Uncommon Descent Serving The Intelligent Design Community

Genes that appear from nowhere — a tutorial

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
arroba Email

A friend notes — about these de novo (from nowhere) genes — that narrator Anne-Ruxandra Carvunis stresses that the genetic patterns she studies don’t fit the evolutionary theory learned “since I was an undergraduate.” The de novo gene literature mirrors that, we are told.

Well, if she has a job story instead of a sob story, eventually, the discrepancies will add up.

Comments
Alan Fox: I'll await your next response; however, in the meantime, this is from the link that you provided:
Further a 1:1 stoichiometric ratio of purine and pyrimidine bases (i.e., A+G=T+C) should exist. This pattern is found in both strands of the DNA. They were discovered by Austrian-born chemist Erwin Chargaff, in the late 1940s.
This is exactly what I said: no preferences exist. There are slight preferences that we now know about (since the 1940'w), but Chargaff's Rules still fundamentally and generally apply. This means that as far as basic biochemistry within the cell, there are no known forces pushing nucleotides in one direction or another, to say nothing of there being a bias of this kind sort of on demand. The mathematics, therefore, are straight forward. That you would point to Chargaff's Rules in this discussion is like telling a college student that "i comes after e except after c." On this blog, the "ivory tower" is left behind, I'm afraid. :) PaV
PaV, trying to comment on a phone is too much trouble. I'll pick this up tomorrow when I have time and a larger screen. Alan Fox
PaV
We know that the probability of a particular nucleotide base to find itself in a sequence of such bases is the same, more or less, for all four nucleotide bases.
The Wikipedia article on Chargaff's Rules summarizes much research over the years into the distribution of nucleotide bases in DNA/RNA sequences. It's not just probability, it's a result of physical and chemical properties, critically: the property of pair-bonding. Alan Fox
Alan Fox: Let's start here:
Only? Your method doesn’t (nor can it) show that. It’s a mathematical model that does not approach reality.
The "islands" I referred to were 'islands of functionality.' The connection between these islands shouldn't, generally speaking, easily happen. We know that mutation and selection can move alleles around in the island they belong to, and even allow them (I would think on extremely rare occasions) to move to another island of functionality. All this means is that the sequence space must be extravagantly large. For human beings in labs, this is difficult. For an All-Powerful God, this is much easier--though the Good Lord "rested" from his "work." I'll leave it at that. As to the mathematical model I used not "approach[ing] reality," we obviously differ here. We know that the probability of a particular nucleotide base to find itself in a sequence of such bases is the same, more or less, for all four nucleotide bases. Hence, back of the envelope calculations give us quite some insight. Sir Fred Hoyle did such a calculation. If the argument is that, "he's not an evolutionary biologist," well, neither is Szostak, whose paper you cited and I looked at. He's a "molecular biologist," just like, if I may add it here, Michael Behe. In Szostak's April 2001 paper, he concludes thusly:
we suggest that functional proteins are sufficiently common in protein sequence space (roughly 1 in 10^11) that they may be discovered by entirely stochastic means, such as presumably operated when proteins were first used by living organisms.
Life can't exist without proteins. And here he's assuming that life does already exist. This is circular reasoning because his thesis is this: since life exists, then protein function can be "discovered by entirely stochastic means," which proves that "entirely stochastic means" can give rise to life. Isn't this logically incoherent? As to the paper itself, I understand the method he employed and why he employed it; however, he ends up on some kind of strange "island" of functionality:
A NetBLAST7 search of the NCBI protein sequence databases shows that the most closely related known protein sequence to the 45 amino acids of the minimal functional sequence of this protein has only a 33% identity. This is not a significant homology for a sequence this short, and did not include any of the four conserved cysteines.
It seems strange that there is hardly any homology at all with anything found in nature. But there was another problem. Unlike ATP-binding that happens in biological systems, this Family B mutated and selected protein, "protein 18-19," seemed to need help for it to bind.
These observations suggested that family B proteins might require a coordinated metal ion to be functional. Elemental analysis by atomic absorption spectroscopy revealed the presence of one equivalent of bound zinc, and no other divalent metals. Incubation of the protein with EDTA results in a concentration-dependent loss of ATP-binding activity. Activity can be restored to protein that has been extensively dialysed in the presence of EDTA by the addition of Zn2+, but not Mg2+, ions.
And a little later:
We suggest that the family B proteins bind to ATP with a folded structure nucleated around, or stabilized by, a Zn2+ ion coordinated to the four invariant cysteines of the CXXC sequences. None of the other three protein families selected in this study contains this zinc binding motif, and no known biological nucleotide-binding domain is a zinc-stabilized structure, although the glucocorticoid receptor contains a similar pair of CXXC sequences and binds to DNA in a zinc-dependent manner.
So the ATP-binding activity of protein 18-19 is brought about in a way that isn't found in nature. No homology, and a binding mechanism that is not found in nature, and a mechanism that relies on a metal ion to fold sufficiently for it to bind to the ATP. So what is it that they've mutated themselves to? If it weren't for nascent blood in the petri dishes, Zn2+ would not have been available and protein 18-19 would not have bound to ATP. The other three sequence lines had a very low level of binding to ATP, even after, IIRC, being mutated and amplified. So, yes, they produced, in random fashion, a sequence that could 'bind' to ATP; however, as far as living cells are concerned, this "protein" must seem like a pile of junk. It feels like something of a stretch to say they really found a "functional protein." PaV
This is a good place for an insightful assessment
To paraphrase someone much smarter than me. A little bit of science inclineth one to atheism A lot of science inclineth one to God
So true! https://twitter.com/HotHarveyW/status/1557578480912543750 jerry
You only have to ensure that the various islands of probability within the total sequence space are probabilistically far enough away from each other that they effectively don’t mix.
