The mitochondrion isn’t the bacterium it was in its prime, say two billion years ago. Since getting consumed by our common single-celled ancestor the “energy powerhouse” organelle has lost most of its 2,000+ genes, likely to the nucleus. There are still a handful left—depending on the organism—but the question is why. One explanation, say a mathematician and biologist who analyzed gene loss in mitochondria over evolutionary time, is that mitochondrial DNA is too important to encode inside the nucleus and has thus evolved to resist the damaging environment inside of the mitochondrion. Their study appears February 18 in Cell Systems.
Despite our long-term relationship with mitochondria, a lot of how our cells and these commensal organelles work together is still mysterious and controversial. We know that acquiring mitochondria may have sparked one of the most important evolutionary events in history by giving the common ancestor of eukaryotes (our kingdom of life) the energy to go multicellular. And we know that each of our cells can possess dozens or hundreds of mitochondria, which are essential for powering everything from our muscles to our brain. But what’s strange is that in nearly all multicellular organisms, mitochondria have stayed independent by holding on to a few vital genes—despite the fact it may be safer for the cell to store these genes in the nucleus.
To figure out what makes the few genes in mitochondria so essential, Williams and lead author Iain Johnston, a research fellow at the University of Birmingham, took all of the data generated about mitochondrial genes and threw them into a computer. After a few weeks, with the algorithm Johnston developed, the computer threw back a timeline for mitochondrial gene loss over evolutionary history.
The analysis revealed that the genes that are retained in the mitochondria are related to building the organelle’s internal structure, are otherwise at risk of being misplaced by the cell, and the DNA in these genes use a very ancient pattern that allows the mitochondrial DNA to strongly bond together and resist breaking apart. Williams and Johnston believe this design, not typically found in our own DNA, is likely what keeps the mitochondrial genes from breaking apart during mitochondrial energy production.
As energy is produced within the mitochondria, in the form of ATP, free radicals are emitted—the same free radicals that are a common byproduct of radiation. In essence, the power produced by the mitochondria comes with a certain amount of destruction, and it could be that the mitochondria are capable of withstanding this damage. “You need specialists who can work in this ridiculously extreme environment because the nucleus is not necessary the best fit,” says Williams.
The investigators also observed that the mitochondrial gene loss that’s taken place across the eukaryote kingdom has followed the same pattern. This is a lesson that evolution may follow the same path many times over, and it’s not always this entirely random process. In the cellular environment, the evolution of mitochondrial gene loss became nearly predictable between different organisms. “If we can harness data on what evolution has done in the past and make predictive statements about where it’s going to go next, the possibility for exploring synthetic biology and disease are massive,” says Johnston.
Using their algorithm, the duo next plans to explore the reasons for chloroplasts as well as where mitochondrial diseases, which are often quite devastating, fit into this bigger picture. While this study doesn’t close the door on why we still have mitochondrial DNA, the authors say it does find a middle ground for many different arguments in the debate.