It is always fascinating to see when theoretical predictions are validated by empirical evidence. As a scientists, this is the ultimate vindication of your hard laborious work to obtain knowledge about a particular subject. And that is what is happening at this moment in evolutionary biology. In the forthcoming issue of Nature Genetics several authors try to examine the empirical foundations of adaptive evolution.
Adaptive evolution is the process in which traits evolve by means of natural selection. In general those adaptations contribute to the fitness and survival of individual organisms. For several decades it was already known that three broad concepts underlie adaptive evolution.
- The probability of fixation of an allele depends on the effective population size (Ne) of the population in question
- The fate of the allele depends on the frequency (P0)when positive selection begins to act. So for de novo mutations initial frequencies are low and alleles are more likely to be lost
- The size of the beneficial effect determines how efficient selection is on a particular allele. This is called the selection coefficient
In recent decades it became more feasible and possible to analyse the signatures of selection in a genome. For example by the development of molecular techniques, like genomics, it has become possible to quantify the amount of variation that occurs in a population for a given allele and indeed validate much predictions that were made by theoretical evolutionary biologist in recent decades.
The authors tried to review the empirical evidence that is found of adaptive evolution. Their results are quite striking and give a nice overview about what is known and proven in adaptive evolution.
Recent empirical evidence supports some major theoretical predictions but not others. For instance, the implication of both small-effect and large-effect QTLs in genetic adaptation suggests that both the infinitesimal and Mendelian models may be correct. Similarly, the importance of epistasis and recombination in adaptive evolution is well-supported, and examples of adaptive alleles originating both from new mutations and standing genetic variation have been documented.
But they also emphasized that not all theoretical predictions are supported by the emperical evidence.
However, conflicting results prevent resolution of long-standing theoretical debates about the roles of hard and soft selective sweeps, and the effect of Ne on the efficiency of selection. It is possible that these contradictions are simply due to inherent difficulties in detecting sequence signatures of adaptive evolution; the availability of more sequences and improved analytical methods may eventually lead to more conclusive results. Additionally, although some studies validate predictions from molecular network theory, other examples consistently defy expectations, indicating that the effects of pathway and network position on adaptive value are more complex than previously thought
In short these conclusions indicate that in the past decade there have been found much more empirical evidence to vindicate the theoretical predictions that have been been proposed much earlier. But they also show that much is not known that that more research is needed into adaptive evolution to get insight into the dynamics and mechanisms behind adaptive evolution.
There is – of course – always an implication for creation science. As creation scientists we have to admit that adaptive evolution is a fact. An example for that is the development of antibiotic resistance of many dangerous bacteria. So let that be clear.
And as creation scientist we all know that John Sanford wrote in his book ‘Genetic entropy & and the mystery of the genome’ that the accumulation of mutations and the low effective population size of humans do not allow much progress to be made and that in fact the human race was deteriorating (or should we say de-evolving).
You probably know that when a trait is polygenic, and that when many genes are involved the effects of selection on each individual gene decreases. And that as a consequence this will cause that the strength of selection on any of thos loci is decreased… And with a lower selection strength, beneficial mutations are more easier lost.
Let’s keep that in mind and turn to networks. An organism is complex and many metabolic pathways are sophisticated and a lot of interaction is going on between several pathways. So in that way you could talk about a network of interactions. It is obvious that the relative importance of an gene or regulatory element depends on the position in such a network.
So it is clear that the adaption of a mutation is context-dependent. And indeed it is the case that the effect size is also dependent on the network, in which a particular genetic element interacts.
This paper shows that it is not yet clear what is resolved. And indeed the second theoretical foundation of adaptive evolution (bigger population, more adaptive evolution) is not yet supported by the empirical date. In fact, conflicting conflicting results are found.
So let’s turn to the fruit flies. In Drosophila melanogaster and a sister species, in which researchers looked at the variation of many protein-coding regions and compared them between the species and subsequent make the following conclusion:
“Despite evidence for different demographic histories, differences in population size have apparently played little role in the dynamics of protein evolution in these two species, and estimates of the adaptive fraction (α) of protein divergence in both species remain high even if we account for recent 10-fold growth.”
And in other studies is found that with a higher population size the most adaptive evolution occurred (i.e. Arabidopsis). What are the implications of that? This implies that it is not yet known whether bigger populations had the most adaptive evolution, but because of the conflicting results, this clearly shows that other factors are responsible for this change.
And think back to the period after the flood. An enormous diversification happened. Populations were small, but the ‘evolutionary’ effects were huge. In a matter of years diversification should have taken place, and for that diversification an explanation is needed.
John Sanford assumes that a small population cannot adapt, because the many (slightly) deleterious mutations that occur, on which selection does not have the power to select. I think his case is quite justified for the current human population. But again, I am still wondering how the small populations after the Flood were able to cope with the mutational overload..
In order to justify Sanford’s claim, you will need to invoke the assumption that after the Flood, mutations were occurring more (which we will never know, but is quite probably), and caused a deterioration of mechanisms behind the diversification process.
It is quite reasonable to assume that other evolutionary explanations could cause the removal of mutations in a population. It is widely known that mutations are not randomly distributed across the genome and that organisms have the ability to ‘silence’ the mutational overload by a variety of mechanisms. More robustness of those mechanisms would allow to cope with those detrimental mutation effects for quite some time.
Either way, this is really speculation and it would be nice to see whether creation scientists could come up with with a set of theoretical predictions backed up with empirical data to show how such an extremely fast diversification happened and why it did stop some time after the flood.
This is really a lengthy post, and those who toke the effort to read it all trough are welcome to leave their thoughts in the comments!