Only? Your method doesn't (nor can it) show that. It's a mathematical model that does not approach reality. Alan Fox
Yes, I'm aware of "sauce for the goose". Alan Fox
Oops just noticed messed up blockquote. PaV said:
My answer makes more sense than your question.
I replied: If you are referring to your back-of-envelope calculation, then I’m sorry to tell you it is based on false assumptions. I’ll repeat, density of functionality, and how similar functions can be achieved by different, unrelated sequences, whether exhaustive search is relevant, undermine your model. I'd add that, of course our own statements make sense to us. The skill in communication is to make sense to others. Beware Dunning and Kruger. Alan Fox
I wasn’t kidding. You asked a silly question.
What question? My answer makes more sense than your question.If you are referring to your back-of-envelope calculation, then I'm sorry to tell you it is based on false assumptions. I'll repeat, density of functionality, and how similar functions can be achieved by different, unrelated sequences, whether exhaustive search is relevant, undermine your model. Alan Fox
Alan Fox: I wasn't kidding. You asked a silly question. My answer makes more sense than your question. PaV
Alan Fox: Yes, Hoyle's is an "all-in-one-go" calculation, as it should be: no cytochrome c, then no duplication. If there is nothing but death, that is not "differential" death. This all is so obvious. I can't believe intelligent people can't see this somewhat immediately. A quick look at Szostak's paper, his abstract, shows that he is NOT calculating the 'density' of functional proteins in 'sequence space,' but rather something along the lines of the density of putative functional proteins in "functional protein space": that is, his denominator is not 2^6x10^9, but something like 2^6000. That's 2^10^6 times smaller. This is a mind-boggling huge difference. From the paper you cite:
The frequency of occurrence of functional proteins in random-sequence libraries appears to be similar to that observed for equivalent RNA libraries
Axe does similar work and comes up with numbers that show the frequency is outstandingly small even within the libraries, let alone all of sequence space for the length of the human genome. JVL: There are 3 billion nucleotides in DNA. There are four nucleotides. So, the denominator (i.e., total sequence space for the human genome) is 2^2 x [2^3 x(10^9)]= 2^6x(10^9). JVL:
You’re proposing a lot of possibilities. It would take some time to check them all out. And how would you check them out.
You don't need to "check them all out." You only have to ensure that the various islands of probability within the total sequence space are probabilistically far enough away from each other that they effectively don't mix. PaV
In the opposite direction, we have Hoyle’s calculation for cytochrome c. How does this form randomly?
I'm guessing Hoyle's is an all-in-one-go calculation like his tornado in a junkyard. Proteins can start as promiscuous and evolve specificity. Alan Fox
...dwarfs the numerator, which is the total number of known functional sequences in the human genome...
What is at issue is the density of functional proteins in sequence space. This is unknown. Jack Szostak threw a little light on it with their seminal paper and work continues. You might like Andreas Wagner's Arrival of the Fittest for an overview. Alan Fox
Why would Doug Axe be wrong?
Well, that's a philosopher's question. I can only tell you Axe's (2004) work is badly flawed. I'd sum it as an elegant example of the Texas sharpshooter fallacy. Alan Fox
As to an approximate figure for infinity, it’s this: infinity minus one.
I'll give you the benefit of the doubt and assume you are joking. Alan Fox
PaV: how could a designer come up with a design unless he’s aware of the parameters available You're proposing a lot of possibilities. It would take some time to check them all out. And how would you check them out. divide that by the total number of sequences in sequence space for human cells. 2 raised to the six billionth power, which is the divisor Could you explain how you get to 2 raised to the 6 billionth power? JVL
JVL: Yes, 1 in 22^105. As to your doubts about a designer, how could a designer come up with a design unless he's aware of the parameters available? What makes you think that God lives in time? He's an Infinite Being. Now that's who I think is the Designer, because otherwise I can't see who could have devised biological life with our puny human intelligence. PaV
Jerry, The quote you include in your last post mention concepts and ideas that Ruth presents in the video. Why would Doug Axe be wrong? He did the experiments--actual experiments, versus notions of proto-genes, whose operation and existence present problems to evolutionary theory. But, I'll take a look. PaV
Alan Fox: Take the total number of functional sequences we know of, multiply that number by a million, and then divide that by the total number of sequences in sequence space for human cells. 2 raised to the six billionth power, which is the divisor, completely overwhelms and dwarfs the numerator, which is the total number of known functional sequences in the human genome multiplied by a million. In the opposite direction, we have Hoyle's calculation for cytochrome c. How does this form randomly? How can cell life take place, let alone divide, without it? Where did it come from? Either way, the astronomically small probability makes thinking this can be explained by physical forces alone, in my opinion, nothing more than metaphysics. As to functionality and specificity, what you write indicates you don't understand either concept as it's presented by ID advocates. You confuse "particular" modes of functionality and specificity with the more "general" modes of what function and specificity is. As to an approximate figure for infinity, it's this: infinity minus one. PaV
PaV: a 105 a.a. long protein has the probability of randomly coming about (assuming it won’t be destroyed upon appearance) of 22^ 105. Umm . . . probabilities are between 0 and 1 so I assume you meant something like 1 in 22^105 OR 22^-105. Not that that makes sense anyway since I doubt even your designer has the 'time' to check out all the possible combinations. JVL
Alan Fox: Can you give me a approximate figure for infinity, then? Which one? :-) JVL
Here is Anne Carvunis’s website. She is from France. https://carvunislab.csb.pitt.edu/ Also https://www.csb.pitt.edu/people/faculty/anne-ruxandra-carvunis/ This is very provocative. Does this contradict Doug Axe?
