Now I’m confused.
There are (at least) 2 bad assumptions in this first part:
A functional protein has to be 275 amino acids long.
The proteins we see in modern organisms are the required proteins for life to exist, and no others. You ignore the possibility that proteins with very different functions could support life.
Dennis Venema over at BiLogos wrote a great essay on the ability of random DNA sequences to produce function. You might want to check it out:
The peer reviewed paper can be found here. Here is the abstract:
With a little more time on my hands, I would enjoy interacting on a couple more interesting topics you raised.
In computer science, an evolutionary algorithm has three parts:
- a stochastic “creative” function that generates new variants, and
- a deterministic selection function that identifies the fittest variants
- a propagation function that discards the least fit variants and passes the most fit to the next generation. (This is usually deterministic, but it can be stochastic.)
Either Dennett misunderstands evolutionary algorithms, or you misunderstand Dennett. I will leave the assessment to you, because I haven’t read Dennett.
Your probabilistic analysis of protein formation relies every bit as much on a multinomial distribution as the analogies you criticize.
So do I! Note: I classify my conclusion as faith rather than the ineluctable conclusion of scientific investigation.
The origin of first life problem remains unsolved by biology, but it does not intersect with the theory of evolution. The theory of evolution simply assumes that the first life came into existence by whatever means. The theory focuses on what has happened subsequent to that first event. Thus it is possible to trust the theory of evolution while at the same subscribing 100% to the miraculous creation of the first organism.
If you look at the text i quoted, it originally didnt have the clarifying text for who you were quoting. So i thought you were being unintentionally ironic.
I withdraw my complaint.
Golly, T. Just because proteins can be less than 275 AA’s doesn’t change the basal probability for those that are 275 or longer. That’s like saying that the odds of being dealt 4 aces are changed by the better odds of getting three.
And for someone regularly spouting aggressively that one’s argument must be science, your second criticism is pure speculation.
As regards Venema’s article, as far as I’m concerned, he showed extreme and sloppy ideological bias there. Let me give you an example: the Bible says, “twisting the nose produces blood” so if I twist your nose and you bleed, that proves the Bible. Seriously, his article is like that. We have no idea why random sequences poked into cell cultures 25% of the time produced improved viability, therefore evolution is true. It’s evolution-of-the-gaps! This is why many scientists need some training in philosophy.
All I’m saying is that I don’t share your faith that randomness can come up with all this. (BTW - please give me a chance to read the paper Chris linked.)
If you can win by getting 3 aces then you don’t need to get 4 aces. The same for proteins. If you can get a functional protein with fewer amino acids then the probabilities for 275 amino acids can be ignored.
I am saying that your claims are speculation. You are assuming that the proteins we see in modern life are the only proteins that can lead to life. This is speculation.
Doesn’t change the fact that 25% of random proteins increased fitness which means that those proteins are functional by definition.
I don’t need faith since I have evidence.
Hi Chris. Enjoyed the paper, but let me share some thoughts.
First, their ideological bias is evident from the first sentence. They crack me up, lumping together those four areas of science. But then the focus of the paper demonstrates with utmost clarity that they don’t have a clue what people actually object to in evolution. And that, I think, is what ideological bias does to people: it prevents them from being able to listen. People are indoctrinated these days instead of educated, and these folks have apparently never talked to someone who has thoughtful objections.
Anyway, what they have done is rigorously demonstrate microevolution. I don’t dispute microevolution, and I don’t know anyone who does. It’s the “arrival of fitness” that bugs me, not how it changes over time after it arrives. Where did the first working protein of the types studied in the paper come from?
The paper is actually a very good mathematical argument for microevolution and common descent. But the aggressive triumphalism is unfounded, since they don’t know the right question. Reminds me of “42.”
I don’t find it that complex. I think Behe’s argument does partly rest on a statement of his that the CR mutations tend to revert when Chloroquine is removed. In other words, when the selectionist pressure is removed, they are less likely to survive, natural selection starts to weed them out, and the CR problem needs to be solved again from scratch. Levin does not say if the wild types with one of the mutations were from an area where CR had arisen, and these were in the process of reverting.
But let me point out that if one or the other of the mutations is common as Levin claims, that may raise different questions as to why CR did not arise sooner. I think most fundamentally, Behe makes the case that CR has arisen at approximately the rate predicted by the math. I think that’s a very profound point! Unless he’s wrong about that, Levin’s diatribe is unfounded.
I don’t think I misread him. I’m not fond of these “just so” stories. Show me the money. And that could be very difficult, I realize, because you would need to show for quite a few examples that the five AA binding site did arise from a two. Now, could that happen? Of course! But then we’re not in the realm of science. We’re in the realm of materialistic metaphysics, where it had to arise that way cuz, well, the math is too difficult for five to show up at the same time.
