No passive sidekick: mitochondrial compensatory evolution during adaptation of ETC mutant lines in Caenorhabditis elegans
Proper mitochondrial function is reliant on favourable mitonuclear epistatic interactions between two genomes, the mitochondrial (mtDNA) and the nuclear with contrasting rates of mutation, copy-number and modes of replication and transmission. The compactness and limited coding capacity of animal mtDNA along with their high mutation rates, uniparental inheritance and lack of recombination has…
Mitochondrial function depends on intricate interactions between two genomes, the mitochondrial and nuclear, both with differing mutation rates and replication methods. Due to their small size and high mutation rates, animal mitochondria are often considered prone to accumulating harmful mutations. However, a prospective evolution study in Caenorhabditis elegans has revealed that mtDNA can rapidly adapt to mitochondrial dysfunction caused by harmful mutations in nuclear genes.
Nonsynonymous changes in mtDNA protein-coding genes were more frequent and positively correlated with fitness, suggesting positive selection. The mitochondrial gene nd-1 was identified as a crucial driver of compensatory mitonuclear adaptation. Additionally, compensatory mutations were more likely to occur when they affected ETC subunits in the same complex as the initial harmful mutation.
These findings highlight the significant role mitochondria play in mitonuclear adaptation, despite their small genome size and limited coding capacity.
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