A new study from the University of Colorado Boulder has revealed the crucial role of maternal mitochondrial DNA (mtDNA) in determining our energy production and overall health. Released on October 4 and published in Science Advances, the research reveals that mtDNA, passed exclusively from mother to child, is essential for synthesising adenosine triphosphate (ATP) — the chemical that supplies energy to the cells of the body. Unlike nuclear DNA, which combines genetic material from both parents, mtDNA’s unique inheritance pattern highlights its significance in shaping our vitality and well-being.
Mitochondria are double membrane-bound organelles that contain their own DNA, distinct from nuclear DNA, and are involved in several metabolic pathways, such as oxidative phosphorylation, which is crucial for ATP synthesis.
The study shows that paternal mtDNA is actively destroyed soon after sperm penetration through a process known as paternal mitochondrial elimination (PME), which involves the selective removal of mitochondria via a form of apoptosis. This mechanism has evolved to ensure that only maternal mitochondria are passed on to future generations. When PME does not occur and paternal mtDNA remains intact, researchers discovered that developmental problems and embryonic energy shortages arise.
The researchers were able to delay the onset of PME by about 10 hours using a model organism similar to human biology—C. elegans. This delay was found to affect ATP levels in developing embryos, which subsequently impacted the neurological and reproductive output of the worms later in life. Collectively, these results underscore the necessity of proper mitochondrial segregation for correct development and functionality.
According to the study, the findings have far-reaching implications for advancing our understanding of mitochondrial disorders, which are diseases caused by dysfunctional mitochondria that result in energy production deficits affecting roughly 1 in every 5,000 people. The researchers suggest that some more complex illnesses may be linked to PME, which is impeded by the presence of paternal mtDNA.
The study also found that administering a specific type of vitamin K2, known as MK-4, could help restore ATP levels to normal, thereby addressing issues related to memory and fertility in worms. This discovery opens up possibilities for preventive measures or treatments in families with a history of mitochondrial disorders. According to the study’s author, Ding Xue, prenatal vitamin K2 supplementation could be a potential option for such families.
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