Researchers at the Broad Institute of MIT and Harvard, Cambridge, have interrogated several interconnected questions related to mitochondrial DNA (mtDNA) heteroplasmy and the influence of nuclear genetics.
In their paper,"Nuclear genetic control of mtDNA copy number and heteroplasmy in humans," published in, the team provides a comprehensive understanding of the molecular mechanisms behind mtDNA interactions and their potential implications for human health and evolution.
The study finds that individuals carrying harmful mtDNA mutations at low heteroplasmy levels displayed intermediate disease traits. This suggests that the level of heteroplasmy can affect the manifestation level of a disease. Nuclear genetic variants were found to influence the levels of mtDNA indels, possibly affecting the replicative efficiency of mtDNA molecules with different alleles. The levels of mtDNA in cells have previously been associated with diseases.Unexpectedly, the study found that approximately 25% of the variation in mtCN between individuals can be attributed to differences in blood-cell composition.
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