Why are we still alive?
The first analysis of evolution in Simulator005 is now available as a free download. Its core result is that the current simple standard model of human mitochondrial DNA evolution is incomplete, as it would predict the extinction of the human line in less than 20 million years. While the hunt for extensions of the standard model is on, this work provides yet another reason to fight any pollution that harms our DNA.
Evolution@home was started in order to combine the power of computers on the Internet for simulating some though problems in evolutionary biology like for example “Muller’s ratchet”, a process that can lead to the accumulation of harmful DNA changes in asexual populations. While the overwhelming majority of species engages in some form of sex (i.e. exchange of genetic material), the rare exceptions are of special interests to biologists, as they provide test cases for various theories. One of these exceptions is the DNA of our mitochondria, the miniature power plants that we have in each of our cells. The mini-genome of mitochondria is exposed to some special hazards and thus harmful DNA changes are relatively frequent. However, nobody so far has simulated the consequences of such mutation accumulation for human mitochondria, as a substantial amount of CPU-time would be required.
In the last few years evolution@home has accumulated over 100 years of computing time in its quest for a better understanding of the consequences of mutations that are slightly harmful and therefore might not be removed from populations by natural selection. The latest study, now freely available (links, PDF 1.7MB), used cutting edge estimates of a classical model of human mitochondrial DNA evolution. The goal was to predict how long it takes to erode the functions of mitochondria to the point where they endanger survival of the human line of evolution.
Results show that this may be less than 20 million years, resulting in a genomic decay paradox, since mitochondria in the human line are older. A sizeable number of potential solutions exists for this paradox and work is under way to determine which particular solutions apply here. These include back mutations, compensatory mutations, rare recombination events and many other biological factors that have been neglected in the standard model. More simulations and new evolution@home simulators will be needed to address these questions.
There is also another more practical result coming from this work. Simulation results have shown that the accumulation of harmful DNA changes is extremely sensitive to the rate at which these changes occur per generation. If we increase this rate, for example by air pollution or by radioactive contamination, then disproportionately many more harmful mutations will get fixed, which means that they will be carried by all humans in some future generation. This implies that genetic diseases of all sorts would become increasingly common and even the most optimistic scenarios of future medical biotechnology will not be able to stem this tide. There are many reasons why we should reduce man-made increases of rates of DNA damage to a minimum, including cancer and Mendelian genetic diseases like cystic fibrosis. The long-term perspective provided by this new work just adds another incentive to act.