I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.
Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.
If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.
One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.
Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.
That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).
Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.
The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”
So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.
So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.
Allan Miller,
Yep the atom, molecule and DNA labs could be inside space time but how do you account for their origin?
Or perhaps, just perhaps, the number of genes uniquely shared between human and zebra fish is not an estimate of the number of genes in their common ancestor. And it isn’t that the ancestor has more genes, it’s that genes are constantly being lost and added, and I suspect that the total number of genes doesn’t change all that much.
Anyway, you haven’t told us how the pattern you note is either expected from or explained by separate creation. Care to go into some detail on that?
And this is in conflict with the observation that cytochrome c is a highly conserved molecule showing deep homology across species?
Alan Fox,
This is Allan’s question. The differences are explained by different function. When I have looked at the substitution differences there is data that shows certain reptiles with closer sequences (13 different) than certain primates (14 different). The same situation occurs with birds and primates. In order to make the tree work you need to invoke the different molecular clock claim which is untestable.
You persist in making claims that have already been shown to be false. Trees do not make any assumptions about molecular clocks, so nothing needs to be invoked. Looking at individual sites should clear up any confusion.
Differences can’t be explained by different function. Even the apoptosis pathway you mention is possessed by many different organisms with different cytochrome c sequences and thus can’t account for those differences. And your explanation can’t account for the nested hierarchical nature of the differences, while common descent can.
John Harshman,
Explain why there are outliers that conflict with what we would expect with common descent. I would not expect a reptile to have more sequence similarity than a primate.
This is clearly a piece of contradictory data. It appears your methods sweep contradictory evidence under the rug.
In addition you are claiming that genes are constantly being lost and added. This is all happening solely due to reproduction?
John Harshman,
Please support this claim. I think it is, in the words of Mung, incoherent at this point.
There are no outliers that conflict with what we would expect, only with what you would expect. What you would or wouldn’t expect is based on your ignorance of evolution and so should not be given much weight. You think it’s contradictory evidence because you are projecting your wishes onto the blank screen of your lack of knowledge.
I’m never sure what you mean by “solely due to reproduction”. It’s due to reproduction, mutation, selection, and drift. If that’s what you mean, then yes. There is no evidence that there is any other cause, and we can see evidence of the process by looking at different genomes.
I can’t support the claim that your explanation can’t account for the differences, there being no way to prove such a negative, but you could refute it by accounting for the differences using your explanation. In the absence of such a refutation, I think I have reasonable grounds for doubting there could be one. Common descent can explain the differences: they arose at various spots on a tree of descent and therefore fit a nested hierarchy. Common descent is an elegant and intuitively obvious explanation for nested hierarchy in data. Nobody has ever suggested a different explanation that survives cursory examination. You would be the first if you can manage it.
John Harshman,
I think what Sal has illustrated is that common descent as a claim without a mechanism that can credibly explain the data observed is not a viable claim.
You are making a huge claim that genes can be gained and lost through lineages through stochastic change which is contradictory with the idea that DNA is a sequence of nucleic acids with an enormous number of ways to arrange the sequence.
Look, make a case for once, rather than relying on ignorant people like Sal to make things up for you. Sal hasn’t demonstrated a damned thing, he’s made a whole lot of idiotic statements that you repeated erroneously, including your bizarre claim that the fact that humans share genes with certain organisms and not others indicates gene loss and regain. It’s not convincing to anyone who thinks.
You certainly haven’t explained why we share so many more genes with mice that we don’t share with chickens or with zebrafish than we share with either of those alone and not with mice–as we’d expect from evolutionary mechanisms. In fact, you’ve never actually explained anything at all.
Why don’t you explain gene families, if it’s such a leap? Oh that’s right, you don’t think you need to explain anything, made up claims are the default while those fitting the evidence are forever suspect.
Glen Davidson
How has he illustrated that? What mechanism can credibly explain the data?
I have no clear idea what that meant. Explain what is contradictory and why. (Incidentally, of the processes I mentioned, I wouldn’t consider selection to be stochastic.) Have you taken into account the evidence that random sequences can frequently perform biological functions? Have you taken into account the evidence that many genes are homologous to sequences in other species that are not genes, i.e. that some new genes have arisen from nonfunctional sequences?
GlenDavidson,
This is John’s claim.
Do facts ever inform your statements?
Glen Davidson
This is not John’s claim. It’s the “regain” part that is your fantasy. The correct claim would be gene loss and gain. Note the absence of “re”. New genes, not old genes returning.
John Harshman,
Yes, I understand these issues but your last claim needs support.
This is speculation and I think highly unlikely.
How do you know they are not genes? Are you claiming that 153 similar non gene sequences exist in the mouse and were de activated by a few mutations?
John Harshman,
How does this change the argument?
Why do you think it’s highly unlikely, given the evidence, which you understand, that random sequences can often be functional?