It has become clear over the past decade that completely novel protein-coding genes can evolve de novo from the “dark matter” of the genome (non-genic sequences). We are investigating a hypothesis according to which such de novo gene birth involves the existence and translation of transitory genetic elements called “proto-genes”. Our work has shown that cellular networks involve many more biomolecules than we thought, and questioned how translation is regulated. We are now actively investigating how these proto-genes evolve and acquire novel functions. Recent results show that yeast proto-genes can provide a growth advantage to the cell upon overexpression, largely due to the presence of transmembrane domains that arise naturally from non-genic sequences. In another study, we analyzed yeast, fly and human evolution, and determined that most species-specific genes cannot be explained by sequence divergence, although the fraction that emerged de novo remains to be determined. To learn more, check out our recent review (also a Wikipedia page!).
https://carvunislab.csb.pitt.edu/wp-content/uploads/2020/09/protogene_review.pdf https://en.wikipedia.org/wiki/De_novo_gene_birth jerry
...effectively infinite since this plays right into the hands of the Design Argument...
There is no theoretical limit to the length of an amino-acid sequence but living organisms employ a small subset of the theoretical possible sequences. As the only way to ascertain the usefulness, functionality, of an unknown protein is to test it, I can claim that unknown theoretical protein sequence space is awash with functionality with as much confidence as anyone claiming the opposite. Probability claims are unjustified assertions. Also, a very important point, functionality and sequence of amino acids in a protein are not the same thing. It is perfectly possible for unrelated proteins to have the same function. Also specificity is not required for function. Enzymes can act on more than one substrate, be promiscuous. Specificity can evolve. Alan Fox
PaV:
...we can’t exactly calculate infinity...
Can you give me a approximate figure for infinity, then? Alan Fox
Alan Fox: First, Alan, thanks for responding. Second, I think I'll just go down the list of your entries one by one, if that's okay.
So there’s one term we can’t reliably calculate. Now for protein sequences that have function? In all this vast sea of theoretically possible proteins, of the ones not yet having been synthesized neither in vivo nor vitro, how can anyone say whether they have a function in some scenario or not?
I would say that from the fact that we can't exactly calculate infinity we shouldn't conclude that the concept of infinity is of no utility here. Physicists and mathematicians quite often substitute zero for the term 1/infinity. I'm puzzled that you consider 22 raised to the nth power ('n' being a very number) to be effectively infinite since this plays right into the hands of the Design Argument. As to your question, ". . . of the ones not yet having been synthesized neither in vivo nor vitro, how can anyone say whether they have a function in some scenario or not?", isn't this an argument from ignorance? If "fitness" is tied to "biological function," and "biological function" is tied to sequences, to say that something is not synthesized in vivo or in vitro only tells us nothing about what could be functional. No. Hoyle was an astronomer. He had no expertise in biochemistry as far as I know. Fred Hoyle was an outstanding mathematician in addition to being an astronomer. He wrote The Mathematics of Evolution. Cells can't reproduce without the help of cytochrome c. Hence, to enter into the Darwinian realm of "selective death," known as NS, life has to reproduce itself. This means cytochrome c must be present. The question Hoyle asks is how did this protein come about randomly. The mathematics then says that a 105 a.a. long protein has the probability of randomly coming about (assuming it won't be destroyed upon appearance) of 22^ 105. An "astronomical" figure if you can pardon the pun. I'm just a lit bit surprised you weren't aware of his book (although no one seems to want to publish it. Maybe evolutionary biologists aren't interested) Are [you] mixing up your Hoyles, PaV? No, it isn't the "Hoyle's Rule" Hoyle I'm thinking about. No more time now. PaV
Gould, for his part, seems to rely almost completely on what ‘cannot’ be seen.
Just the opposite. It’s all based on what can be seen. First, there is the change represented by the new species which happens suddenly after eons. Second, there is the mechanism for this change which can be seen in the genome. The basis for the new species has been silently developing over millions of years until it is exapted for expression as a physical difference. Brosius provides a description of the origin of the second part and why it suddenly happens after millions of years of development. It’s very simple and straightforward. The term exaptation was developed by Gould with Elizabeth Vrba. They were more interested in taking current proteins and finding new uses. Brosius explains how exaptation can happen for the development of new proteins. Gould used the word “exapt” several hundred times in his final work, “The Structure of Evolutionary Theory. All these ideas show up in the above OP video. Nothing said in any of Gould’s or Brosius’s work is threatening to ID. I doubt it explains much. But ID should be aware of just what it is. iD can easily debunk it with good research. Here is another article on this.
More Evidence on the Real Nature of Evolutionary DNA Change Our data revealed >280,000 mobile element exaptations common to mammalian genomes covering ~7 Mb..., a considerable expansion from the ~10,000 previously recognized cases. Of the ~1.1 million constrained elements that arose during the 90 million years between the divergence from marsupials and the eutherian radiation, we can trace >19% to mobile element exaptations
https://www.huffpost.com/entry/more-evidence-on-the-real_b_1158228 What this means may be nothing but it should be looked at. jerry
Jerry:
Again, you obviously do not understand what was claimed as the mechanism for punctuated equilibrium. You are confusing the claimed observations with the proposed mechanism for those observations. You also cite 1970 studies.
