It is difficult to imagine how point mutations, a large number of which are neutral, a certain number of which are deleterious, and a tiny number of which are fitness-enhancing, can add up to the sorts of evolutionary diversity and adaptive elegance we see in real life. However, there are only two possible explanations for what we see in nature: 1) Evolution happened more or less as we think it did or 2) God created life and made it look exactly like evolution happened. Take your pick. I’m betting on number 1.
People will get mad at me for suggesting that it is hard to figure how all this Saganian starstuff turned into the amazing diversity of life that we see, but that would only be if they weren’t paying attention during the last paragraph. I’m not making a statement about how current evolutionary science does not really explain life. Notice that I blamed the point mutation subject to selection (or not) for being unimpressive. This says nothing about the rather amazing dance of DNA that occurs over generational time, especially among organisms that exchange genes (and that includes a lot of organisms) or those that simply reproduce at all. In animals, there are dozens of molecules coded for by distinctly different genes that serve a variety of purposes that fall into the category of “globins” because of their basic morphology. The probability of having so many different globins all evolve independently from point mutations is so low that if I was convinced that they did in fact arise from independent staring points via point mutations subsequently selected, I’d probably start going to church. But we know that these important molecules did not evolve that way. Rather, a primordial globin got cloned, as it were, during a “gene duplication” event. That is how much of the molecular disparity we see in living organisms has arisen over time.
But there are other mechanisms that are less well understood, that are also not point mutations, that shepherd along the evolutionary process, or provide opportunity for molecular change that is subject to selection. Here’s the thing: Changes that occur one base pair at a time (which are then subject, potentially, to selection) are analogous to a person trying to figure out a very complex problem that requires many steps … say, assembling a baby carriage from the parts that come in the box … with no instructions or models, and no prior experience. Go watch someone who is doing that, and see what your brain does as a result of your personal frustration at observing the futility of it all. You will want to find an identical baby carriage and show it to the person. You will be happy with a different baby carriage if that’s all you’ve got, because it may demonstrate some basic principle that the person can use as a guidelines as to what parts to put together. Or, you might even want to grab the instructions and point to them and yell, “did it ever occur to you to read this??? Huh????” Or, you might even realize that you’ve got a baby carriage already assembled that you are not using any more, and just hand it to them.
Homologous recombination, non homologous juxtaposition, and gene duplication are ways in which the ‘information’ that is a genetic code can come from a previously worked out part of the genome to change, constrain, or just become the genetic code for a different part of the genome. (See Bogarad and Deem citation below for a key paper on this topic.) We probably don’t know about all the possible mechanisms for genomes to change over time, we certainly don’t know the relative importance of various mechanisms, but simple inspection as well as various experiments have demonstrate that the point mutation model alone is part of the story, but not the whole story, and simulation modeling and in vitro experimentation have demonstrated this further.
A paper from 2006 by Hayashi et al, published in PLoS ONE is an example of one such study. From the abstract:
The fitness landscape in sequence space determines the process of biomolecular evolution. To plot the fitness landscape of protein function, we carried out in vitro molecular evolution beginning with a defective fd phage carrying a random polypeptide of 139 amino acids in place of the g3p minor coat protein D2 domain, which is essential for phage infection. After 20 cycles of random substitution at sites 12-130 of the initial random polypeptide and selection for infectivity, the selected phage showed a 1.7×104-fold increase in infectivity, defined as the number of infected cells per ml of phage suspension. Fitness was defined as the logarithm of infectivity, and we analyzed (1) the dependence of stationary fitness on library size, which increased gradually, and (2) the time course of changes in fitness in transitional phases, based on an original theory regarding the evolutionary dynamics in Kauffman’s n-k fitness landscape model. In the landscape model, single mutations at single sites among n sites affect the contribution of k other sites to fitness. Based on the results of these analyses, k was estimated to be 18-24. According to the estimated parameters, the landscape was plotted as a smooth surface up to a relative fitness of 0.4 of the global peak, whereas the landscape had a highly rugged surface with many local peaks above this relative fitness value. Based on the landscapes of these two different surfaces, it appears possible for adaptive walks with only random substitutions to climb with relative ease up to the middle region of the fitness landscape from any primordial or random sequence, whereas an enormous range of sequence diversity is required to climb further up the rugged surface above the middle region.
That’s a lot of heavy terminology, but the main point that relates to the present discussion is this: When you use this approach to understanding Darwinian evolution, point mutations and subsequent selection does not explain the apparent success of that evolutionary process to solve problems unless you assume a baseline of potential mutations that is to large to be real. The authors, in this paper and elsewhere, as well as others, have suggested for some time that there are other mechanisms that have to do with gene shuffling to speed up the process significantly. I would add that although we see some amazing things in adaptive evolution, it is also probably the case that we see many systems that are far from perfect, either because they are in transition, because we are missing some competing evolutionary factor that overrides selection in the featurew we are observing, or because, in the end, evolution is in fact hard and the whole mutation-selection thing is probably not fast enough to solve certain problems as well as one might expect.
The reason I bring this up now is because I just came across a post on a creationist blog that quote mines the Hayashi et al paper and uses it to prove that evolution is not true. The quote mining runs like this:
One cannot observe birds evolve nor flowers, nor trees or humans so evolution is measured in terms of fitness which has been very elusive in evolutionary research. In a recent paper in PLoS, called; “Experimental Rugged Fitness Landscape in Protein Sequence Space” where it makes the following statement…
“Experimental molecular evolution from randomly generated polypeptides has been employed to determine how and to what extent a functional protein can evolve according to the principles of Darwinian evolution -. One of the most remarkable findings of these studies is that relatively small degrees of sequence diversity, e.g., 10 different random sequence for esterase activity, are sufficient to allow Darwinian selection of random polypeptides composed of about 140 amino acid residues .”
“By extrapolation, we estimated that adaptive walking requires a library size of 10^70 [a one followed by 70 zeros] with 35 substitutions to reach comparable fitness. Such a huge search is impractical and implies that evolution of the wild-type phage must have involved not only random substitutions but also other mechanisms, such as homologous recombination.”
This is not something a student would not hear in their biology, in fact the response of the teacher would most likely be that evolution is an absolute indisputable fact…
The blog post goes on to note that the authors give some crazy-ass explanations for how evolution manages to happen (i.e., those I mention above) and asserts that these other ideas are post-hoc excuses that would never work. Which is pretty much what I would expect from someone who does not understand science and who has faith that the scientists are wrong. Such faith would lead anyone to assume that ideas that explain the observations we make of nature are made up and incorrect.
Bogarad, L. (1999). A hierarchical approach to protein molecular evolution Proceedings of the National Academy of Sciences, 96 (6), 2591-2595 DOI: 10.1073/pnas.96.6.2591
Hayashi, Y., Aita, T., Toyota, H., Husimi, Y., Urabe, I., & Yomo, T. (2006). Experimental Rugged Fitness Landscape in Protein Sequence Space PLoS ONE, 1 (1) DOI: 10.1371/journal.pone.0000096
“Michael”, Peer Reviewed Paper Says Evolution is Not Practical. New Discoveries and Comments About Creationism: Promoting Curiosity of True Science which Verifies God’s Word.