, with a massive gene transfer from the original proteobacterium to the host nucleus. Thus, mitochondrial performance relies on a mosaic of nuclear gene products from a variety of genomes. [...] Read more.
The origin of eukaryotic organisms involved the integration of mitochondria into the ancestor cell, with a massive gene transfer from the original proteobacterium to the host nucleus. Thus, mitochondrial performance relies on a mosaic of nuclear gene products from a variety of genomes. The concerted regulation of their synthesis is necessary for metabolic housekeeping and stress response. This governance involves crosstalk between mitochondrial, cytoplasmic, and nuclear factors. While anterograde and retrograde regulation preserve mitochondrial homeostasis, the mitochondria can modulate a wide set of nuclear genes in response to an extensive variety of conditions, whose response mechanisms often merge. In this review, we summarise how mitochondrial metabolites and proteins—encoded either in the nucleus or in the organelle—target the cell nucleus and exert different actions modulating gene expression and the chromatin state, or even causing DNA fragmentation in response to common stress conditions, such as hypoxia, oxidative stress, unfolded protein stress, and DNA damage. Full article
(This article belongs to the Special Issue Mitochondria as a Core of Cell Signals)
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22 pages, 1465 KiB  
Review
Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury
by Robert W. Siggins, Patrick M. McTernan, Liz Simon, Flavia M. Souza-Smith and Patricia E. Molina
Int. J. Mol. Sci. 2023, 24(10), 8650; https://doi.org/10.3390/ijms24108650 - 12 May 2023
Cited by 5 | Viewed by 3334
Abstract
Alcohol misuse, directly or indirectly as a result of its metabolism, negatively impacts most tissues, including four with critical roles in energy metabolism regulation: the liver, pancreas, adipose, and skeletal muscle. Mitochondria have long been studied for their biosynthetic roles, such as ATP [...] Read more.
Alcohol misuse, directly or indirectly as a result of its metabolism, negatively impacts most tissues, including four with critical roles in energy metabolism regulation: the liver, pancreas, adipose, and skeletal muscle. Mitochondria have long been studied for their biosynthetic roles, such as ATP synthesis and initiation of apoptosis. However, current research has provided evidence that mitochondria participate in myriad cellular processes, including immune activation, nutrient sensing in pancreatic β-cells, and skeletal muscle stem and progenitor cell differentiation. The literature indicates that alcohol impairs mitochondrial respiratory capacity, promoting reactive oxygen species (ROS) generation and disrupting mitochondrial dynamics, leading to dysfunctional mitochondria accumulation. As discussed in this review, mitochondrial dyshomeostasis emerges at a nexus between alcohol-disrupted cellular energy metabolism and tissue injury. Here, we highlight this link and focus on alcohol-mediated disruption of immunometabolism, which refers to two distinct, yet interrelated processes. Extrinsic immunometabolism involves processes whereby immune cells and their products influence cellular and/or tissue metabolism. Intrinsic immunometabolism describes immune cell fuel utilization and bioenergetics that affect intracellular processes. Alcohol-induced mitochondrial dysregulation negatively impacts immunometabolism in immune cells, contributing to tissue injury. This review will present the current state of literature, describing alcohol-mediated metabolic and immunometabolic dysregulation from a mitochondrial perspective. Full article
(This article belongs to the Special Issue Mitochondria as a Core of Cell Signals)
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15 pages, 1792 KiB  
Review
Mitochondrial Signaling Pathways Associated with DNA Damage Responses
by Tsutomu Shimura
Int. J. Mol. Sci. 2023, 24(7), 6128; https://doi.org/10.3390/ijms24076128 - 24 Mar 2023
Cited by 5 | Viewed by 2390
Abstract
Under physiological and stress conditions, mitochondria act as a signaling platform to initiate biological events, establishing communication from the mitochondria to the rest of the cell. Mitochondrial adenosine triphosphate (ATP), reactive oxygen species, cytochrome C, and damage-associated molecular patterns act as messengers in [...] Read more.
Under physiological and stress conditions, mitochondria act as a signaling platform to initiate biological events, establishing communication from the mitochondria to the rest of the cell. Mitochondrial adenosine triphosphate (ATP), reactive oxygen species, cytochrome C, and damage-associated molecular patterns act as messengers in metabolism, oxidative stress response, bystander response, apoptosis, cellular senescence, and inflammation response. In this review paper, the mitochondrial signaling in response to DNA damage was summarized. Mitochondrial clearance via fusion, fission, and mitophagy regulates mitochondrial quality control under oxidative stress conditions. On the other hand, damaged mitochondria release their contents into the cytoplasm and then mediate various signaling pathways. The role of mitochondrial dysfunction in radiation carcinogenesis was discussed, and the recent findings on radiation-induced mitochondrial signaling and radioprotective agents that targeted mitochondria were presented. The analysis of the mitochondrial radiation effect, as hypothesized, is critical in assessing radiation risks to human health. Full article
(This article belongs to the Special Issue Mitochondria as a Core of Cell Signals)
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