I find neither Gould's thesis nor Brosius "proposed mechanism" persuasive. I've scanned an article Brosius wrote recently, in 2019, I believe. I look for stuff of substance. I can't find anything. Is this because I'm biased and my mind is made up? Possibly. However, I don't consider either exaptation by Gould or exaptation by Brosius to be compelling or reasonably plausible. Gould, for his part, seems to rely almost completely on what 'cannot' be seen. His is an inference. So is the "Design Inference." I find the Design Inference plausible. Why? Because intelligence does not act blindly as does nature. And invoking blind forces to explain the origin of life and its subsequent development seems unreasonable based on my experiences in this life. Let's leave it at that. OK? PaV
Again, what proof is there of “exaptation”? Why aren’t we inundated with examples of it being “demonstrated” to be true
I never said there were lots of examples. Again, you obviously do not understand what was claimed as the mechanism for punctuated equilibrium. You are confusing the claimed observations with the proposed mechanism for those observations. You also cite 1970 studies. Gould was eulogized by an evolutionary biology journal with a special issue in 2005, 30 years after what you cite. See above. Jurgen Brosius was given the premiere spot in that issue. Brosius had collaborated with Gould and obviously knew what he thought. Brosius was recommended by Allen MacNeill who said Darwinian Evolution was dead. This got me curious. I suggest you read what Brosius wrote. As I said it relates to the OP. Whether it explains much is another issue. I never said it did. Though Brosius claims it does. I provided a research approach that would solve everything. jerry
Are mixing up your Hoyles, PaV? Alan Fox
I’m sure you’re familiar with Fred Hoyle’s calculations involving cytochrome c, right?
No. Hoyle was an astronomer. He had no expertise in biochemistry as far as I know. Alan Fox
Is a Royal Flush rare? Why? Can we calculate it?
Any particular set of cards in a hand is rare compare to the total possible dealable hands but the calculation is straightforward. The chance of receiving a particular card in a deal if one card is 1 in 52.
Can this calculation be extended to genetic sequences? If not, why not?
No because we (well, I am) are talking about putative function in amino-acid sequences. First it is simple to generate the number of possible sequences by taking (for argument's sake) twenty as the choice of amino-acid and "n" as the sequence length giving us 20 to the power n as the total possible proteins of length "n". The total space becomes 1 to 1th power + 2 to 2th power + 3 to 3th power + ... which is logically, if not practically, infinite. So there's one term we can't reliably calculate. Now for protein sequences that have function? In all this vast sea of theoretically possible proteins, of the ones not yet having been synthesized neither in vivo nor vitro, how can anyone say whether they have a function in some scenario or not? Alan Fox
Jerry,
None of what you wrote is what punctuated equilibrium is.
That is no more than your view of things. Gould and Eldredge clearly state in their 1972 article that their theory is an "inference" about the tempo and modes of evolution. That Brosius is supposedly the author of a "mechanism" for punk eek, doesn't mean that's what the theory is. What Brosius describes is his "molecular genetic" notion of how things happen. In the 1977 article, if I'm not mistaken, Gould and Eldredge encourage one of their fellow scientists to investigate their theory in terms of molecular genetics. Brosius took the challenge. But that doesn't make the "putative" genetical version of punctuated equilibria the replacement of what punctuated equilibria was originally stated to be. From your quote above:
Interestingly, where relevant, the genomic perspective is consistent with Gould’s agenda.
Being "consistent with" is not the same as being "equivalent to." You conclude thusly:
These ideas are part of what is outlined in OP video.
Yes, these are ideas are mainstream evolutionary biology these days. But how does she end the video? By saying the basics of evolutionary theory have to be broken down into its elements and studied individually because the theory doesn't seem to be working. From the OP, News concludes with a comment from a friend:
. . . narrator Anne-Ruxandra Carvunis stresses that the genetic patterns she studies don’t fit the evolutionary theory learned “since I was an undergraduate.
Again, what proof is there of "exaptation"? Why aren't we inundated with examples of it being "demonstrated" to be true? Alan Fox: You never seem to want to respond to my posts. Is there a 'good' reason?
It is impossible to quantify the rarity of function in theoretical sequences.
Is a Royal Flush rare? Why? Can we calculate it? Can this calculation be extended to genetic sequences? If not, why not? I'm sure you're familiar with Fred Hoyle's calculations involving cytochrome c, right? If a Royal Flush is NOT rare, then I would conclude that an intelligent being is involved. How about you? PaV
but unfortunately for you
Why is it unfortunate? I explained what the supposed mechanism is. This mechanism is also being advocated by the researchers in the OP video. I also have at several times explained how this could be researched. Your comment is a non sequitur. jerry
Jerry The mechanism for punctuated equilibrium is
:) It's impressive you know what punctuated equilibrium is but unfortunately for you such a mechanism do not exist . Punctuated equilibrium is a just-so story invented to explain contradiction between "gradual" evolution and "explosions" observed in fossils (strata). Darwinism is a just so story and require billions of other just-so stories to be "explained". whistler
Because the process is well understood and quantifiable.
Nope. It is impossible to quantify the rarity of function in theoretical sequences. I wonder if Jerry is led astray by Axe's flawed papers on protein folding. Alan Fox
I don’t see what’s complicated here.
None of what you wrote is what punctuated equilibrium is. The mechanism for punctuated equilibrium is exaptation of various genetic elements that were not coded for eons but then were translated and eventually became working proteins. That’s why the changes were sudden after possibly millions of years of stasis. All during these millions of years something was happening that wasn’t being coded. That’s the theory as outlined by Brosius. The question is whether it is true or not. Easily verified by right research approach. Here is the journal article by Brosius who was given the lead article in an entire journal edition published to honor Stephen Gould.
