scholarly journals Mitochondrial DNA copy number is regulated in a tissue specific manner by DNA methylation of the nuclear-encoded DNA polymerase gamma A

2012 ◽  
Vol 40 (20) ◽  
pp. 10124-10138 ◽  
Author(s):  
Richard D. W. Kelly ◽  
Arsalan Mahmud ◽  
Matthew McKenzie ◽  
Ian A. Trounce ◽  
Justin C. St John
2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Laura Bordoni ◽  
Vanessa Smerilli ◽  
Cinzia Nasuti ◽  
Rosita Gabbianelli

Abstract Background Since both genomic and environmental factors are involved in obesity etiology, several studies about the influence of adiposity on both nuclear DNA and mitochondrial DNA methylation patterns have been carried out. Nevertheless, few evidences exploring the usage of buccal swab samples to study mitochondrial DNA epigenetics can be found in literature. Methods In this study, mitochondrial DNA from buccal swabs collected from a young Caucasian population (n = 69) have been used to examine potential correlation between mitochondrial DNA copy number and methylation with body composition (BMI, WHtR and bioimpedance measurements). Results A negative correlation between mitochondrial DNA copy number and BMI was measured in females (p = 0.028), but not in males. The mean percentage of D-loop methylation is significantly higher in overweight than in lean female subjects (p = 0.003), and a specific CpG located in the D-loop shows per se an association with impaired body composition (p = 0.004). Body composition impairment is predicted by a combined variable including mtDNA copy number and the D-loop methylation (AUC = 0.785; p = 0.009). Conclusions This study corroborates the hypothesis that mitochondrial DNA carries relevant information about body composition. However, wider investigations able to validate the usage of mtDNA methylation from buccal swabs as a biomarker are warranted.


Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 247 ◽  
Author(s):  
Ji Baek ◽  
Hyeonwi Son ◽  
Young-Hoon Jeong ◽  
Sang Park ◽  
Hyun Kim

The changes in telomere length and mitochondrial DNA copy number (mtDNAcn) are considered to be aging markers. However, many studies have provided contradictory or only fragmentary information about changes of these markers in animal models, due to inaccurate analysis methods and a lack of objective aging standards. To establish chronological aging standards for these two markers, we analyzed telomere length and mtDNAcn in 12 tissues—leukocytes, prefrontal cortex, hippocampus, pituitary gland, adrenal gland, retina, aorta, liver, kidney, spleen, skeletal muscle, and skin—from a commonly used rodent model, C57BL/6 male mice aged 2–24 months. It was found that at least one of the markers changed age-dependently in all tissues. In the leukocytes, hippocampus, retina, and skeletal muscle, both markers changed age-dependently. As a practical application, the aging marker changes were analyzed after chronic immobilization stress (CIS) to see whether CIS accelerated aging or not. The degree of tissue-aging was calculated using each standard curve and found that CIS accelerated aging in a tissue-specific manner. Therefore, it is expected that researchers can use our standard curves to objectively estimate tissue-specific aging accelerating effects of experimental conditions for least 12 tissues in C57BL/6 male mice.


2014 ◽  
Vol 91 (4) ◽  
Author(s):  
Meiping Tian ◽  
Huaqiong Bao ◽  
Francis L. Martin ◽  
Jie Zhang ◽  
Liangpo Liu ◽  
...  

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