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.
Bill, here’s the issue you seem to be having: “the same number of genes” were not lost independently in two lineages. In actuality, a whole slew of different genes were lost in the two lineages. It just so happened that both of the loses included an overlap of 73 genes. That’s hardly amazing considering the actual number of genes in a genome. There are over 30,000 in the human genome for instance. Why are you hung up on 73?
It gets even better, as they have shown how these very same transcription factors could have evolved in literally hundreds of different ways.
To borrow a phrase from Sal, “from the prestigious scientific journal nature“:
Starr TN, Picton LK , Thornton JW:
Alternative evolutionary histories in the sequence space of an ancient protein. Nature (2017). DOI: 10.1038/nature23902 Pubmed: PMID: 28902834.
Key question for IDcreationists: If the reconstructed evolutionary history of this family of hormone-receptor controlled trancsription factors did not actually take place in history, and if the inferred ancestral molecules never really existed on Earth, how come scientists are able to use the phylogenetic methods you reject to infer the ancestral states of ancient molecules, reconstruct them in the laboratory, and test them for function, find them to be functional and in the way predicted?
How come scientists can use this very method to also show that there are HUNDREDS of possible alternative ways these functions can evolve, mutation by mutation?
Erik,
Can you draw a tree on the words ‘cup’, ‘bowl’, ‘vase’, ‘saucer’ such that the tree for the first letter converges on that for the second letter, and that for the third, and the fourth? No, you cannot. And yet this is very much what you can do with gene sequences. The order of genes on chromosomes is conserved, very closely in closely ‘related’ species, as well as the order of bases within the gene.
The analogy crashes and burns at this point. You think it impossible to construct a phylogeny on versions of Canterbury Tales without knowing what the story is about, why it was written and such? We know as much about the general term ‘organism’ as we do about the general term ‘manuscript’; there is no special extra knowledge required to construct a phylogeny.
Shouldn’t we be doing something more productive, like teaching logic to cats?
Glen Davidson
I taught my pet budgies how to signal me that their seed-tray is empty. Not kidding.
GlenDavidson,
Heh. I’m off to the pub!
Robin,
How does reproduction along with random variation lead to the genes being lost twice?
colewd,
Think, Bill.
How would the loss of a gene in one lineage “reach over” and prevent the loss of that same gene in another lineage?
You had me until this point, Sal. Why does it require the ancestor of mice, humans, and chickens to get a bit of poof of all these genes in the first place and then lose them? I don’t know what you mean by that.
All organisms have genes. So the origin of mice, humans, and chicken genes should not be that hard to understand. They all got their genes from a common ancestor. Splits from the common ancestor are the product of modification of those genes. Right there we expect that different groups are going to have some different genes from one another.
Sal, in checking a few genomes research bits doing a Internet search, there aren’t that many examples of orphan genes, so it doesn’t appear to me that there’s all that much ‘poof’ going on. And considering that there’s some good research on the mechanisms and origin of orphans, I don’t see ‘poof’ even being valid. So where are you getting that impression?
I’d prefer something a little more credible than a reference to some silly debate. Got any actual research or published analysis?
Well, the results and subsequent claims from ENCODE are rather dubious. I’ll wait until they are fully peer reviewed and some legitimate analysis published on the subject before drawing any conclusions.
That’s not what I’ve found.
Well, until there’s something a little more studied, I’ll reserve judgement.
Why don’t you read posts where things like this are explained to you? Like back here.
Here it is again:
There has been multiple independent but paralell gene-losses in the twelve different isolated lineages in Richard Lenski’s Long-Term Evolution Experiment with E coli. Some lineages have lost multiple genes to large deletions.
See for example:
Richard E. Lenski. Convergence and Divergence in a Long-Term Experiment with Bacteria.
Am Nat. 2017 Aug;190(S1):S57-S68. doi: 10.1086/691209.
