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<img src = "http://micetimes.asia/wp-content/uploads/2018/07/0151290af9fdbf6986013a70c2863dff.jpg" style = "float: left; width: 200px; height: 150px; margin: 5px;" alt = "Researchers have contributed to DNA mutations of mitochondrial mutations in DNA.
Scientists from the University of Alabama in Birmingham (USA) have managed to research findings on mitochondrial mutations, mouse wear and rejuvenation, controlling gene activity in mitochondria Scientific articles published in the journal Cell Death & Disease.
Researchers contributed to mutations in mitochondrial DNA that affect the POLG gene, encoding the DNA of the enzyme Gamma polymerase, localized in mitochondria and involved in the replication and repair of mitochondrial DNA (mtDNA ), shows that the POLG lesion causes mitochondrial dysfunction, particularly a dysfunction of oxidative phosphorylation, which contributes to efficient storage of energy, resulting in the development of scientists have i Nested in the fertilized egg of mice an additional copy of the mutation of the POLG gene. This defective DNA begins to participate in the production of the only polymerase in the presence of the doxycycline antibiotic. Doxycycline began to add to the consumption of food and water rodents, genetically modified animals have reached the age of eight weeks. After two weeks of antibiotic in the mice began to show signs of aging. The black fur began to turn gray and to fall, the skin began to shrink, and the spine curved.
Eliminate the consumption of doxycycline that blocked the activity of the mutant copy of POLG, increased the content of mitochondrial DNA. This has contributed to the decline and almost complete disappearance of aging symptoms in rodents. According to scientists, the observation of the process of rejuvenation in animals with the restoration of mitochondrial function was held for the first time.
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