Paybacks are hell? Actually glad you picked up on that, cuz it was intentional.
Well, what we’re after here is what actually happened, right? Not what can happen. The math says the first protein doing X did not arise at its current length by randomness, so we can speculate on plausible mechanisms. Then we need to demonstrate one. We would need a genetic (or protein) analysis like in the paper you posted that shows much longer proteins, perhaps in Eukaryotes, doing the same basic task as shorter proteins somewhere, perhaps in Archaeans, and showing some plausible pathway from the Archaean protein to the Eukaryote. Demonstrate this for a number of proteins, and that would be something I would need to consider.
Regarding “each step”, while probabilities of individual mutations do not multiply (that’s microevolution again), probabilities of finding cooperating proteins with working binding sites in a protein complex do. Now again, there are values to add to the numerator even at this level. But it seems to me the numbers of zeroes in the denominator grow way too quickly.
This one, Chris, makes me giggle. Fact is, I am only different from genetic material of my parents by about 1e-10 (if I remember my mutation rates). The argument that I am of infinitesimal probability is (if I’ve got my logical fallacies right) a post hoc fallacy. It is also a tautology, because the odds of this keyboard I am typing on being made from these particular keys is also infinitesimal. By that argument, probability is kinda meaningless, yet we know probability works.
But to me, that’s not the right analogy. Instead, take a billion scrabble tiles and dump them on the floor. Find any meaningful sentence of, maybe, 150 letters. I think this is a great analogy to coming up with the first protein that does X. Even as you add orders of magnitude to the number of tiles you’re working with, well, good luck finding even one.
Ahhhh, thanks Chris! What a guy!
Let me add, I appreciate how you are trying to exchange views thoughtfully. Glad to try continue as we have time.
To help focus on perhaps the most important point, if Behe’s argument is wrong, why does his math align pretty well with how frequently CR has arisen ? If Levin is right, why has CR not arisen several orders of magnitude more frequently (and so, consequently, chloroquine would never have gained the traction it did as a treatment)?
Hope this is all helpful!
Then tell us how you think these proteins came about, and produce the same type of evidence that you require from other explanations for your own explanation. Remember, no “just so” stories or speculation. Let’s see the evidence.
With all due respect, you did not fully grasp the paper’s methods and conclusions. Take another look at Table 2, p. 6. You will see that the analysis by White, et al., establishes common ancestry among the following groups:
- vertebrates, sea squirts (urochordata), echinoderms (e.g., sea urchins), and hemichordates (e.g., acorn worms): common ancestor ~600MYA
- chlorophytes (members of protist kingdom) and streptophytes (land plants): common ancestor ~700MYA
- ferns and seed plants: common ancestor ~390MYA
The way I have seen advocates of microevolution define the term is that it admits some amount of evolution (e.g., antibiotic resistance) while denying common ancestry beyond narrowly constrained boundaries, such as species or perhaps genera. But this paper demonstrates common ancestry that spans beyond family…beyond order…beyond class… and beyond phyla (e.g., vertebrate humans alongside acorn worms). And even beyond the very highest taxonomic category, kingdoms (protist chlorophytes alongside plant streptophytes).
The only way I see to accept White’s results and “microevolution” simultaneously is to redefine microevolution so it’s basically the same thing as macroevolution.
This is a really good question, Marty. It also has nothing to do with the theory of evolution.
Let me repeat that, Marty, because you seem to be confusing categories within the study of biology. The theory of evolution helps us understand how life, once it existed on earth, came to have the many forms and processes that we observe today.
It is akin to the Big Bang theory in astronomy in that it assumes a starting condition and explains what happens thereafter. The starting condition in the Big Bang theory is the initial singularity. The Big Bang theory does not try to explain that starting condition; it assumes the starting condition and works from there. Likewise with the theory of evolution: it assumes a starting condition (a primitive form of life billion years ago) and works from there.
Your concern has everything to do with the branch of biology known as origin-of-life studies.
Your concern has nothing to do with the theory of evolution.
You seem to be justifying the violation of the standards you hold other people to. Is that really where you want to go?
This is not the right analogy for working biologists, because they see strong evidence for an inheritance process that, to adopt the language metaphor, allows simple words to form, then longer words, then word combinations, then sentences, then paragraphs.
I don’t understand how you got on this track, Marty. Neither of them disagree as to the frequency of CR appearance. Their disagreement centers on whether a probabilistic analysis of mutation frequency and other genetic mechanisms supports an evolutionary explanatory model (Levin’s position) or whether it places CR appearance beyond the edge of evolution (Behe’s position).
