Comment on Dr. Jason Rosenhouse “Among the Creationists” by Nick (Matzke).

Hi Sean,

No one is asking for “evolution from scratch”. All that I’m asking for here are the odds of evolving something new at a various levels of functional complexity.

That is incorrect. Your arguments and probability calculations are based on the effects of many simultaneous mutations, with no opportunities for selection between them. Thus, under your model, large moves in sequence space have to happen all-at-once. Your criticisms of that model are valid, but they say nothing about the evolutionary model, which is stepwise.
An example from your own comment:

Now, is it in fact true that your argument that most proteins are flexible so that most positions can be mutated, one at a time, without a complete loss of function. However, it isn’t quite like you claim. After all, pretty much all of the letters in this paragraph could be mutated, one at a time, without a significant qualitatively loss in the intended meaning of the paragraph. However, the more and more mutations that occur at the same time, the exponentially less and less likely it is that the sequence will maintain beneficial functionality.

This doesn’t matter, since in evolution, all the mutations don’t occur at the same time. Each is exposed to long periods of selection, drift, etc. The real process is that after a substitution happens in a population (either beneficial, beneficial but with some negative side effects, or neutral, or nearly neutral but slightly deleterious), a variety of new mutations accumulate over subsequent generations. Some of these mutations are neutral, some are slightly deleterious, and some compensate for some deleterious feature introduced by a previous substitution. Compensatory substitutions, in particular, are crucial to include in the model. Creationist arguments, including yours, universally ignore the role they play.

Also, proteins are much more flexible than, say, English. It is commonplace to find protein families where 50% or even 80% of the amino acids have changed, yet the structure and function remain the same. Not so for English. Protein evolution is more like language evolution, where most / all of the words can be modified, the resulting languages are incomprehensible to each other, but the same message can be communicated via different sentence, each within the overall context of its language.

Your arguments are rather like arguing that French and Romanian could not have evolved from a common ancestor, because if you take a French sentence and randomly mutate most of the letters in each of the words, you get something incomprehensible. This is nothing like the actual proposed historical process, and so is not a rebuttal of it.

Language space is surely huge just like sequence space, and it is surely true that most random assemblages of sounds don’t mean anything in any modern or extinct language, yet languages have evolved nonetheless, through a long process of step-by-step changes, with the participating humans mostly or completely oblivious.

Other examples of this mistake in your comment:

The reason for this is because there is an “experimentally observed exponential decline in the fraction of functional proteins with increasing numbers of mutations (Bloom et al. 2005).”

…and again:

Bloom goes on to point out that,

“Experiments have demonstrated that proteins can be extremely tolerant to single substitutions; for example, 84% of single-residue mutants of T4 lysozyme and 65% of single-residue mutants of lac repressor were scored as functional. However, for multiple substitutions, the fraction of functional proteins decreases roughly exponentially with the number of substitutions, although the severity of this decline varies among proteins.”

…and again:

In short, most mutations that affect a region or island cluster of thermodynamically stable sequences in sequence space are destabilizing in such a way that each additional mutation has an exponentially destabilizing effect. Obviously, this means that the vast majority of sequences in sequence space would not produce viably stable proteins.

It is true that most mutations have this effect, but this doesn’t matter, since they happen for the most part one at a time, and (1) selection removes the severely deleterious mutations, and (2) the slightly deleterious ones can later be corrected by compensatory substitutions.

The “vast majority of sequences” therefore don’t matter, since evolution doesn’t have to search through all possible sequences in order to explain the data. To explain the data, it just has to, *sometimes*, find *some* of the paths between proteins with different-but-related sequences but the same function, and, occasionally, find *some* of the paths between proteins with different-but-related sequences and different functions. It doesn’t have to do it *all* the time for *everything*, because the data indicates that failures are common (extinctions are observed, imperfect adaptations are observed), and the data indicate that biology doesn’t occupy all of functional space or sequence space, just little bits of it.

It also suggests that as sequence space increases in size by 20^N, the ratio of viable vs. non-viable sequences, not just systems, decreases exponentially.

This is just the all-at-once fallacy repeated again.

You conclude with:

And, this effect only gets exponentially worse and worse with each step up the ladder of functional complexity.

This is raw assertion, not something your references say, and you haven’t defined the “ladder of functional complexity” anyway. Most of protein complexity involves fusing protein domains or evolving binding sites between them, these are pretty trivial processes.

JUNK DNA

It isn’t just bits and pieces of function, it is a significant proportion of non-coding sequences that appear to have functionality to one degree or another.

This is false, based on the ENCODE project’s claim that any measurable binding to any bit of DNA, even at negligible/noise levels (say, <1 binding event per cell) constitutes "function." Most of this just shows that DNA binding is a sloppy process and our techniques have gotten good enough to detect the noise.

Does this mean that all functional aspects are therefore vital to life? No, not at all. However, the notion that non-coding sequences are largely or almost entirely evolutionary garbage doesn’t make much sense. Even from an evolutionary perspective, it makes no sense to maintain junk that is expensive to reproduce and maintain, from one generation to the next.

This isn’t really a modern evolutionary perspective, this is 1960s-style panadaptationism, most famously corrected by Stephen Jay Gould in his articles on “spandrels”, “exaptation”, etc. Most modern evolutionary biologists read these critiques of panadaptationism as part of routine coursework, but some molecular biologists/genome jockeys, and virtually all creationists, remain clueless.

Also, it’s intuitively “obvious”, but mistaken, to think that having a large amount of junk DNA in the genome is “expensive”. The energetic & material cost of replicating/maintaining the genome in a typical large eukaryotic cell is trivial compared to the costs of protein synthesis, energy generation for muscle action, etc.

This is junk DNA 101 stuff, and you are getting it wrong.

While we’re at it, why do some ferns and salamander have genomes the same size or smaller than the human genome, and other ferns and salamander have genomes 50 times the size of the human genome? And all with approximately the same number of genes, and the difference being due mostly to parasitic repetitive elements? If your discussion of junk DNA doesn’t include these facts, it’s just uninformed, no more useful than a poorly researched undergraduate research paper.

FLAGELLUM

I’ve discussed this topic with you before, quite extensively. In my fairly lengthy discussion of your arguments (Link), where have I gone significantly off base with my homology numbers?

See the table at Panda’s Thumb from Pallen & Matzke 2006. There is a lot more to the argument than just the 10 proteins homologous to nonflagellar T3SS.

The key problem with your argument is that you assume that the novel steppingstones that you list off are actually close enough in sequence space to be easily found from the perspective of the previous steppingstone. This simply isn’t true. The steppingstones that you yourself list off are far too far away from each other for random mutations to get from one to the other in what anyone would consider to be a reasonable amount of time.

There is no point in discussing this until we resolve your misconception about the ability of single proteins to evolve along narrow paths through huge sequence space, in some cases retaining the same function, in other cases changing function.

Those paths exist. Phylogenies of proteins are one of the proofs. The branches of the phylogenies are actual statistical estimates of these paths. They exist both for cases where all the proteins at the tips have the same function, and for cases where some of the proteins at tips of the tree have different functions.

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