MITOCHONDRIA AND MAKING NEW SPECIES

How do new species arise? Many biologists are intrigued by this question:we are obviously not the same species as chimpanzees, so identifying different species can be simple. However, the process of speciation occurs gradually and is much harder to measure. Scientists want to know what changes occur between reproductive compatability, when two populations fully interbreed; and reproductive isolation, when two populations can't interbreed and become independent species. An early step in this process is called hybrid breakdown,where offspring with parents from different populations have reduced fitness,which gets in the way of successful interbreeding. The causes of hybrid breakdown are poorly understood, prompting Christopher Ellison and Ronald Burton from University of California San Diego to explore how mitochondrial function contributes to this process.As the powerhouse of the cell, mitochondria generate energy during respiration in the form of ATP. The final part of respiration involves an electron transport chain that contains five `complexes', each made up of many enzymes. All of the enzyme complexes, except complex II, contain proteins encoded by both nuclear and mitochondrial DNA, and these proteins must interact properly for mitochondria to work effectively. Offspring can inherit nuclear DNA from either parent, but mitochondrial DNA is inherited only from the mother, and these genomes normally co-evolve to keep proteins in the mitochondria interacting properly. Ellison and Burton suspected that hybrid breakdown is caused when mismatched proteins from genomes that haven't evolved together are combined. This could occur when mitochondrial DNA from a mother in one population is combined with nuclear DNA from a father in a different population.To test this idea, they collected marine crustaceans (Tigriopus californicus) from several different populations along the western coast of North America. There are strong genetic differences between wild populations, and hybrid breakdown occurs when different populations interbreed and produce offspring. To assess the effects of hybrid breakdown on mitochondrial function, the team interbred individuals from different populations and produced hybrids, then isolated their mitochondria to measure how well they made ATP.They found that mitochondria from hybrids produced much less ATP than their parents' mitochondria. The authors suspect this reduces hybrid fitness because efficient ATP production is essential for survival; however, they didn't know how ATP production was being reduced. To address this, they measured the activity of enzyme complexes I-IV from the mitochondrial electron transport chain. Complexes I, III and IV had reduced activity in hybrids. The team already knew that these complexes contain proteins encoded by mitochondrial and nuclear DNA, so concluded that incompatibilities between both protein types was causing the mitochondria in hybrids to produce less ATP.This idea was supported when they found that the activity of enzyme complex II, which is encoded by nuclear DNA only, was the same in hybrids and their parents. This shows that proteins encoded by nuclear DNA are unaffected by interbreeding, while incompatibilities between proteins encoded by nuclear and mitochondrial DNA from different populations might lead to reduced fitness and contribute to hybrid breakdown. By understanding how mitochondria can contribute to this early step in the process of speciation, Ellison and Burton have brought us one step closer to understanding the origin of species!

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