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Significance Mitochondria, the powerhouses of the cell, possess their own DNA, which encodes proteins involved in cellular ATP production. During the aging process deleted versions of mtDNA accumulate inside cells and replace the wild type form. Currently no explanation exists that can explain the mechanism behind this accumulation, which is also compatible with experimental observations. We present here a new idea based on the distinctive connection between transcription and replication of mtDNA. Analysis of mtDNA deletion spectra strongly supports our hypothesis and computer simulations show the mechanism to be compatible with data from short- and long-lived species. We believe that this idea may provide a major breakthrough in understanding the complex links between mitochondrial mutations and their accumulation in aging.

Transcription could be the key to the selection advantage of mitochondrial deletion mutants in aging