The key differentiator is that Behe’s position assumes the the mutation events are I.I.D., whereas Levin’s incorporates survival analysis that dramatically increases the probability of co-occurrence of CR-aiding mutations. To use the Scrabble tile analogy, Behe assumes the sentence has to come together all at once. Levin, on the other hand, proposes that individual words and n-grams can form along the pathway to the sentence.
Levin provides strong evidence for his position by showing that we see the words and n-grams in the wild. The sentence did not appear out of nowhere.
EDIT: I think I misunderstood something that you wrote, Marty, so I want to try as much as possible to clarify. While you are genuinely skeptical about the claim that anything short of an intervention by an intelligent designer could have created the first cell, you are also skeptical of the claim that the mechanisms described by the theory of evolution could account for the appearance of complex proteins later in history. And that was what you were trying to communicate. Do I have that right?
Let’s see what phylostratigraphy can turn up. It might take a little while, though.
Dipping my feet into the waters quite tentatively here, because I can’t pretend to have followed everything so far. But I am fairly sure, as I understand Marty’s position, that he doesn’t actually deny common ancestry, necessarily. He’s just not sure that random mutations and natural selection will get us to macroevolution. I myself have held this position in the past, so I’m sympathetic to it. The idea is, yes of course, small changes add up to big ones, and yes of course, the tree of life by common ancestry is fairly hard to deny once you get into the details, but the only remaining question really is, did God himself introduce those little changes because random mechanisms couldn’t really have done the heavy lifting, or did they really come about through apparently scientifically random processes?
Marty, correct me if I’m wrong.
My best to all,
It’s always a good morning (or afternoon or evening) when you post.
That’s not how I would summarize the theory of evolution. It has a strong non-random component (natural selection) for one thing. And stochastic is a far better term than random to describe changes in DNA and environment.
I mention these things because the word random is theological red meat to the dedicated Calvinist. Why get drawn into a theological maelstrom when you can avoid it with careful terminology?
We have observed the natural process of mutagenesis producing all the types of differences that we see between the genomes of different species. This includes indels, substitutions, insertion of mobile elements, and small to large recombination events. The real question is why someone would say that any difference between two genomes could not be produced by the known mechanisms of mutagenesis, or why these changes would not accumulate with each generation.
Protein length/size and evolution is fairly well covered in the literature. A “plausible pathway” across a billion years isn’t necessary to see interesting trends across phylogeny in protein structure, including size. A couple of papers below, to illustrate the kinds of analyses that have been done.
Thanks so much for these excellent articles, Steve! They provide a great overview of the kinds of selection pressures on proteins in different kingdoms, and how archaic proteins differed from modern proteins. Great stuff.
I think that Marty is looking for a study of a protein that appears in many higher taxa, and whose evolutionary history can be reasonably inferred. I understand that there is not enough information to identify the exact sequence in which changes occurred. However, if some kind of phylogeny across a broad set of taxa could be created based on protein structure, that would be extremely helpful. I don’t know if any such studies have been done, or could even be done given our current data and tools.
Look for papers on phylostratigraphy. That will launch you (or Marty) pretty well, I think.
Thanks so much, Stephen!
“Phylostratigraphy” led me to “de novo”, where phylostratigraphy is one of the 2 main approaches for identifying novel genes. The other approach is to identify a transcribed gene under selection pressure that has synteny with near-equivalent, non-coding region of multiple other species. Instances identified by the second approach provide very strong evidence of relatively recent mutation(s) that activate the non-coding region (it is now transcribed, when before it was not) and yield functionality (demonstrated by the transcription and selection pressure).
I hope I explained that correctly. I would be happy to have a well-trained biologist clarify anything that needs clarification!
Anyway, here are some de novo genes that code for proteins:
- CLLU1 (121 codons), C22orf45 (159 codons), and DNAH10OS (163 codons) - Knowles and McLysaght, 2009
- YHR180W-A (61 codons) and YGL165C (173 codons) - Wu and Knudson, 2018. Note that these resulted from DNA shuffling of two widely separated non-coding regions.
- Lu, Leu, and Lin (2017) identified 10 de novo protein-coding genes under selection pressure in yeast (see Table 1).
Food for thought.
Hi @AMWolfe. Yes that’s a good summary.
We’re getting there! And I really appreciate the continued engagement.
Yes, but mutation is random, within the laws of physics and appropriate distributions. Without mutations, nothing new arises on which Selection can work. So it seems to me that this foundation of development is fundamentally random.
Given the known selectionist mechanisms which are not properly “random”, functional sequences must still arise to be selected. Can Mutation, which is fundamentally random, provide enough information to produce the complexity we see in the biosphere?
I’ll be checking those papers out. Thanks!
But I would still like to get a good answer to these questions: