A prominent ID supporter at UD, gpuccio, has this to say:
My simple point is: reasoning in terms of design, intention and plans is a true science promoter which can help give new perspective to our approach to biology. Questions simply change. The question is no more:
how did this sequence evolve by some non existent neo darwinian mechanism giving reproductive advantage?
but rather:
why was this functional information introduced at this stage? what is the plan? what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?
Gpuccio references actual biology in his writings and is one of the few at UD that do, and as such I’m prepared to take him at his word that the ID project is now ready to move from simply determining design to answering the questions he posed:
- why was this functional information introduced at this stage?
- what is the plan?
- what functions (even completely unrelated to sheer survival and reproduction) are being engineered here?
If any ID supporter would like to provide a specific example with answers for those 3 points for discussion that would be perfect.
Gpuccio’s OP concludes:
The transition to vertebrates was a highly engineered process. The necessary functional information was added by design.
In response I simply repeat back the question what is the plan?
Question for the experts. Is there any know case in which a relatively or even highly conserved protein(s) at some point in some lineage have undergone a faster evolution? IOW, some protein has stopped being subject to significant selective pressure?
Not that I’m an expert, but off the top of my head, genes involved in eye development in blind cave fish. Opsins perhaps. Maybe the regulatory genes such as PAX6 if does not have important, unrelated pleiotropic effects.
Another thing could be genes involved in tooth formation in toothless birds.
In general, most pseudogenes would more or less qualify. GULOP in humans is rather heavily degraded, having many substitutions and is missing several exons.
Rumraket,
Thanks, makes complete sense.
Seems to me that in order to provide some meaningful metric of conservation in vertebrates that might help measure functional constrain in vertebrates for those proteins, one would need to align the proteins for ALL current vertebrates and determine what’s conserved across the board. Does that make any sense?
I still wouldn’t call that a measure of “functional information”
Yes, there are many such examples. In fact, one popular method for identifying sequences under positive selection is to look for lineages in a phylogeny that have undergone relatively rapid amino acid substitution in comparison with lineages in which the sequence is more highly conserved is (more specifically, looking for elevated rates of non-synonymous substitutions compared to synonymous substitutions).
Here is an example of such a case from my own research (as yet unpublished, though I’m working on it!). This is small snippet of an alignment of tropomyosin sequences found in six spider species from 3 genera (two species per genera). There are very few amino acid substitutions in any of the species over most of the length of the sequence, but here toward the middle there is a relatively high concentration of non-synonymous substitutions in two of the species from the same genera. This is a pretty strong signal of positive selection acting in the ancestor of these two species.
There many more published examples of this kind of analysis.
Dave Carlson,
Thanks so much, Dave.
So in this case, a loss of conservation led to speciation, or played a roll in it. I guess that would imply a loss of functional restraint and therefore, a loss of information according to gpuccio?
I have repeatedly asked you to present some of this evidence against common descent. Usually you ignore me, but occasionally you present evidence against the power of natural selection (or at least you think it’s evidence). Do you understand that natural selection and common descent are two very different things?
What is the evidence against common descent?
I think that at the very least you would have to ignore pseudogenes. I presume the question would be how much a protein could vary and still retain the same function. Proteins that have lost all function (really, genes that don’t produce proteins any more) should not count, nor should proteins that have significantly altered function. And now you have to ask what “significantly” means. Even proteins like cytochrome c, which does the same thing in all eukaryotes, must adapt to their cellular environments: operating temperatures, pH, changes in associated proteins, etc. It’s not a simple question.
Actually, there is no particular reason to think that these amino acid changes have anything to do with speciation. They happened somewhere on the branch connecting those two species, but there’s no way to tell where on that branch. They merely must have happened after that branch had separated from other branches.
What John said. I don’t have any particular reason to believe that these changes are related to speciation. For the record, the three genera I used in the analysis are not that closely related (the data I used were a small subset of a larger analysis being conducted in conjunction with multiple labs – these six species were just the ones that I had access to). To get a better understanding of when and in what specific lineages these changes took place in, we would need to use more dense sampling of species to put these changes in to a more complete phylogenetic context.
Understood. But it still seems to me it undermines gpuccio’s metric if loss of conservation can produce positive selection. Obviously this can be easily explained by evolutionary mechanisms: environmental changes affecting selection for the ancestor of these spiders.