In this paper we find this gem:
”For example, all 12 populations completely lost their ability to grow on another sugar, ribose, over the first 2,000 generations of the LTEE (Cooper et al. 2001). In this case, the parallel losses resulted from deletion mutations that were demonstrably beneficial in the glucose-based medium and, moreover, occurred spontaneously at an exceptionally high rate. The high mutation rate was caused by a transposable element adjacent to the ribose operon that transposed into the operon and then underwent homologous recombination, leading to a deletion. These losses were so consistent across the replicate populations as to generate convergent, not divergent, outcomes.”
In this paper there’s a nice graph that shows some large deletions:
Barrick JE1, Yu DS, Yoon SH, Jeong H, Oh TK, Schneider D, Lenski RE, Kim JF.: Genome evolution and adaptation in a long-term experiment with Escherichia coli.
Nature. 2009 Oct 29;461(7268):1243-7. doi: 10.1038/nature08480.
I have highlighted some rather large deletions (losses) with green arrows in this figure: See this link if the image quality is bad.
So there you go Bill, there is an explanation for how the same gene can be lost, in parallel, several times independently, through evolution. Observed in real time.
Got it.
Took me reading ahead to catch on to that. Yeah. Hopefully my explanation showing that nothing need “reappear” makes sense
Umm…bill…without reproduction, the loss of genes (or the gain of some new gene) can’t spread through a population and become diversity. So really, reproduction is a rather large part of diversification.
Naw mayn, you’re forgetting the…
See my previous response and Harshman’s lengthy explanation as well. Lots of genes are lost or modified throughout the millions of years of evolution. So the fact that groups of organisms lose 73 similar genes really isn’t that amazing.
Robin,
I agree with this point there are around 3000 genes lost by each the chicken and the mouse so 73 is under .3% common. Keiths and John, I concede the gambit.
I agree that reproduction can spread new genes. The problem is how does it generate new genes? How is the loss of 3000 genes in the mouse and chicken tolerated and survival maintained without a planned change?
Well…
Reproduction with mutation generates new genes. Such mutations can be of several types, all of which have been mentioned to you at one time or another. Loss of genes is tolerated because only genes that aren’t needed are lost. Genes become redundant all the time, and that’s been mentioned to you also. If a gene is duplicated, the common fate is for one copy to be deactivated, for example. To pick another example, humans have lost a great many smell receptor genes. You can probably figure out why they were preserved in, say, dogs, but not in humans.
A different subject, but a good one. Reproduction doesn’t generate new genes. There are other mechanisms, like mutation and horizontal transfer that do that.
An interesting question. As I see it, it’s totally happenstance. There are likely billions of metaphorical graveyards filled with organisms that lost genes that were vital. Hard to say of course because evolution doesn’t leave traces of the changes that didn’t work.
No Bill. The number is closer to 2500, and they’re not just losses, they’re also gains. Again you’re misreading the graph. The area of the ellipsis without any overlap simply shows genes which are not present in the other species in the graph. The reason they’re not present in the other species can be both a combination of multiple losses, or gains. And again, many of those gene gains are simple duplications.
John Harshman,
I have yet to see the claim that reproduction leads to the generation of new genes supported.
Are you claiming that 15% of our genes are not needed? Or 3000 out of 20000 in the mouse and chicken.
Robin,
Don’t you agree that this happens in the germ line so the changes are passed forward by reproduction?
We lack experimental evidence that supports new genes being formed by reproduction and other accompanied variation.
Gene duplication, and the mechanisms whereby they happen when cells copy their genomes before cell division, is an observed fact.
Here’s an overview: Mechanisms of Gene Duplication and Amplification.
Not to mention the fact that I gave two references up above that describe how multiple historical duplications over deep time have created an entire family of hormone receptor controlled transcription factor genes and even describe how there are literally hundreds of other ways it could have happened.
Evolution by un-poofing! The exact same genes lost in two separate lineages. What are the odds. Looks like devolution due to common design to me.
Rumraket,
I agree but duplication is not a new gene.
– I have 2918 for chickens and 2785 for mice. I agree there are gains and losses.
colewd,
Think, Bill. After the duplication event, are the two copies going to evolve in lockstep?
Mung,
That’s because you’re bad at thinking.
ETA: Let me ask you the same question I asked Bill:
That’s probably because nobody can figure out what you mean by that. What do you mean?