There are a number of ways to recognize non-genes (in this case, non-protein-coding sequences). The common forms of deactivating mutations are new stop codons and out of frame indels, and those are easy to spot. Deactivating mutations in promoters are tougher. One could of course also search for mRNAs and translated proteins. I would suppose that some of those missing genes are pseudogenes in mice. But some of them may have been lost by large deletion or became inactive long enough ago that a series of mutations has made them unrecognizable, somewhere between the origin of Euarchontoglires and the present day. Mind you, you started asking about the origin of new genes and ended up asking about deletion of old genes instead, which suggests that you are very confused about all this.
Radically. The return of old genes (unless we’re talking about the reversal of a very recent pseudogenization) would be difficult to explain by common descent, but new genes are actually evidence of common descent.
John Harshman,
Functional is a vague term. Some simple binding may take very little sequence integrity. A nuclear protein that binds to several proteins is very different and requires much more precision.
It looks like some data mining is in order to see if there is a reasonable explanation.
How are the appearance of new genes evidence of common descent?
So you agree that some new proteins could arise from translation of random sequences. That’s a start. Of course many proteins do not arise from translation of random sequences but from duplication and divergence of existing genes. How about that?
Knock yourself out.
Because they fit a nested hierarchy: each one arises at some single spot on the tree. Like other features that show nested hierarchy, common descent is the only explanation.
John Harshman,
Really? A gene existed in Zebra fish, a single spot on the tree, and then arose again in humans.
John Harshman,
I think this is highly unlikely on any protein we can identify in multicellular organisms.
I can’t believe someone hasn’t already pointed you to Keefe and Szostak PDF and their work on ATP affinity with randomly generated sequences.
No!!! For common descent to be true, that a gene is homologous with a distantly related organism, there must be an unbroken chain of descent from the most recent common ancestor, in this case to both humans and Zebra fish.
How many times is it necessary to correct this misconception of yours? No. We’re talking about a gene that existed in the common ancestor of zebrafish, chickens, mice, and humans, but was lost in one or more of those lineages. No re-appearances need apply. This has nothing to do with new genes. You are consistently confusing new genes, gene loss, and gene re-appearance (which is not a thing).
Graphs always help. Here’s how gene-gains and losses can look on a phylogenetic tree.
Alan Fox,
So what is your explanation when genes don’t appear in other lineages that share the same ancestor. In Sal’s case both chickens and mice.
Alan Fox,
How many proteins in multicellular organisms sole function is to bind with ATP?
Surely you are capable of figuring that one out yourself: gene loss.
John Harshman,
I know your opinion. I am wondering if Alan has the same opinion.
Damn, Bill. This isn’t difficult. If you can’t picture it mentally, then draw the relationships on a piece of paper.
Humans are more closely related to mice than to chickens, which means they share a most recent common ancestor (MRCA) that is not shared with chickens. Draw that and label the ancestor AHM, for “ancestor of humans and mice.”
AHM shares a most recent common ancestor with chickens. Draw that and label the ancestor AHMC, for “ancestor of humans, mice and chickens.”
You should now have a tree with AHMC at the root. One branch leads from AHMC to chickens; the other leads from AHMC to AHM.
There are two branches from AHM. One leads to humans and the other leads to mice.
You are trying to explain why a particular gene G is present in humans and chickens but not in mice. The obvious answer is that G was present in AHMC and AHM. It got passed to chickens and humans, but somewhere on the path from AHM to mice it got lost.
Just one event: a gene loss. No genes lost and regained.
In your graph after the last duplication event, why is the green line named “spo” and the blue line “spok” when otherwise in the rest of the graph the blue line is named “spo”?
Erik,
My best guess is that it’s a mistake, and that they intended to label the green line “spok” and the blue line “spo”.
It’s hard to be sure, though, since there’s no legend explaining the colors.
Yes I think that is a mistake. It seems the mistake is repeated in the legend for the figure, the source is this: Lineage-specific duplications and losses of spo-like genes in Daphnia and insects.
The green duplicate should probably have been called ‘spok’. The renaming of the spo-like gene into spok, and a subsequent duplication of it named spo, like it’s orthologues in other species, is rather illogical.
I have pointed that out to Bill like at least three times independently on this forum. It’s in my OP on Axe and protein sequence space. And to make matters worse for Bill and other deniers of de novo protein evolution, it isn’t the only or even the best or most interesting work.
Every time the subject comes up, Bill likes to imagine that the only work that has ever been done on the subject is the Keefe & Szostak paper. The implication purportedly being that it is a kind of statistical fluke, and that ATP binding proteins are irrelevant.
I happen to think the implications of this paper is far worse for Bills misconceptions about protein sequence space:
Yuuki Hayashi, Takuyo Aita, Hitoshi Toyota, Yuzuru Husimi, Itaru Urabe, Tetsuya Yomo
Experimental Rugged Fitness Landscape in Protein Sequence Space
Published: December 20, 2006https://doi.org/10.1371/journal.pone.0000096
Pay attention to the part I highlighted in bold there.
“Based on the landscapes of these two different surfaces, it appears possible for adaptive walks with only random substitutions to climb with relative ease up to the middle region of the fitness landscape from any primordial or random sequence…”.
So rather than an in vitro test of small molecule binding for a small 80 amino acid protein, they test the ability of in vivo infectivity (an actual biological function critical for the ability of phages to infect bacteria) of a ~140 amino acid protein. And they find that simply through iterative mutations of a random sequence, the random sampling of sequence space can find and substantially improve sequences that yield infectivity for phage.
In the discussion of the paper we find this:
So the protein is unrelated to the functional protein found in wild-type phage. Proving that a different protein fold has been found in sequence space, by a random sampling process, and improved it to detectable levels of phage infectivity.
They even find there are more than one such peaks, which is why they call the fitness landscape of the protein “rugged”. There are many hills in that landscape.
Yes, of course. What can happen to genes, the pattern of descent, is analogous to species. Genes can mutate, duplicate and be eliminated, as species adapt, bifurcate and go extinct. You can consider evolution both at the level of the gene and the level of phenotypes in a species.
Rumraket,
Thanks for that, Rumraket. Must read!
stcordova,
No, the bulb remains dim as ever. I – along with all biologists – am too stupid to grasp your unassailable logic, which seems to me unutterably dumb. You are confusing evolution with ‘front-loading’. From where I sit, you have really gone off the rails.
colewd,
That is absolutely no answer to my question. Why is there a Rabbit way to initiate apoptosis, and a Horsehoe Crab way, and (maybe, I can’t be bothered to check) a Dandelion way?
colewd,
Let me turn that around. How do you account for ‘DNA labs’? I don’t regard them as even a thing. At least, not until recently.
colewd,
You don’t need to invoke a ‘different molecular clock’. Even with a constant clock, changes are stochastic, not … deterministic. A difference of 1 or 2 either way is not highly significant. It also depends on taxonomic coverage.
colewd,
And the non sequitur award goes to …
John Harshman,
I would. If a selection coefficient changes from 0 to (say) 0.001, or population size changes to render an effectively neutral allele non-neutral, stochasticity doesn’t just go away.
The stupid thing about all this is that gene loss is itself a phylogenetic signal. People are bamboozled by their lack of grasp of underlying genetics.
It might help to forget entirely about gene functions and just look at strings of DNA. There are a limited number of manipulation operations that are possible on a string:
1) Substitution – SEQUENCE to SEBUENCE
2) Deletion – SEQUENCE to SEENCE
3) Insertion – SEQUENCE to SEQSINEUENCE
4) Duplication – SEQUENCE to SEQUQUENCE
5) Transposition – SEQUENCE to SENCEEQU
6) Inversion – (not readily represented in WP!)
All of these can be a phylogenetic signal, because once it has happened, it will be inherited by all descendant sequences – at least until the next change, which is itself inherited. Gene loss is simply an example of 2 [eta – or a cumulative result of one or several of them all].
The idea that the common ancestor of all organisms must have had all modern genes can actually be tested – using phylogenetics. To me, it appears equivalent to claiming that Latin must have had every word in all Romance languages. We are certainly seeing the legendary unembarrassability of Creationists here, that they should cling to that position so assiduously.
Isn’t it great? We are 645 comments into the thread and we haven’t seen a single post addressing how common design trumps common descent as a explanation of the nested hierarchy. We just keep reverting to the origin of derived characters, which is completely irrelevant.
It seems to me the people who think common design (or any design) is a better explanation don’t even know what it is they’re required to explain. They have no idea what it even is.
Or what explanation means, what the point of explaining could possibly be. Attacking the “other side” seems to be what they think science really entails, and the value of theoretical understanding is unimagined.
Bill thinks it’s fine for ID to fail to explain anything because it’s “limited.” But its only limits are that its results are anything and everything, not even distinguishable from the results of unintelligent evolution. He does seem to realize that it doesn’t really tell us anything, other than that life is “designed.” What he doesn’t seem to realize is that it does so only by emptying “designed” of any meaning precisely by its becoming unlimited in meaning.
ID isn’t limited, in fact, it is unlimited, hence meaningless. It’s the flip side of “explaining everything,” the claim doesn’t become limited, it becomes nothing. Dividing by infinity.
Glen Davidson
And how is it known that it is inherited? Because what you seem to be saying is both circular and convenient at the same time: “Studying phylogenetic signals we can demonstrate that genetic sequences are inherited (nevermind that “phylogenetic signal” means presupposing that the sequence is inherited, not demonstrating it). If the sequence is the same, then it was inherited without loss. If the sequence is different, it means it was inherited with loss.”
Erik,
Because of the basics of template-directed DNA replication. Learn some genetics.
What a load of nonsense.