Disparity, adaptation, exaptation, bookkeeping, and contingency at the genome level Journal: Paleobiology / Volume 31 / Issue S2 / 2005 Jurgen Brosius 08 April 2016 pp. 1-16 Abstract The application of molecular genetics, in particular comparative genomics, to the field of evolutionary biology is paving the way to an enhanced “New Synthesis.” Apart from their power to establish and refine phylogenies, understanding such genomic processes as the dynamics of change in genomes, even in hypothetical RNA-based genomes and the in vitro evolution of RNA molecules, helps to clarify evolutionary principles that are otherwise hidden among the nested hierarchies of evolutionary units. To this end, I outline the course of hereditary material and examine several issues including disparity, causation, or bookkeeping of genes, adaptation, and exaptation, as well as evolutionary contingency at the genomic level–issues at the heart of some of Stephen Jay Gould's intellectual battlegrounds. Interestingly, where relevant, the genomic perspective is consistent with Gould's agenda. Extensive documentation makes it particularly clear that exaptation plays a role in evolutionary processes that is at least as significant as–and perhaps more significant than–that played by adaptation.
These ideas are part of what is outlined in OP video. jerry
Same paper as above: p 139:
In this perspective, speciation is the raw material of macroevolution, and genetic substitution within populations cannot be simply extrapolated to encompass all events in the history of life. We therefore challenged the central assumption that secured the admission of paleontology into the modern synthesis of evolutionary theory (Simpson 1944 and 1953): change in gene frequency within populations is the building block of major evolutionary events. We wrote (1972, p. 112): A reconciliation of allopatric speciation with long-term trends can be formulated along the following lines: we envision multiple 'explorations' or 'experimentations' (see Schaeffer 1965)-i.e. invasions, on a stochastic basis. of new environments by peripheral isolates. There is nothing inherently directional about these invasions. However, a subset of these new environments might, in the context of inherited genetic constitution in the ancestral components of a lineage, lead to new and improved efficiency. Improvement would be consistently greater within this hypothetical subset of local conditions that a population might invade. The overall effect would then be one of net, apparently directional change: but, as with the case of selection upon mutations, the initial variations would be stochastic with respect to this change. We postulate no 'new' type of selection.
PaV
Eldredge and Gould, 1977: p 125:
But our model of punctuated equilibria predicts that no transitional forms will be found between ancestors and descendants in local sections.
p 129:
We must not make up stories about the power of natural selection, just because modern theory favors it as an evolutionary agent. In so doing, we do not strengthen the Darwinian cause, but only display our biases
PaV
Have I got it wrong, Jerry? Subpopulations get isolated from the larger population, the gene pool gets small, genes are able to be "fixed" more quickly, and "new" species form. I suppose I could add that when these "new" species reemerge into the larger population, any "intermediate" genes that existed while the ancestral line developed into a "new" species will no longer be found. When comparing the genomes, one finds an ancestral gene performing a new function. The gene has been "exapted." This is from memory, so please, anyone, feel free to correct. I don't see what's complicated here. Again, what is said to have occurred, the mechanism of exaptation, is not visible to anyone. You won't find it in extinct or extant species. I'm not one to believe blindly. PaV
I’m wondering to whom your comments are addressed.
Everyone.
Punctuated equilibria is not a complicated idea
Yet everyone on UD gets it wrong. I haven’t seen anyone here who understands it. Punctuated equilibrium is based on a biological process/mechanism and no one addresses the viability of the process.
Is “exaptation” believable
I certainly don’t know but some researchers claim it happens. It seems possible for it to have happened especially when lots of stuff gets translated. It’s testable but nobody’s doing the research to verify it or not. Brosius claims it has worked but again I haven’t seen a research project that says it has or hasn’t. Seems unlikely but it’s definitely a possible process. But how likely is the process to generate usable proteins? Certainly Allen MacNeill believed it happened. jerry
Alan Fox @ 10 :
Allow me to point out the flaw in your conjecture. It is impossible to allocate a probability to an unknown quantity. In this case, how rare useful amino acid sequences are in the space of all sequences.
