Rogue mitochondrial DNA spreads despite crippling host cells
Scientists discovered a spontaneous DNA mutation in mitochondria that spreads aggressively through cells while severely damaging fitness—a finding that could reshape how we understand cellular inheritance and disease. The research reveals how genetic conflicts emerge inside cells, with implications for treating mitochondrial disorders and understanding why some harmful mutations persist in populations.
Originaltitel: Friend turned foe: selfish behavior of a spontaneously arising mitochondrial deletion in an experimentally evolved <em>Caenorhabditis elegans</em> population
<p>Selfish mitochondrial DNA (mtDNA) mutations are variants that can proliferate within cells and enjoy a replication or transmission bias without fitness benefits for the host. mtDNA deletions in <em>Caenorhabditis elegans</em> can reach high heteroplasmic frequencies despite significantly reducing fitness, illustrating how new mtDNA variants can give rise to genetic conflict between different levels of selection and between the nuclear and mitochondrial genomes. During a mutation accumulation experiment in <em>C. elegans</em>, a 1,034-bp deletion originated spontaneously and reached an 81.7% frequency within an experimental evolution line. This heteroplasmic mtDNA deletion, designated as <em>meuDf1</em>, eliminated portions of 2 protein-coding genes (<em>coxIII</em> and <em>nd4</em>) and tRNA-<em>thr</em> in entirety. mtDNA copy number in <em>meuDf1</em> heteroplasmic individuals was 35% higher than in individuals with wild-type mitochondria. After backcrossing into a common genetic background, the <em>meuDf1</em> mitotype was associated with reduction in several fitness traits and independent competition experiments found a 40% reduction in composite fitness. Experiments that relaxed individual selection by single individual bottlenecks demonstrated that the deletion-bearing mtDNA possessed a strong transmission bias, thereby qualifying it as a novel selfish mitotype.</p>