His previous work had shown that not only did the nuclear genomes of T. californicus vary among populations, so did their mitochondrial genomes.
Since proper mitochondrial functioning required the interaction of proteins made by both genomes, Burton hypothesized that a mismatch between mitochondrial and nuclear DNA sat at the heart of the F2’s problems.
Because mitochondrial DNA lacks capabilities for checking DNA for errors and repairing it, in animals it mutates on average 10 times as frequently as its nuclear counterpart does.
To evolutionary biologists, this high mutation rate posed an interesting question: How does the nuclear genome respond to this mitochondrial variability and its sabotage of their partnership? Moreover, an organism inherits its mitochondrial DNA only from its mother, instead of from both parents like its nuclear genome.
The mismatch of evolutionary forces on mitochondrial and nuclear genomes could be seen in Burton’s F2 copepods.
He extracted mitochondria from their cells and measured their mitochondria’s energy output in the form of ATP. The F2 hybrids produced significantly less ATP than their nonhybrid counterparts did, a clear indication of mitochondrial dysfunction.
Jonci Wolff at Monash University in Australia and colleagues irradiated male flies to generate large numbers of DNA mutations, and then mated these flies with females that had identical nuclear genomes but one of six different mitochondrial genomes.