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Research on Mitochondrial Genetics and Epigenetics
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Research on Mitochondrial Genetics and Epigenetics

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

Deadline for manuscript submissions: 20 October 2025 | Viewed by 2607

Special Issue Editor

Dr. Arianna Montanari

E-Mail Website
Guest Editor
Department of Biology and Biotechnologies “C. Darwin”, Sapienza University of Rome, Piazzale Aldo Moro, 5, 00185 Rome, Italy
Interests: mitochondria; mitochondrial mutations; yeast model; C. elegans model; epigenetic regulation

Special Issue Information

Dear Colleagues,

The Special Issue of the International Journal of Molecular Sciences, titled "Research on Mitochondrial Genetics and Epigenetics”, is focused on molecular research regarding the genetics and epigenetics of the mitochondria. Mitochondria are cellular mediators of energy metabolism whose physiology is maintained either by nuclear or mitochondrial gene functions. The peculiar dynamics of mitochondrial (mt)DNA, such as a high mutation rate, the balance between homoplasmy and heteroplasmy, as well as the copy number variability and maintenance, contribute to the complex regulation of the mitochondrial genetics and are associated with the onset of pathological conditions ranging from metabolic alterations to neurodegenerative diseases and cancer.

The crosstalk between nucleus and mitochondria is finely tuned; in particular, alterations in mitochondrial functionality can trigger cellular stress signaling and changes in nuclear gene expression by retrograde regulation. In this scenario, the epigenetic modifications also occurring in mtDNA play an important role in regulating gene expression, influencing the maintenance of cellular health by leading the cellular homeostasis, the oxidative stress responses, and the energy production. Furthermore, non-coding RNAs, both mitochondrially and nuclearly encoded, can be involved in the epigenetic regulation of mitochondrial gene expression, as well as are the modifications of mtDNA-binding proteins within mitochondrial nucleoids.

Dr. Arianna Montanari
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • mitochondrial DNA dynamics
  • retrograde regulation
  • epigenetic modulators
  • mitochondrial diseases
  • cellular homeostasis

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Published Papers (2 papers)

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Research

17 pages, 3159 KB  
Article
Csn5 Depletion Reverses Mitochondrial Defects in GCN5-Null Saccharomyces cerevisiae
by Angela Cirigliano, Emily Schifano, Alessandra Ricelli, Michele M. Bianchi, Elah Pick, Teresa Rinaldi and Arianna Montanari
Int. J. Mol. Sci. 2025, 26(14), 6916; https://doi.org/10.3390/ijms26146916 - 18 Jul 2025
Viewed by 481
Abstract
In this study, we investigated the mitochondrial defects resulting from the deletion of GCN5, a lysine-acetyltransferase, in the yeast Saccharomyces cerevisiae. Gcn5 serves as the catalytic subunit of the SAGA acetylation complex and functions as an epigenetic regulator, primarily acetylating N-terminal [...] Read more.
In this study, we investigated the mitochondrial defects resulting from the deletion of GCN5, a lysine-acetyltransferase, in the yeast Saccharomyces cerevisiae. Gcn5 serves as the catalytic subunit of the SAGA acetylation complex and functions as an epigenetic regulator, primarily acetylating N-terminal lysine residues on histones H2B and H3 to modulate gene expression. The loss of GCN5 leads to mitochondrial abnormalities, including defects in mitochondrial morphology, a reduced mitochondrial DNA copy number, and defective mitochondrial inheritance due to the depolarization of actin filaments. These defects collectively trigger the activation of the mitophagy pathway. Interestingly, deleting CSN5, which encodes to Csn5/Rri1 (Csn5), the catalytic subunit of the COP9 signalosome complex, rescues the mitochondrial phenotypes observed in the gcn5Δ strain. Furthermore, these defects are suppressed by exogenous ergosterol supplementation, suggesting a link between the rescue effect mediated by CSN5 deletion and the regulatory role of Csn5 in the ergosterol biosynthetic pathway. Full article
(This article belongs to the Special Issue Research on Mitochondrial Genetics and Epigenetics)
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19 pages, 4321 KB  
Article
Impact of Cold Stress on Hepatopancreas Transcriptomic and Metabolomic in Red Swamp Crayfish Procambarus clarkii
by Xiaochen Zhu, Aidi Peng, Yueying Zou, Yingdong Li, Hua Wei, Xianhu Zheng and Yingying Zhao
Int. J. Mol. Sci. 2025, 26(3), 1221; https://doi.org/10.3390/ijms26031221 - 30 Jan 2025
Viewed by 1401
Abstract
The aquaculture industry of red swamp crayfish (RSC), Procambarus clarkii, has grown significantly in recent decades due to increasing market demand. In China, low water temperatures, particularly during overwintering, pose a challenge, hindering the development of the RSC aquaculture industry in northern [...] Read more.
The aquaculture industry of red swamp crayfish (RSC), Procambarus clarkii, has grown significantly in recent decades due to increasing market demand. In China, low water temperatures, particularly during overwintering, pose a challenge, hindering the development of the RSC aquaculture industry in northern regions. Understanding the molecular mechanism of RSCs’ responses to cold stress could be beneficial for its aquaculture practices. In this study, we exposed RSCs to 4 °C (T4) and 22 °C (T22: control) for 96 h. Transcriptomic and metabolomic analyses of hepatopancreas tissues were performed to identify key genes and metabolites that participate in cold stress response. A total of 787 differentially expressed genes (DEGs) and 198 differentially expressed metabolites (DEMs) were identified between T4 and T22. DEGs were significantly enriched in KEGG pathways related to carbohydrate, lipid, amino acid, and nucleotide metabolism, immunity, and signaling, while DEMs were significantly enriched in pathways associated with lipid and amino acid metabolism and membrane transport. The results indicated that cold stress altered RSCs’ metabolism and their innate immune system. This study provides valuable information to increase our understanding of cold stress responses in RSCs. Full article
(This article belongs to the Special Issue Research on Mitochondrial Genetics and Epigenetics)
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