How does ID explain the loss of conservation in those genes? It simply can’t
Can someone help me with this? Seems to me if purely neutral variation was going on, it would make no sense to talk about function, therefore function couldn’t remain exactly the same (well, unless “no function” is considered function)
Am I missing something?
Allan Miller,
I respectfully disagree with this point. I don’t think we have a clue how novel genes arrive.
John Harshman,
I don’t see them as separated. For common decent you need a mechanism of how the process occurred or how can you claim the descent actually occurred? The evidence against is the differences in genes and regulatory RNA between species. The evidence for common descent is the similarities.
colewd,
When you say ‘we’, you just mean you.
eta – a paper all about not having a clue
colewd,
You just don’t. The mechanism by which two sequences are related is simply descent. Not selection, not drift, not HGT, not even a step by step history of every generation, but simple descent – implemented by template copying of DNA in separate lineages.
It is clear that descent occurs. It would be perverse to deny it. You don’t need an additional mechanism.
colewd,
Differences between lineages are not evidence against common descent! If there was nothing but difference, then maybe. But that is not the case.
By the same token, one does not need a mechanism for solar development to infer the components, shape, and the movement of the planets and the sun in our solar system indicate they are all related in terms of their origin. Similarly, one does not not need a mechanism for plate tectonics to infer that geological features around the world indicate that the landmasses move around.
There appears to be some hurdle for some people in understanding the difference between patterns that indicate relationships and the explanations for how those relationships come about.
Devil’s advocate:
Patterns are the bailiwick of ID mongers. Patterns plus mechanisms are provided by biology.
We can observe mutations in controlled experiments. We can observe mutations in lineages of people and plants and animals and bacteria. This is the mechanism of change and the source of variation. It is indisputable.
We can observe that some mutations are synonymous, some are neutral, some are nearly neutral, some are advantageous in some environments and deleterious in other environments, some are deleterious in most environments, some are lethal.
We can do the math for the fixation of variants. We can do so for various values of neutrality or non-neutrality.
We can deduce the rate of mutation from laboratory experiment and from differences in close lineages. We can extrapolate the rates of change in lineages that are more distant.
There are lots of other lines of evidence. Common descent is not just a pattern.
The pattern is icing on a cake that was baked a century ago.
Do you know the mechanism that causes snow to fall? And if you do, was this mechanism known 1000 years ago? In either case, don’t you and didn’t people then know that there was snow? No, you don’t have to know why genetic changes happen in order to use them to determine that common descent happens. Differences are not evidence against common descent. In fact they’re evidence for common descent, since the differences are arranged in a nested hierarchy. Can you explain why that’s the case?
A mechanism really is crucial to common descent. To be sure, we have one–reproduction, the copying and transmission of DNA information.
Languages also bear the marks of common descent, but the mechanism surely is different (and obvious).
On the other hand, early American rockets were much like V2 rockets (later ones, too, since the Germans got a lot right, but not as much like V2, of course). Common descent? Well, clearly in some sense that’s the case, in the sense of ideas having a kind of descent from earlier ideas, but it’s not really “common descent” as we generally understand that to be. Common design can yield some commonalities that common descent would, but clearly the overall patterns have never been very similar at all, which is why it’s very annoying to constantly have that failure bandied about as an “alternative.”
It’s really a matter of cause and effect, and one must know how the two relate in order to infer one from the other (hint, ID isn’t really an inference at all, not in the scientific sense, as there’s no specific connection between cause and effect). Hence mechanism matters. Reproduction is such a familiar mechanism that we tend to forget that it is a mechanism, but it is the only good inference that can be made for the patterns of similarities (along with differences) among organisms. It’s the mechanism that Behe invokes, indeed, as a kind of normal scientific inference from effect to cause, while he breaks from science in claiming that differences arise by design (even though they’re clearly limited by reproduction and the mechanisms of mutation, etc.).
We don’t often really invoke a mechanism for common descent because it’s so obviously reproduction, the only mechanism ever observed for it in the realm of biology (even HGT is a kind of reproduction, just an unusual type). It’s just that it’s still a mechanism, or a number of mechanisms if you prefer.
Glen Davidson
Reproduction with heritable variation.
It would seem so.
Glen Davidson
Sure, but colewd isn’t asking about the mechanism of common descent, though he thinks he is. He’s asking about the mechanism of evolutionary change. He thinks they’re the same thing.
