Mitochondrial genetics regulate nuclear gene expression through metabolites

Fetterman, Jessica L.; Ballinger, Scott W.

doi:10.1073/pnas.1909996116

Cited by 12 publications

(12 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This effect on mitochondria is expected to affect the nuclear genes expression including the genes families coding to these receptors. 60 This hypothesis also correlates with the current data with the previously suggested underlying mechanisms for APs diabetogenic effect.…”

Section: Discussionsupporting

confidence: 92%

“…This supposed mechanism can be further explained according to the current study data that APs affect Beta cells bioenergetics with further oxidative damage of the mitochondria and their DNA. This effect on mitochondria is expected to affect the nuclear genes expression including the genes families coding to these receptors 60 . This hypothesis also correlates with the current data with the previously suggested underlying mechanisms for APs diabetogenic effect.…”

Section: Discussionsupporting

confidence: 91%

See 1 more Smart Citation

Antipsychotics inhibit the mitochondrial bioenergetics of pancreatic beta cells isolated from CD1 mice

Elmorsy

Alelwani

Kattan

et al. 2020

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Antipsychotics (APs) are mainly used as long-term medications for many psychiatric conditions, such as schizophrenia, bipolar disorder and Alzheimer's disease. 1,2 The number of individuals receiving APs worldwide is surprisingly high. 3 APs are classified as either old typical (conventional) or newer atypical APs with different common side effects, including extrapyramidal manifestations, 4 atropine-like action 5 and metabolic disorders. 6 Since the mid-1960s, AP treatment was associated with the aggravation of already existing DM or the development of new-onset type II DM with reported higher risk of hyperglycaemic emergencies. 7-12

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Antipsychotics inhibit the mitochondrial bioenergetics of pancreatic beta cells isolated from CD1 mice

Elmorsy

Alelwani

Kattan

et al. 2020

Basic Clin Pharma Tox

View full text Add to dashboard Cite

show abstract

“…The crosstalk between mitochondria and the nucleus, not just as a cellular response to acute mitochondrial stress but also an adaptation of the nuclear epigenetic landscape to changes in metabolism due to mtDNA variants, deserves revisiting. In this regard, we might need to be more careful in interpreting data that are generated with mouse models harboring mtDNA variants ( Fetterman and Ballinger, 2019 ; Wei et al, 2019 ). Also, even though the mtDNA molecules of most higher organisms have been sequenced, the list of new mtDNA-encoded peptides is still growing ( Kim et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial function in development and disease

Rossmann

Dubois

Agarwal

et al. 2021

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

Mitochondria are organelles with vital functions in almost all eukaryotic cells. Often described as the cellular ‘powerhouses’ due to their essential role in aerobic oxidative phosphorylation, mitochondria perform many other essential functions beyond energy production. As signaling organelles, mitochondria communicate with the nucleus and other organelles to help maintain cellular homeostasis, allow cellular adaptation to diverse stresses, and help steer cell fate decisions during development. Mitochondria have taken center stage in the research of normal and pathological processes, including normal tissue homeostasis and metabolism, neurodegeneration, immunity and infectious diseases. The central role that mitochondria assume within cells is evidenced by the broad impact of mitochondrial diseases, caused by defects in either mitochondrial or nuclear genes encoding for mitochondrial proteins, on different organ systems. In this Review, we will provide the reader with a foundation of the mitochondrial ‘hardware’, the mitochondrion itself, with its specific dynamics, quality control mechanisms and cross-organelle communication, including its roles as a driver of an innate immune response, all with a focus on development, disease and aging. We will further discuss how mitochondrial DNA is inherited, how its mutation affects cell and organismal fitness, and current therapeutic approaches for mitochondrial diseases in both model organisms and humans.

show abstract

“…Future insights into the interplay between mtDNA and nDNA methylation could involve the study of mitochondrial heteroplasmy. In fact, recent findings suggest that epigenetic histone methylation is regulated by mtDNA heteroplasmy [ 64 , 65 ]. Defining the mechanisms involved in such phenomena could be important to determine mitochondrial disease penetrance.…”

Section: Effects Of Mitochondria On Nuclear Dna Methylationmentioning

confidence: 99%

“…Finally, the impact of mitochondrial respiratory complex dysfunctions on DNAm is starting to appear. Notable examples are seen in studies where rotenone-induced complex I dysfunction resulted in global changes in DNAm levels in rats, human cybrid cells, and even when induced in mother mice and measured in the offspring [ 64 , 65 , 67 , 68 ]. Together, these studies enforce the notion that differences in mtDNA are signalled to the nucleus, influencing its DNA, and are consequently associated with nuclear DNAm [ 6 , 69 ].…”

Section: Effects Of Mitochondria On Nuclear Dna Methylationmentioning

confidence: 99%

Mitochondrial metabolism and DNA methylation: a review of the interaction between two genomes

Lopes

2020

Clin Epigenet

View full text Add to dashboard Cite

Mitochondria are controlled by the coordination of two genomes: the mitochondrial and the nuclear DNA. As such, variations in nuclear gene expression as a consequence of mutations and epigenetic modifications can affect mitochondrial functionality. Conversely, the opposite could also be true. However, the relationship between mitochondrial dysfunction and epigenetics, such as nuclear DNA methylation, remains largely unexplored. Mitochondria function as central metabolic hubs controlling some of the main substrates involved in nuclear DNA methylation, via the one carbon metabolism, the tricarboxylic acid cycle and the methionine pathway. Here, we review key findings and highlight new areas of focus, with the ultimate goal of getting one step closer to understanding the genomic effects of mitochondrial dysfunction on nuclear epigenetic landscapes.

show abstract

Mitochondrial genetics regulate nuclear gene expression through metabolites

Cited by 12 publications

References 10 publications

Antipsychotics inhibit the mitochondrial bioenergetics of pancreatic beta cells isolated from CD1 mice

Antipsychotics inhibit the mitochondrial bioenergetics of pancreatic beta cells isolated from CD1 mice

Mitochondrial function in development and disease

Mitochondrial metabolism and DNA methylation: a review of the interaction between two genomes

Contact Info

Product

Resources

About