Bedrock radioactivity influences the rate and spectrum of mutation

All organisms on Earth are exposed to low doses of natural radioactivity but some habitats are more radioactive than others. Yet, documenting the influence of natural radioactivity on the evolution of biodiversity is challenging. Here, we addressed whether organisms living in naturally more radioactive habitats accumulate more mutations across generations using 14 species of waterlice living in subterranean habitats with contrasted levels of radioactivity. We found that the mitochondrial and nuclear mutation rates across a waterlouse species’ genome increased on average by 60% and 30%, respectively, when radioactivity increased by a factor of three. We also found a positive correlation between the level of radioactivity and the probability of G to T (and complementary C to A) mutations, a hallmark of oxidative stress. We conclude that even low doses of natural bedrock radioactivity influence the mutation rate possibly through the accumulation of oxidative damage, in particular in the mitochondrial genome.

Bedrock radioactivity influences the rate and spectrum of mutation

All organisms on Earth are exposed to low doses of natural radioactivity but some habitats are more radioactive than others. Yet, documenting the influence of natural radioactivity on the evolution of biodiversity is challenging. Here, we addressed whether organisms living in naturally more radioactive habitats accumulate more mutations across generations using 14 species of waterlice living in subterranean habitats with contrasted levels of radioactivity. We found that the mitochondrial and nuclear mutation rates across a waterlouse species’ genome increased on average by 60 and 30%, respectively, when radioactivity increased by a factor of three. We also found a positive correlation between the level of radioactivity and the probability of G to T (and complementary C to A) mutations, a hallmark of oxidative stress. We conclude that even low doses of natural bedrock radioactivity influence the mutation rate through the likely accumulation of oxidative damage, in particular in the mitochondrial genome.

Mitochondrial genome variation affects the mutation rate of the nuclear genome in Drosophila melanogaster

Mutations are the raw material for evolutionary change. While the mutation rate has been thought constant between individuals, recent research has shown that poor genetic condition can elevate the mutation rate. Mitonuclear genetic conflict is a potential source of poor genetic condition, and considering the high mutation rate of mitochondrial genomes, there should be ample scope for mitochondrial mutations to interfere with genetic condition, with concomitant effects on the nuclear mutation rate. Moreover, because theory suggests mitochondrial genetic effects will often be male-biased, such effects could be more strongly felt in males than females. Here, by mating irradiated male Drosophila melanogaster to isogenic females bearing six distinct mitochondrial haplotypes, we tested whether mitochondrial genetic variation affects DNA repair capacity, and whether effects of mutation load on reproductive function are shaped by interactions between sex and mitochondrial haplotype. We found mitochondrial genetic effects on DNA repair, and that the mutational variance of reproductive fitness was higher in males bearing haplotypes characterized by high female fitness. These results suggest that mitochondrial genome variation may affect the mutation rate, and that induced mutations interact more strongly with male than female reproductive function. The potential for haplotype-specific effects on the nuclear mutation rate has broad implications for evolutionary dynamics, such as the accumulation of genetic load, adaptive potential, and the evolution of sexual dimorphism.

Mitochondrial Respiratory Electron Carriers Are Involved in Oxidative Stress during Heat Stress inSaccharomyces cerevisiae

ABSTRACT In the present study we sought to determine the source of heat-induced oxidative stress. We investigated the involvement of mitochondrial respiratory electron transport in post-diauxic-phase cells under conditions of lethal heat shock. Petite cells were thermosensitive, had increased nuclear mutation frequencies, and experienced elevated levels of oxidation of an intracellular probe following exposure to a temperature of 50°C. Cells with a deletion in COQ7 leading to a deficiency in coenzyme Q had a much more severe thermosensitivity phenotype for these oxidative endpoints following heat stress compared to that of petite cells. In contrast, deletion of the external NADH dehydrogenases NDE1 and NDE2, which feed electrons from NADH into the electron transport chain, abrogated the levels of heat-induced intracellular fluorescence and nuclear mutation frequency. Mitochondria isolated fromCOQ7-deficient cells secreted more than 30 times as much H2O2 at 42 as at 30°C, while mitochondria isolated from cells simultaneously deficient in NDE1 and NDE2 secreted no H2O2. We conclude that heat stress causes nuclear mutations via oxidative stress originating from the respiratory electron transport chains of mitochondria.