This seems to be no more than another way of saying that miracles happen. As to the video, as best I could understand, the cunundrum she is wrestling with is this: in the yeast cells she studies, proto-genes exist and are expressed; however, a single mutation in a proto-gene severely compromises the growth of the organism. If, however, the same proto-gene with the mutation reversed is supplied to the organism via a plasmid insertion, then 'functionality' is restored. On this basis of both these things happening, she concludes that NS should be at work. That is, "purifying" selection should have eliminated the proto-gene. But, there the proto-gene is. Why? For her, this flies in a completely different direction than the one she was trained in, the central dogma. She wonders if "different forces" are at work within the organism/cell; that is, a "different force" than NS. I would comment that this seems to be really no more than what Kimura found in the 60's. Using the techniques of protein variant identification via the new technique then of gel electrophoresis, all kinds of protein variants (tied to sequence variants) were showing up in animal populations. Too many, though, since the level of "purifying" selection needed to cause genes to be "fixed" and all of these various loci needing to be "purified" would then require lots of offspring to die off. That is, all of this variability should have killed off the populations (Haldane's Dilemma). It was as if NS had been "turned off." So, Motoo Kimura "turned off" NS via his "Neutral Theory." But, of course, the Neutral Theory ended up being exapted by Darwinian theorists. Alas. Jerry @ 15: I'm wondering to whom your comments are addressed. Punctuated equilibria is not a complicated idea. The question is: is it believable? Is "exaptation" believable. "Exaptation" is itself a "miracle." It says, "There used to be something there that was useful at the time, but no longer needed, and now it's gone." IOW, don't bother "looking for it." Is this really a testable theory? PaV
It is impossible to allocate a probability to an unknown quantity
Incredible stupid statement. Why? Because the process is well understood and quantifiable. Again, shows that many commenters here do not understand what they are talking about. They just mouth cliches. jerry
I have been pointing to Jurgen Brosius for years after Allen MacNeill introduced him about 15 years ago. No one has paid attention till PAV posted an article by him the other day. He has more faithful followers in the world than UD certainly does. His ideas which are not his alone are the basis for punctuated equilibrium. Which as pointed out here several times no one who posts here understands. Hint: It has to do with Junk DNA which is hot this morning. Most posters at UD do not understand the theories of those they oppose. They just rant at how stupid they are. Aside: the theories they oppose are stupid but they fail to understand why. Most of the world believe these stupid ideas. People on UD haven’t a clue how to change this. jerry
Fasteddious, Thanks for taking the time to 'decipher' the video. I too had a hard time understanding her and quit watching the video after a few minutes. Anyways, from your synopsis,
Her example is one gene in a yeast species, which she traces back through a supposed evolutionary tree to other yeast species, which has almost the same gene as a non-functional (or perhaps minimally functional?) proto-gene. The tracing back shows which codons were changed at each step to create a proper open reading frame, followed by improved functionality. Mind you, she said they don’t know what the function is yet for that new gene.
So basically, they did no experimental work, and don't even know the function of the new gene, but only assumed that the common ancestry of a yeast gene was true. My first thought was that yeast, all by themselves, have already thrown a big monkey wrench into the entire Darwinian assumption of common ancestry. As one researcher out, “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.”
Here Are Those Incongruent Trees From the Yeast Genome - Case Study - Cornelius Hunter - June 2013 Excerpt: We recently reported on a study of 1,070 genes and how they contradicted each other in a couple dozen yeast species. Specifically, evolutionists computed the evolutionary tree, using all 1,070 genes, showing how the different yeast species are related. This tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. Yet one of the fundamental predictions of evolution is that different features should generally agree. It was “a bit shocking” for evolutionists, as one explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.” In fact, as the figure above shows, the individual gene trees did not converge toward the concatenation tree. Evolutionary theory does not expect all the trees to be identical, but it does expect them to be consistently similar. They should mostly be identical or close to the concatenation tree, with a few at farther distances from the concatenation tree. Evolutionists have clearly and consistently claimed this consilience as an essential prediction. But instead, on a normalized scale from zero to one (where zero means the trees are identical), the gene trees were mostly around 0.4 from the concatenation tree with a huge gap in between. There were no trees anywhere close to the concatenation tree. This figure is a statistically significant, stark falsification of a highly acclaimed evolutionary prediction. http://darwins-god.blogspot.com/2013/06/here-are-those-incongruent-trees-from.html
So basically, the common ancestry of yeast can be dealt a severe, even fatal, experimental blow, and it is apparently of no consequence for Darwinists. Business, and/or 'just-so stories', simply carry on as usual for Darwin's theory. Again, whatever Darwin's theory is, it is certainly not experimental science. As to her belief, "that mutations can accumulate in these proto-genes and that they can then be selected for due to their unknown function (proto-function?). As they get mutated, and their function starts to be useful, they get further selected and over time, become actual new genes, properly expressed." Yet again, experimental evidence contradicts her Darwinian 'just-so story',
Right of Reply: Our Response to Jerry Coyne - September 29, 2019 by Günter Bechly, Brian Miller and David Berlinski Excerpt: Indeed, Harvard mathematical biologist Martin Nowak has shown that random searches in sequence space that start from known functional sequences are no more likely to enter regions in sequence space with new protein folds than searches that start from random sequences. The reason for this is clear: random searches are overwhelmingly more likely to go off into a non-folding, non-functional abyss than they are to find a novel protein fold. Why? Because such novel folds are so extraordinarily rare in sequence space. Moreover, as Meyer explained in Darwin’s Doubt, as mutations accumulate in functional sequences, they will inevitably destroy function long before they stumble across a new protein fold. Again, this follows from the extreme rarity (as well as the isolation) of protein folds in sequence space. Recent work by Weizmann Institute protein scientist Dan Tawfik has reinforced this conclusion. Tawfik’s work shows that as mutations to functional protein sequences accumulate, the folds of those proteins become progressively more thermodynamically and structurally unstable. Typically, 15 or fewer mutations will completely destroy the stability of known protein folds of average size. Yet, generating (or finding) a new protein fold requires far more amino acid sequence changes than that. Finally, calculations based on Tawfik’s work confirm and extend the applicability of Axe’s original measure of the rarity of protein folds. These calculations confirm that the measure of rarity that Axe determined for the protein he studied is actually representative of the rarity for large classes of other globular proteins. Not surprisingly, Dan Tawfik has described