No. Genes that aren’t needed tend to be deactivated fairly quickly in evolutionary terms. When the environment changes, including the portion of the environment consisting of other genes in the genome, some genes that were once useful may become useless. And so there will be a sprinkling of losses over time.
Why is experimental evidence the only kind you will accept when it comes to evolution, but you will take just about anything as evidence for whatever you already want to believe?
John, to colewd:
You really should think about that, Bill. It’s a huge problem in your thinking.
keiths,
How does it evolve at all? The gene is a functional sequence. What mechanism gets it to find another functional sequence? The mechanism that avoids the disaster of a random walk through a functional sequence is the DNA repair mechanism.
John Harshman,
Because I see bad science being generated with just hypothesis by inference. The data we see is lots of genes coming and going through Sal’s flower. Reproduction itself accompanied by variation is not a good explanation.
Robin,
The problem is how did they both lose exactly the same genes? What are the chances?
My guess is that they each actually lost hundreds of genes, there just happen to be 73 that chickens and humans lost and mice didn’t. And there are probably many more than 73 that mice and humans lost but chickens didn’t. Am I right?
colewd,
Think, Bill. (You’ll notice I’m repeating the exhortation. That’s quite deliberate.)
After the duplication event, there are two copies of the gene. One of them is free to evolve while the other continues to serve its prior purpose.
keiths,
We all have cognitive bias. Evolution is supposed to be science. Do you see a problem holding the theory to scientific standards?
colewd,
Why? Specific reasons, please.
colewd,
Of course not. That’s how I concluded that evolutionary biologists are right to accept common descent and reject common design.
Creationism is truly flat-earth, Rain-Fairy stupid. Crackpot “science”.
keiths,
So you are claiming that the duplicated gene will not be repaired by the repair mechanism.
If the repair mechanism is turned off it will suffer many mutations and soon will be non functional.
My objection to this theory is that the evidence contradicts the claims.
DNA repair isn’t all or nothing, Bill. This is not a secret. Read about it!
keiths,
It has an accuracy of 10^-9 and is running constantly. Based on what I quoted it is mission critical for multicellular organisms survival. It had to be functional in the Cambrian animals for them to survive. Its existence contradicts the claim that reproduction and variation are responsible for new genes over long periods of time.
colewd,
No, it doesn’t.
Christ, Bill. Do we have to spoon-feed everything to you?
Not every error is fixed by DNA repair mechanisms. Is this really news to you?
ETA: The third sentence of the Wikipedia article on gene duplication:
Is it really too much to ask that you do some reading before issuing your categorical pronouncements?
keiths,
It sounds like you automatically discount evidence coming from the creation side.
keiths,
You need enough errors to sneak out even if you have the miss conception that errors are going to do anything else but move the sequence to non function. 10^-9 accuracy and running constantly. It is run prior to gene transcription. .1% human to human variation .2% for dogs. Cells are not designed to evolve, they are designed to remain the same.
Think about it Keiths, the reality of cell function discovered over the last 50 years is contradicting the theory.
colewd,
Not at all. I was raised as a creationist and I deeply wanted creationism to be true.
Once I learned enough science, I saw that creationism was simply too stupid to believe, so I rejected it.
Creationism requires stupidity, whether that stupidity comes naturally, via religion, or both.
ETA: I should add that ignorance can substitute for stupidity. People who aren’t familiar with the science, or who simply haven’t thought about it carefully, can be creationists with relatively little cognitive dissonance.
keiths,
What do think errors due to mutation in the repair mechanisms cause?
Cancer.
keiths,
Maybe its time to take a fresh look.
colewd,
So every single mutation causes cancer. No exceptions.
Is that your final answer?
I’m off to run some errands. Perhaps someone else will take over your education in the meantime.
colewd,
The DNA repair mechanism does not catch all mutations. Indeed, it is to some extent mutagenic itself (ask me how). Therefore mutation occurs, therefore yadda yadda yadda. Been here before. Sure we’ll be here again.
Genes don’t evolve. Think, keiths.
colewd,
Whaaat? You really need to understand the mechanism(s) of DNA repair. I can’t see how DNA repair has any information about whether a gene is a duplicate or not.