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.
keiths:
colewd:
I’ve been paying attention, and the arguments for creationism are still crap, Bill. I simply cannot summon the stupidity required to be a creationist again.
Creationism really is bottom-of-the-barrel, flat-earth, Rain-Fairy stupid.
Allan Miller,
This is true but to generate the diversity we see its accuracy would have to be a lot less then it is.
colewd,
How many mutations will occur per genome replication in a human at that rate?
My thinking is just highly evolved.
Spooky action at a distance. Quantum entanglement. Gene fairies. The yin/yang theory of evolution.
keiths,
I am not asking you to become a creationist. I am asking you to evaluate evolution more objectively. Evaluate the fine tuning arguments more objectively and let the facts fall where they may.
colewd,
One thing you are confusing here is DNA repair as a per-base thing, and gene duplication which involves very many bases. The two have little to do with each other. Gene duplication occurs due to slippage, often in meiosis. Tandem repeats are very common. DNA repair – the 10^9 thing – is completely blind to this.
Allan Miller,
What errors occur during replication will be cleaned up prior to transcription due to additional passes of the repair mechanism.
As is usual with you, you didn’t answer the question. Experiment is not the only way to get good data. And experimental results are interpreted by inference. How else could they be? Why isn’t reproduction accompanied by variation (and selection, don’t forget selection) not a good explanation?
Usually. Not always. That’s the point.
This just isn’t true. If it were true, there would be no accumulation of genetic variation within populations, which even you admit to.
colewd,
I’ve asked you before to supply a number for that threshold, rather than just waving your arms. You have been silent.
Anyhoo, 10^-9 is enough to account for all the point-mutational differences between human and (your favourite species) chimp, given 6-7 million years.
We’ll have to get some evidence worthy of the name before we’ll know that.
And we know you don’t have any, or you’d present it rather than latching onto every dumb anti-evolutionary claim that comes along.
Glen Davidson
Allan Miller,
Perhaps but for new genes to serendipitously find a new gene SNP’s are required.
This is where the design argument is much better at explaining the origin of new gene complexes like DNA repair.
Couple of points. First, what’s this about repair before gene transcription? And do you realize that the .1% and .2% figures are the mean distance between randomly chosen individuals, and that in the human population there’s scarcely a site that isn’t variable?
Allan Miller,
If it only ran once yes, but Its multi pass capability kills that argument.
OK, explain it for once, instead of saying that it explains it.
You’ve never even tried to use design to explain it, that anyone can see.
Glen Davidson
That’s 10^-9 per cell replication. How many cell replications per generation in the human germ line? (It’s different for males and females.)
colewd,
Prior to transcription? That’s a curious thing to bring in, not sure why you mention it.
The repair mechanism has only a limited source of corrective information. For a base mismatch on a strand, it has the other strand. It’s not always going to make the right call as to which was the ‘correct’ base.
For a double strand break, it has to go for another chromosome. For most of the cell cycle, it has the just-replicated sister, which is pretty accurate, though not 100% guaranteed. But in the G1 phase, it only has the ‘homologue’ (pause for Mung to make hay with a term with two meanings), which is not an identical copy. It actually avoids that pathway, and goes for nonhomologous end-joining (NHEJ), which can be mutagenic. This suggests that the mutagenic effect of NHEJ is preferable to that of homologous repair.
GlenDavidson,
In all this discussion you have not seen one interesting argument. What are you doing on this blog every day?
colewd,
However many times it runs, it only has one go at getting it right. Once it’s got it wrong, that’s the new normal.
John Harshman,
Sorry, yes, that is what I meant.
Clearly not learning anything of value from you.
There are interesting things, like how wrong you can be while you think that you’re ultimately right. There’s also interesting information from the pro-science side. PRATTs, not so much.
Glen Davidson
John Harshman,
10^9 is the base error rate. That is reduced by multiple passes.
GlenDavidson,
Ok. Good bye Glen.
I should mention that slippage in meiosis (and elsewhere) is the reason for loss of DNA, as well as its duplication. The mechanism is such that one gamete ends up with the duplicate, the other with a (ligated) gap. So, gene duplication and gene loss are down to the same thing.
colewd,
Whats the net error rate then?
Best you can do, I guess.
You certainly won’t clean up your act, just blame the ones who ask for what you can’t provide.