the origination of a truly novel protein or fold as “something like close to a miracle.” Tawfik is on Coyne’s side: He is mainstream. https://quillette.com/2019/09/29/right-of-reply-our-response-to-jerry-coyne/ Dan S. Tawfik Group - The New View of Proteins - Tyler Hampton - 2016 Excerpt: Tawfik soberly recognizes the problem. The appearance of early protein families, he has remarked, is “something like close to a miracle.”45,,, To the extent that Tawfik’s selection experiments were successful, it is because mutations were localized and contextualized. Mutation had a key but confined role. If evolution proceeded, the prevailing architecture of the active sites and protein shapes nonetheless remains intact. Changes were not to central structures, but to peripheral loops. A great deal of flexibility was discovered. Still, it is hard to see how any of this could build proteins—that is, in the sense of building their fundamental shapes, or scaffolds; and build proteins in terms of explaining the key catalytic strategies of each active site. Even in the impressive demonstration of a transition through nine orders of magnitude, in which a full exchange of a promiscuous activity for the primary activity was seen, the overall geometry of the protein was unchanged, and, although substrates had changed, the fundamental active site strategy stayed the same. ,,, “Modern neo-Darwinism and neutral evolutionary treatments,” remark Leonard Bogarad and Michael Deem, “fail to explain satisfactorily the generation of the diversity of life found on our planet.” It is not that they did not evolve, they say, but that “... most theoretical treatments of evolution consider only the limited point-mutation events that form the basis of these theories.” Their sober conclusion is that “point mutation alone is incapable of evolving systems with substantially new protein folds.”60,,, “In fact, to our knowledge,” Tawfik and Tóth-Petróczy write, “no macromutations ... that gave birth to novel proteins have yet been identified.”69 http://inference-review.com/article/the-new-view-of-proteins Chase Nelson At Inference Review: Reconstructing Ancestral Proteins - August 13, 2021 Excerpt: The deepest questions about the origins of novel gene families remain shrouded in mystery. https://uncommondescent.com/evolution/chase-nelson-at-inference-review-reconstructing-ancestral-proteins/
And from another angle of experimental evidence, i.e. 'quantum criticality', here is yet more experimental evidence that functional proteins, (and other functional biomolecules), are exceedingly rare in sequence space.
Quantum criticality in a wide range of important biomolecules - March 2015 Excerpt: “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” they say. That’s a discovery that is as important as it is unexpected. “These findings suggest an entirely new and universal mechanism of conductance in biology very different from the one used in electrical circuits.” The permutations of possible energy levels of biomolecules is huge so the possibility of finding even one that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,, “what exactly is the advantage that criticality confers?” https://medium.com/the-physics-arxiv-blog/the-origin-of-life-and-the-hidden-role-of-quantum-criticality-ca4707924552 Quantum Critical Proteins - Stuart Lindsay - Professor of Physics and Chemistry at Arizona State University - 2018 Excerpt: The difficulty with this proposal lies in its improbability. Only an infinitesimal density of random states exists near the critical point.,, Gábor Vattay et al. recently examined a number of proteins and conducting and insulating polymers.14 The distribution for the insulators and conductors were as expected, but the functional proteins all fell on the quantum-critical distribution. Such a result cannot be a consequence of chance.,,, WHAT OF quantum criticality? Vattay et al. carried out electronic structure calculations for the very large protein used in our work. They found that the distribution of energy-level spacings fell on exactly the quantum-critical distribution, implying that this protein is also quantum critical. There is no obvious evolutionary reason why a protein should evolve toward a quantum-critical state, and there is no chance at all that the state could occur randomly.,,, http://inference-review.com/article/quantum-critical-proteins Gábor Vattay et al., “Quantum Criticality at the Origin of Life,” Journal of Physics: Conference Series 626 (2015); Gábor Vattay, Stuart Kauffman, and Samuli Niiranen, “Quantum Biology on the Edge of Quantum Chaos,” PLOS One 9, no. 3 (2014)
Verse:
1 Thessalonians 5:21 but test all things. Hold fast to what is good.
bornagain77
Alan Fox writes:
It is impossible to allocate a probability to an unknown quantity
This has always been the problem ID has when they argue against evolution using probability. Ford Prefect
Why do people insist on ignoring natural selection?
who is ignoring natural selection? You obviously have no idea what it means. Or you wouldn’t be making such stupid statements. jerry
Intrigued by the post, I watched the video presentation. Basically, she says that between recognized genes in the genome, there are long stretches of non-coding DNA which contain many more "proto-genes". Those are sequences that are sometimes partially expressed but which have no known function. She claims that mutations can accumulate in these proto-genes and that they can then be selected for due to their unknown function (proto-function?). As they get mutated, and their function starts to be useful, they get further selected and over time, become actual new genes, properly expressed. This seems like a fancy version of the old "new-genes from mutating junk DNA" theory. A lot of intermediary proto-genes exist between the random junk and the true genes, and these proto-genes can be selected for and can evolve into new genes expressing useful proteins. Her example is one gene in a yeast species, which she traces back through a supposed evolutionary tree to other yeast species, which has almost the same gene as a non-functional (or perhaps minimally functional?) proto-gene. The tracing back shows which codons were changed at each step to create a proper open reading frame, followed by improved functionality. Mind you, she said they don't know what the function is yet for that new gene. This seems like a combination of "junk DNA" that is not really junk, plus a mutation-selection chain from partial/maybe function to full-function. She did find that when the proto-gene in another experiment is knocked out, the yeast grows slower. So clearly this "proto-gene" sequence had some real function, but it could not be called a "gene" because it wasn't expressed the same way other genes are. To me that seems more like, "We don't really know everything about genes, expression, proteins, and functions, but we are trying to fit what we see into a Darwinian mould." Somehow I doubt whether this approach can rescue Darwinism. Sure, there may be ten times as many "proto-genes" than "true genes" in the genome, but that does not significantly change the probability of random sequences yielding a useful gene. Perhaps it is more that cells have some backup sequences for special purposes which get used only when needed. If they are used often (a new environment), then they get improved through selection. If they are not needed, they are ignored and may start to degrade via mutations, until needed again, when they could be rescued again from the archive, cleaned up and put back to work. Yes, natural selection sometimes works on small changes to either maintain genes or improve partially functional genes. But as we know, Darwinian processes cannot work if there is nothing to select for. I'd best stop speculating before I exceed my limited knowledge. :-) Fasteddious
The idea is that any random assembly of amino acids more than 150 units long has a 10^-74 (or thereabouts) chance of being a useful protein, at least according to Doug Axe’s experiments and subsequent mathematical logic.
