For 1.5 billion years, the mitochondrial and nuclear genomes have been coevolving. Over this time, the mitochondrial genome became reduced, retaining only 37 genes in most animal species, and growing reliant on the nuclear genome to fulfill the organelle’s primary function—to produce ATP by oxidative phosphorylation. Mitochondrial gene products interact with those encoded in nuclear genes, and sometimes with the nuclear genome itself. Because the mitochondrial genome mutates faster than the nuclear genome, it takes the lead in the mitonuclear evolutionary dance, while the nuclear genome follows, evolving compensatory mutations to maintain coadapted gene complexes. Researchers are now coming to appreciate that this has consequences for physiology and even macroevolution.
Researchers have long known that many proteins are made of several components, some of which are coded for in the mitochondrial genome, and others being coded for in the nuclear...
Researchers have long known that many proteins are made of several components, some of which are coded for in the mitochondrial genome, and others being coded for in the nuclear genome. Cytochrome oxidase, the last enzyme in the respiratory electron transport chain, is one example.
Mitochondria require nuclear gene products to continually produce energy for the cell. For example, mitochondrial protein translation requires aminoacyl tRNA synthetases (aaRS) encoded by the nuclear genome to attach amino acids to the corresponding tRNAs encoded by the mitochondrial genome.
Nuclear gene expression
Mitochondrial gene products can influence the expression of nuclear genes, though the mechanisms are as yet unclear.
CONSEQUENCES OF MITONUCLEAR INTERACTIONS
The intimate relationship between the mitochondrial and nuclear genomes comes into play as populations evolve. For example, the relatively fast mutation rate of mitochondrial DNA (mtDNA) means that the nuclear genome (nDNA) has had to evolve compensatory mutations to keep pace and maintain collaborative functionality. This process causes populations to drift apart due to mitonuclear incompatibilities.
Copepods on the Pacific coast of North America are the best-known example of this phenomenon. Researchers have successfully bred animals from different tide pools, and while the first-generation hybrids do fine, second-generation individuals develop slower and have fewer offspring.
When F2 hybrids are backcrossed to the paternal line, they show no improvement in fitness. When they are backcrossed to their maternal line, however, their fitness is rescued, most likely because the backcross in this direction reintroduces the nuclear genome to the mitochondrial background it is co-adapted with.
F2 hybrid females crossed with paternal line, where mitochondria types do not match, leads to no fitness improvement:
F2 hybrid females crossed with maternal line, which carries the same mitochondrial type, improves fitness:
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Correction (November 5): The illustration in this story has been updated to correctly label the red copepods as coming from San Diego. The Scientist regrets the error.