Glen Davidson
I was unaware of a ‘multiple pass’ aspect to DNA repair. Can anyone provide a reference? [eta – yes, I’ve tried Google]
Allan Miller,
Good question. Need to think about how much the error rate is reduced per pass but mutations are going to be very rare except the ones the mechanism cannot see which is also infrequent.
colewd,
Well, you do need to bear in mind that the machinery only has limited information. It’s got the other strand, in the case of mismatch, or one/two other chromosomes in the case of a complete double strand break – one a close copy but not there for the whole cell cycle, the other a (possibly distant) relative in diploids. Other than that, it does not know what is ‘right’.
Since we’re talking about human genetic diversity, I got an alert earlier this week about a new pre-print that seems apropos. It’s free for anybody to read:
Multi-platform discovery of haplotype-resolved structural variation in human genomes
That’s a lot of variation in only 9 individuals!
No, that’s the base error rate after correction. What “multiple passes” could you possibly be talking about, and how is it possible for children to have a significant number of differences from both parents’ genomes if what you think is true?
Allan Miller,
per wiki
John Harshman,
Genetic recombination.
No, recombination only results in parental genes switching chromatids. This results in no new variation at any site, though it may result in new combinations of variation at multiple sites. Anyway, this can’t account for SNPs.
This is a serious misunderstanding of wiki. For one thing, the quoted bit, for which you provide no citation, seems to be referring to soma, not germ line.
Glen is keeping this blog safe from the likes of us. And isn’t he doing a great job of it! 🙂
That’s not what the evidence shows.
John Harshman,
There are more citing when I have time. There is no reason to have a different repair in the germ line. Without constant repair we could not have successful reproduction.
Yeah, you’re confused. DNA lesions aren’t mutations. Repair of DNA lesions causes mutations, though it’s a minor factor, especially in the germ line. Most mutations happen during replication. This repair process you’re talking about doesn’t fix mutations.
You certainly can on cognate words in related languages. It’s what historical linguistics (linguistics that studies the history of languages) does. And you can on *actual* cups, bowls, vases and saucers, not the words “cup” or “bowl” etc. (wherever you got that idea)
So what? Manuscript lineages show a similar pattern. It does not make manuscripts multiply and evolve by themselves. Activity of scribes multiplies them.
Harshman at some point actually admitted this. Let’s see,
At first deny the significance of orphan systems and next assert that many of them fit the tree. I of course cannot comment much because I have no idea if any of this purported data is real or how it’s been extracted.
It doesn’t matter whether you think a duplicated gene counts as “new”. The authors who make the graph you find so confusing count gene duplications as new. So a whole-genome duplication in one species would to them, count as a doubling in the species number of genes.
Not that the exact number here is particularly important, but your numbers are wrong then. The area of the mouse ellipsis that doesn’t overlap others says “2596”, and “2657” for the chicken.
But you said there were 3000 losses in chickens and mice. There can’t be 3000 losses if the number represents both a mix of independent gains and independent losses.
Seriously Bill, you have no idea how to read the graph do you?
So far everything you’ve said about this graph and subjects that relate to our discussions about it have been flat out wrong.
You think gene duplications don’t count. Wrong.
You think DNA repair prevents or reduces the frequency of mutations so much it would basically eliminate variation. Wrong.
You think transcription removes mutations. Wrong.
You think DNA error correction is “multiple pass”, I suspect because you confuse mutated sequence with damage to the DNA strands. Wrong.
You think the numbers without overlap on the venn-diagram represent losses only. Wrong.
You think DNA repair prevents duplications. Wrong.
You think genetic recombination would cause mutational variation. Wrong.
You think that “without constant repair there would not be successful reproduction”. Wrong.
It’s all wrong. How could you end up with so many demonstrable misconceptions Bill?
I second this, never heard of this before and nothing comes up when I try googling around.
Rumraket:
Yet the depth of his own incompetence never seems to sink in, and he goes on blithely believing that he’s right and the entire evolutionary biology community is wrong.
Take a look at the flat-earthers, Bill. Like you, they believe they’re right. Like you, they believe the scientific community has made a terrible blunder that they are able to see through. Like you, they ignore the evidence except when they think they can spin it to their advantage. Like you, they are scientifically incompetent and make ridiculous arguments.