I’m rarely clear about what he thinks, other than that evolution is wrong because he’s sure that some long-ago changes couldn’t happen “naturally.” And, ID can be properly inferred without any specifics whatsoever being known, let alone confirmed (because it’s been limited to the point of meaninglessness, although he seems clueless about its meaninglessness).
But yes, he does seem to muddle together change and continuity, from what I’ve seen. Evolutionary theory shall be done in by blunt force trauma!
Glen Davidson
Colewd is not simply denying the evidence for evolution and common descent; he is denying that there is a description of evolution as history and a description of descent with variation. In other words, he is denying that textbooks on evolution exist, that general articles like Douglas Theobald’s 29 Evidences exist.
He does not even bother to argue against the literature. He denies it exists. He is JoeG without the foul mouth.
And you have zero formal education and you don’t work with any of it for a living. And multiple people have corrected dusins of misconceptions you have before, including me.
For some strange reason I can’t put my finger on I just don’t take your disagreement very seriously.
John Harshman,
Now that I have seen Allan’s definition of common descent, I agree. The question in my mind is does is explain anything. If differences is not evidence against common decent what is evidence against it?
If there is no evidence against it, again, what is it, simply a definition of what is observed like speciation. Does common descent = commonality in DNA sequences?
Rumraket,
If you have a paper the mathematically reconciles how a de novo gene is created other than, a gene is copied, mutations occur and it finds new functional space and is transcribed, I am all ears.
Have you ever wondered how paternity tests work?
What is Allan’s definition and how does it differ from the usual one? I think you may be misinterpreting there. Evidence against common descent could be of many sorts, but generally anything that contradicts what we would expect from it. If, for example, similarities and differences were not arranged in a consistent nested hierarchy, that would be evidence. No, common descent does not equal commonality in DNA sequences. Common descent is just what it sounds like. Certainly we would expect to see similarities in DNA sequences that had a common ancestor not too awfully long ago.
I don’t understand what you aren’t getting here.
John Harshman,
It sounds like you can trace the linage of a group of animals as you can trace human linage.
For humans since you know how reproduction works this is much more straight forward.
You say that common descent is independent of a mechanism.
How do you look at the data and make a decision that two species descended from a common ancestor?
Since the nested hierarchy was created by some objective criteria isn’t this self evident as long as the creator of the nested hierarchy is competent?
Do you agree with Allan’s statement?:
This is why I asked does similar DNA=Common descent?
I don’t know what you mean by any of that. Could you try harder to say what you mean? I don’t know how you intend to trace human lineage. I’m pretty sure we know how reproduction works in any organism.
I never said common descent is independent of a mechanism. What I said is that our ability to infer common descent doesn’t depend on the mechanism that causes genetic changes. We don’t decide that two species descended from a common ancestor. We decide that lots of species descended from a common ancestor, based on our ability to find a nested hierarchy, and we decide that two species are more closely related to each other than to other species, based on the same thing.
Again, I have no idea what this means. The nested hierarchy wasn’t created at all. It was discovered by analysis of data. I don’t know what is supposed to be self evident.
Similar DNA doesn’t equal common descent. We do not infer common descent based on “similar DNA” but, again, from a nested hierarchical pattern of similarities and differences. I’m not sure what “mechanism” means here, but certainly the more recently diverged two species are, the more their genomes will tend to resemble each other. This ought to be obvious. Replication of DNA is nearly perfect from generation to generation, with errors somewhere around 10^-8 per base. What are you trying to say? Where is your promised evidence against common descent, which you have been so certain of?
If you’re honestly interested in learning what is known about de novo gene origin – and this is for the most part a relatively recent field of study, so research is ongoing – you might start with the following two review papers:
– The evolutionary origin of orphan genes
https://www.researchgate.net/profile/Tomislav_Domazet-Loso2/publication/51606747_The_evolutionary_origin_of_orphan_genes/links/5400dcf20cf2c48563aee9ab.pdf
– New genes as drivers of phenotypic evolution
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4236023/
Dave Carlson to colewd:
He isn’t honestly interested in learning about the evidence for common descent, so it’s doubtful that he’s honestly interested in learning about de novo gene origin.
He’s in constant fear of the evidence. What a way to live.
Dave Carlson,
Thank you.
John Harshman,
Similarities and differences of DNA? What else? At what point is a common ancestor inferred?
