scholarly journals Potential Roles for G-Quadruplexes in Mitochondria

2019 ◽  
Vol 26 (16) ◽  
pp. 2918-2932 ◽  
Author(s):  
Micol Falabella ◽  
Rafael J. Fernandez ◽  
F. Brad Johnson ◽  
Brett A. Kaufman

Some DNA or RNA sequences rich in guanine (G) nucleotides can adopt noncanonical conformations known as G-quadruplexes (G4). In the nuclear genome, G4 motifs have been associated with genome instability and gene expression defects, but they are increasingly recognized to be regulatory structures. Recent studies have revealed that G4 structures can form in the mitochondrial genome (mtDNA) and potential G4 forming sequences are associated with the origin of mtDNA deletions. However, little is known about the regulatory role of G4 structures in mitochondria. In this short review, we will explore the potential for G4 structures to regulate mitochondrial function, based on evidence from the nucleus.

2018 ◽  
Vol 315 (2) ◽  
pp. H206-H215 ◽  
Author(s):  
Anne M. Macgregor-Das ◽  
Samarjit Das

MicroRNAs (miRNAs) are known as the master regulators of gene expression, and for the last two decades our knowledge of their functional reach keeps expanding. Recent studies have shown that a miRNA’s role in regulation extends to extracellular and intracellular organelles. Several studies have shown a role for miRNA in regulating the mitochondrial genome in normal and disease conditions. Mitochondrial dysfunction occurs in many human pathologies, such as cardiovascular disease, diabetes, cancer, and neurological diseases. These studies have shed some light on regulation of the mitochondrial genome as well as helped to explain the role of miRNA in altering mitochondrial function and the ensuing effects on cells. Although the field has grown in recent years, many questions still remain. For example, little is known about how nuclear-encoded miRNAs translocate to the mitochondrial matrix. Knowledge of the mechanisms of miRNA transport into the mitochondrial matrix is likely to provide important insights into our understanding of disease pathophysiology and could represent new targets for therapeutic intervention. For this review, our focus will be on the role of a subset of miRNAs, known as MitomiR, in mitochondrial function. We also discuss the potential mechanisms used by these nuclear-encoded miRNAs for import into the mitochondrial compartment. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/microrna-translocation-into-the-mitochondria/ .


2013 ◽  
Vol 8 (5) ◽  
pp. e24139 ◽  
Author(s):  
Yuan Hu Xuan ◽  
Ryza A. Priatama ◽  
Vikranth Kumar ◽  
Chang-deok Han

2019 ◽  
Vol 30 (24) ◽  
pp. 2943-2952 ◽  
Author(s):  
Enrique J. Garcia ◽  
Janeska J. de Jonge ◽  
Pin-Chao Liao ◽  
Elizabeth Stivison ◽  
Cierra N. Sing ◽  
...  

Loss of mitochondrial DNA (mtDNA) results in loss of mitochondrial respiratory activity, checkpoint-regulated inhibition of cell cycle progression, defects in growth, and nuclear genome instability. However, after several generations, yeast cells can adapt to the loss of mtDNA. During this adaptation, rho0 cells, which have no mtDNA, exhibit increased growth rates and nuclear genome stabilization. Here, we report that an immediate response to loss of mtDNA is a decrease in replicative lifespan (RLS). Moreover, we find that adapted rho0 cells bypass the mtDNA inheritance checkpoint, exhibit increased mitochondrial function, and undergo an increase in RLS as they adapt to the loss of mtDNA. Transcriptome analysis reveals that metabolic reprogramming to compensate for defects in mitochondrial function is an early event during adaptation and that up-regulation of stress response genes occurs later in the adaptation process. We also find that specific subtelomeric genes are silenced during adaptation to loss of mtDNA. Moreover, we find that deletion of SIR3, a subtelomeric gene silencing protein, inhibits silencing of subtelomeric genes associated with adaptation to loss of mtDNA, as well as adaptation-associated increases in mitochondrial function and RLS extension.


Gene ◽  
2016 ◽  
Vol 576 (2) ◽  
pp. 782-790 ◽  
Author(s):  
Gaiping Wang ◽  
Shasha Chen ◽  
Congcong Zhao ◽  
Xiaofang Li ◽  
Ling Zhang ◽  
...  

2016 ◽  
Vol 62 (2) ◽  
pp. 134-140
Author(s):  
A.V. Smirnova ◽  
V.N. Sukhorukov ◽  
V.P. Karagodin ◽  
A.N. Orekhov

MicroRNAs (miRNAs) are small (~22 nucleotides in length) noncoding RNA sequences regulating gene expression at posttranscriptional level. MicroRNAs bind complementarily to certain mRNA and cause gene silencing. The involvement of miRNAs in the regulation of lipid metabolism, inflammatory response, cell cycle progression and proliferation, oxidative stress, platelet activation, endothelial and vascular smooth muscle cells (VSMC) function, angiogenesis and plaque formation and rapture indicates important roles in the initiation and progression of atherosclerosis. The key role of microRNAs in pathophysiology of cardiovascular diseases (CVDs), including atherosclerosis, was demonstrated in recent studies. Creating antisense oligonucleotides is a novel technique for selective changes in gene expression both in vitro and in vivo. In this review, we draw attention to the role of miRNAs in atherosclerosis progression, using miRNA as the potential biomarkers and targets in the CVDs, as well as possible application of antisense oligonucleotides


Medicine ◽  
2017 ◽  
Vol 96 (47) ◽  
pp. e8487 ◽  
Author(s):  
Yong Yang ◽  
Fu-Hao Chu ◽  
Wei-Ru Xu ◽  
Jia-Qi Sun ◽  
Xu Sun ◽  
...  

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