Like you, they believe something mind-bogglingly stupid that’s easily refuted by those with the relevant scientific knowledge.
You’re in very poor company.
Well, I get Google results, no idea how relevant though.
Doesn’t quite tell what multiple passes are, but the words are there.
https://encrypted.google.com/search?hl=en&q=%22dna%20repair%22%20%22multiple%20passes%22
Erik,
The words I chose were not cognate words in related languages. They were the words for the objects you use in your ‘draw a tree on anything’ analogy.
You can’t do multiple trees from those objects and achieve congruence. Try it with a red bowl, plastic vase, pewter cup. Whatever tree you can draw on ‘bowl, vase’, ‘cup’, you cannot sensibly draw the same tree on ‘red’, ‘plastic’, ‘pewter’. Well, you could just stick a tree down and then shove the words on the tips, but that would be a bit stupid.
I got the idea by mashing together your analogy on artefacts with the basics of genetics. I’m trying to persuade you to forget about actual objects and look at the digital evidence – the molecules, DNA strings. This, you steadfastly refuse to do.
The words ‘cup’, ‘bowl’, saucer’ are analogous to genetic strings.
For real? That’s one of the dumber arguments I’ve seen presented. It does not matter how the copying is achieved. On observation, the process of reproduction preserves the order of genes on chromosomes. Scribes don’t copy them. And so, if one finds two chromosomes with the same gene order, common descent is a strong candidate for the cause of that common pattern. It does not stop being so in genetics simply because there are no scribes scratching away at the DNA with quill pens.
Again, the LTEE (Long-Term Evolution Experiment) comes back to refute this.
Several of the lineages in the experiment have suffered deactivating “loss of function” mutations in their nucleotide repair pathways, leading to order of magnitude increases in the mutation rate. These lineages with their defective repair-pathways and hugely elevated mutation rates have still managed to persist, and some of them have even subsequently evolved compensatory anti-mutator phenotypes that reduce the error rate back down to more normal levels.
From: Olivier Tenaillon et al.: Tempo and mode of genome evolution in a 50,000-generation experiment.
Nature. 2016 Aug 11; 536(7615): 165–170. doi: 10.1038/nature18959.
“Genome-wide mutations and hypermutability We sequenced the genomes of 2 clones from each population after 500, 1000, 1500, 2000, 5000, 10,000, 15,000, 20,000, 30,000, 40,000 and 50,000 generations using the llumina platform (Supplementary Data 1). We called mutations, including structural variants, using the breseq pipeline24,25. In total, we found 14,572 point mutations; 500 insertions of IS (insertion sequence) elements; 726 deletions and 1132 insertions each ≤50 bp (small indels); and 267 deletions and 45 duplications each >50 bp (large indels). After 50,000 generations, average genome length declined by 63 kbp (~1.4%) relative to the ancestor (Extended Data Fig. 1). Mutations were not distributed uniformly across the populations. Instead, six populations (Ara−1, Ara−2, Ara−3, Ara−4, Ara+3 and Ara+6) had 96.5% of the point mutations, having evolved hypermutable phenotypes caused by mutations that affect DNA repair or removal of oxidized nucleotides 18,20. Fig. 1a shows the trajectories for the total mutations in all 12 populations; Fig. 1b is rescaled for better resolution of those that did not become point-mutation mutators. Hypermutability tended to decline over time as the load of deleterious mutations favoured antimutator alleles 20. All four populations that were hypermutable at 10,000 generations accumulated synonymous substitutions (a proxy for the underlying point-mutation rate) between generations 40,000 and 50,000 at much lower rates than from 10,000 to 20,000 generations (Extended Data Fig. 2).”
My bolds.
Exactly. Because you had no idea what you were doing or what you were trying to achieve.
Exactly. And my point is – words for some objects are not the same thing as the objects. Also, data for something is not the same thing as that something. Data, particularly statistical data, for languages, manuscripts, populations and genes looks indistinguishable, but languages, manuscripts and genes are all different things with different natures that must be distinguished. And data is yet another thing with its own nature.
The word ‘dog’ is not a dog. It’s a word! Words don’t fetch the stick for you or wag the tail when you get home after work. Dogs do. To mix the two is a most unfortunate category error.
In other words, you are trying to lure me into the category error that master statisticians here employ. Get real.