??? You were just told it was inferred “from a nested hierarchical pattern.” You quoted it! Did you not read what you quoted? Do you not understand the nature of this pattern?
Or stop asking about common descent. It is unseemly to ask what the evidence is, when you have a link to one of the best summaries around.
Dave Carlson,
https://www.researchgate.net/profile/Tomislav_Domazet-Loso2/publication/51606747_The_evolutionary_origin_of_orphan_genes/links/5400dcf20cf2c48563aee9ab.pdf
Both these papers were not legible from the link. The third (pubmed.gov) paper is legible and I have read the abstract. Will finish the body of the paper over the next couple of days.
There were only two papers, actually. Both links work for me, but here’s another version of the first one:
http://bioinfo2.ugr.es/PDFsClase/EvolMol/The%20evolutionary%20origin%20of%20orphan%20genes_2011.pdf
Flint,
What is the original criteria that determines the nested hierarchical pattern? DNA similarity/differences? What else?
Dave Carlson,
This link works. Thanks 🙂
Once more I have no clear idea what you’re asking me. There are other sources of evidence (morphology, mostly), but the DNA is enough by itself. Simply put, the data have some degree of fit to any tree, by some criterion. One such criterion that’s easy to explain is parsimony: the minimum number of changes necessary to account for the distribution of characters are assigned to various branches, which gives a total count of all changes. Then you try that criterion on lots of trees. If some small subsample of all possible trees has a much better (lower) score than for any other trees, the data are hierarchically structured and imply a particular pattern of common descent. If there were no common descent, there would be no reason to expect any tree to be strongly preferred by the data.
colewd, you now have 3 references about the origin of de novo genes, since I provided one as well. Is that enough to be going on with?
Similar DNA (sequentially aligned) is an expectation of common descent. It is not the same as common descent, as your equation seems to be saying/asking.
DNA is copied by unwinding the double strand and regenerating the complementary strand on each single strand, giving two-for-one. This is the fundamental process/mechanism of descent. It keeps going, with the potential for exponential doubling but the reality of much lineage loss.
Separate, independent lineages of copying are an inevitable result, and if more than one lineage survives to be tested, they ultimately trace back (coalesce) to a single molecule. They are commonly descended.
This copying does not solely occur in a parent-child, full-genome manner, but that’s the ‘main line’ process of descent.
colewd,
Why are you so afraid to examine what you claim to have been seeking?
What does it mean to “mathematically reconcile” how a de novo gene is created?
Try to explain yourself:
What are you looking for?
What should be in the paper in your opinion?
Why should that be in the paper?
A gene can be duplicated, that is an observed fact. Are you with me this far? In fact, genes are actually duplicated extremely frequently, much higher than the rate of spontaneous point mutations. Gene duplications are probably the most frequent type of mutation.
See for example: High Spontaneous Rate of Gene Duplication in Caenorhabditis elegans
To give an example of a known duplication that was also transcribed, in the LTEE, the citrate transporter was duplicated into another part of the genome, such that it was immediately transcribed. A copy was made and the copy randomly inserted itself in a place where it came under control of another promoter. So the “and is transcribed”-part is not a separate event that needed to happen also, after the duplication.
It was duplicated and the duplicate is transcribed, full stop. This is an observed fact. You with me so far?
I understand that conservation strongly suggests negative selective pressure and therefore, functional constraint. I also understand that neutral evolution is an indication of lack of function. What I don’t think is meaningful is your metric for “functional information”:
Is seems odd to me to quantify “functional information” by comparing proteins that retain the same function. For all I know most of the “information” that makes a shark different to a bony fish, or a mouse, is in gene regulation anyway.
You’re comparing sequences in one lineage, I would say you’re only measuring divergence, not information.
At the end of the day your argument seems to me like a rehash of Meyer’s Cambrian impossibility with some sciency information pseudo-theory:
yawn
Hi Pucci! I’ve missed you as well!
Unfortunately I can’t comment on your post because (I’m assuming) you had me blocked. I assume this because you were the only person I was really talking to last time I was at UD. I even tried to make a new account while you were gone for a bit, but it appears you guys know my IP.
alicia cartelli,
Hi and welcome to TSZ.
I suspect Barry Arrington keeps a tight hold on the reins of power. It is simple to block IPs from the admin dashboard. I doubt gpuccio had a hand in it.
If anyone here is allowed to comment at UD, please invite Gpuccio to join us here. It’s getting rather silly.