Allow me to point out the flaw in your conjecture. It is impossible to allocate a probability to an unknown quantity. In this case, how rare useful amino acid sequences are in the space of all sequences. Alan Fox
AF @8: The idea is that any random assembly of amino acids more than 150 units long has a 10^-74 (or thereabouts) chance of being a useful protein, at least according to Doug Axe's experiments and subsequent mathematical logic. Others have found similar estimates. Moreover, without a useful function, such an assembly would not be selected for. This is what is meant by searching through the space of possible polypeptides looking for a new protein. The functional ones are so far apart in that space that there is no way to find a new one other than by a random search. And at that level of improbability, there is not enough time or other resources (random trials) in the cells and population to find even one such protein. Fasteddious
Thus, you cannot realistically get a new functional protein by randomly tweaking existing DNA or by chance mixing and matching pieces of genes.
You don't know that until that new or changed sequence is road-tested by selection. Why do people insist on ignoring natural selection? Alan Fox
I haven’t had time yet to look at the video
I only looked at a short amount. Hard to understand her. Seems sincere. Associated with a big medical center. jerry
If you click on the link in my post, just click to the top right in the blue button which says, "Download pdf." Hope that helps. I haven't had time yet to look at the video. Thanks for the heads up on her explanation. PaV
In a 2019 paper, Juergen Brosius writes this
All my references to Brosius turn up as broken links. They were to his publications and linked to Muenster University in Germany. It seemed he left and they took down his links. Doesn’t seem like a good relationship. He was given the privilege of introducing the issue of a journal dedicated to the memory of Gould. In it he described the basis for punctuated equilibrium. It is exaptation and how new proteins arise. This is apparently how the woman in the video above describes the origin of some new genes. Unused regions of the genome mutate away until something then gets transcribed and then exapted for something. Brosius claims to have some examples. Easily assessed with the right research program. jerry
Jerry: Jeurgen Brosius collaborated with S.J. Gould to promote "exaptation" (Gould's invention) at the "genetic level." In a 2019 paper, Juergen Brosius writes this:
Addressing ambiguities involving the term exaptation As exemplified in footnote 2, Wallace used the term adaptation to describe what would be defined as exaptations sensu Gould and Vrba (Gould and Vrba, 1982). Some authors suggest “...it is impossible to differentiate exaptation from adaptation unless we interpret the term teleologically” (Larson et al., 2013). Unlike mathematics with its rules and physics with its laws, biology and especially evolutionary biology, although adhering to the aforementioned, the “guiding” principles are best portrayed as “whatever works”. Hence, for most states or concepts in biology, there are no clear boundaries (Brosius, 2014; Brosius and Raabe, 2016; Pauli et al., 2015); accordingly, there exists a fuzzy area between exaptation and adaptation. In addition, an exaptation event is usually followed by numerous adaptations. Buss and co-authors (Buss et al., 1998) realized that “exaptations themselves often involve further adaptations”. In addition, these authors listed a number of other confusions—chiefly pertaining to culturally useful features of the brain—psychological (including cognitive capacities), human instrumental actions, or motivational mechanisms. They did, however, resolve many of the misunderstandings concerning exaptation."
There's serious problems here, no? PaV
you cannot realistically get a new functional protein by randomly tweaking existing DNA or by chance mixing and matching pieces of genes
This is what she claims has happened. I have a hard time understanding her. So it’s hard to know what’s a claim and what she has evidence for. I will be traveling the next few days so I may take awhile finishing her presentation. I mentioned Doug Axe in my comment. I’m well aware of his claims. It’s just that there are claims to the opposite of Axe’s findings. jerry
Jerry: ORFan genes are one of the arguments in favour of ID. It seems that many (possibly most) species have at least one gene unique to that species. Darwinists cannot explain where those genes (and their proteins) came from except by positing unlikely scenarios. They also like to hype up tiny modifications to existing genes as "new genes". Truly new genes are essentially impossible to create "de-novo" via Darwinian means. What Doug Axe showed (and no one has refuted it, I believe) is that functional (useful) proteins are extremely rare in the haystack of possible amino acid sequences. Thus, you cannot realistically get a new functional protein by randomly tweaking existing DNA or by chance mixing and matching pieces of genes. I don't have a link to the paper and subsequent discussions, but you can search his name on evolutionnews.org . Fasteddious
I am trying to understand her but it is difficult. Basically, she says genes originate in a lot of ways and describes these ways. But she also says some genes come out of no where. Now this is the basis for punctuated equilibrium and described by Jurgen Brosius and originally brought up by Allen MacNeill. Brosius describes the process by which these de novo genes arise. Totally ignored by everyone on UD. Another example of one side not knowing what the other side is claiming. Instead most of the comments here are wasted on meaningless inanity. Aside: Doug Axe has essentially undermined this process of forming de novo genes but there is no formal article that does so. Also there is a research program that would prove or disprove it but no one is interested. Which leads to my assessment that neither side is interested in finding out the answers. What are they afraid of? ID should not be afraid since its basic premise does not depend on Evolution not being true. jerry

Leave a Reply