Michael Denton’s new book is out, Evolution: Still A Theory In Crisis.
Denton’s stance is for structuralism and against functionalism, especially as functionalism appears in it’s current form as the modern synthesis or neo-Darwinism (the cumulative selection of small adaptive changes).
Denton argues for the reality of the types, that “there are unique taxon-defining novelties not led up to gradually from some antecedent form” and that the lack of intermediates undermines the Darwinian account of evolution. He also argues that a great deal of organic order appears to be non-adaptive, including “a great number of the taxa-defining Bauplans,” and that this also undermines the Darwinian account of evolution. Evo-devo is also showing us that “Darwinian selection is not the only or even the main factor that determined the shape and main branches of the great tree of life.”
These arguments are first set forth in Chapters 3 through 5 of the book and then defended throughout the subsequent chapters.
Denton provides a list of some of the Type-Defining Homologs:
The Pentadactyl Limb
The Feather
The Insect Body Plan
The Flower
The Amniotic Membrane
It is not just the major taxa which are characterized by unique defining homologs or novelties:
Centipedes
Beetles
Ants
Butterflies
Even individual species are often defined by unique novelties (autapomorphies in cladist terminology).
To head off a lot of irrelevant objections and nonsense from people who can’t be bothered to read the book, Denton accepts common descent and doesn’t appeal to “goddidit” as a better explanation.
- If types exist, what does that mean for Darwinian evolution?
- Does the existence of non-adaptive order undermine Darwinism?
- Does anyone think neo-Darwinism is even relevant to modern evolutionary theory?
The claims are easy to understand – Sal is trying to cherry-pick misinterpreted factoids with the goal of force-fitting them into a preposterously stupid hypothetical history. But to the extent that this history is preposterous, the required distortions render any argument incoherent.
I gave up when I realized he was deliberately equating sexual with asexual, equating genes with populations with organisms, and all of it embedded in assumptions so false they can’t be extracted.
stcordova,
I have been reading through the post and trying to understand your general hypothesis. Let me try.
The observation of gene variation between specie types can be used to evaluate the date of specie origin.
Interesting hypothesis (assuming I am correct): Can you set up an experiment to validate? Maybe creating a molecular clock that measures the mean time and standard deviation of mutations in ecoli could work. Do several experiments and see if you get repeatability. If you do, then you can create a mathematical model for this specie. If you can’t create a reliable mathematical model (due to lack of repeatability)what then would you say about your hypothesis?
lenski has done the lab work. My reading is that different populations have had different rates of molecular evolution, by a factor of four to one.
stcordova,
If it does, it does. But I trust you are not saying that this would be any evidence at all that these ‘MRCA’s’ themselves lacked a prior evolutionary history, or were unique in their time? Coalescence is an expectation of evolutionary theory, not evidence against it.
stcordova,
So molecular phylogeny is so useless that it is being used to trace disease origins?
colewd,
Molecular clocks have been around for donkeys’ years. Like radioactive and other clocks, apparently they only work when they give Creationist-friendly dates. Then, they are unimpeachable, produced by the finest scientists in the land.
Of course the converse accusation could be made, but that would require treating by far the greater proportion of dates as anomalous.
petrushka,
If anyone can surface Lenski’s data that would be interesting to review.
http://lmgtfy.com/?q=richard+lenski+long+term+evolution
http://myxo.css.msu.edu/ecoli/summdata.html
colewd,
Wow, can’t believe you’d wade through all of this!
Ok, there are a lot of mutliple arguments going on and I’ll start with what should be the most incontestable to the more speculative.
1. The first issues were how similar are yeast-to-yeast, E. Cole to E. Coli, human to human. You’d think I would get as much argument over this as I did, but I got challenged on it! For humans the Wiki figure was:
https://en.wikipedia.org/wiki/Human_genetic_variation
I suspected that one guy is pretty similar genetically to another guy because of what I saw when I was combing through the NIH NCBI databases. It’s like no one would actually accept what I saw, Dave Carlson contested whether I actually may have seen literature that said we were 0.5% different. But now do you notice, after I made the citation in Wiki, no one is contesting the 0.5% figure vigorously?
A lot of comments to the effect that I’m confused, I don’t understand. But I delivered on that figure. I could be not so nice and put people down now that I showed them up on that simple point, but that’s not why I’m here.
Then I claimed high levels of similarity between the genes common to all E. Coli. I said I suspected it while looking at NIH NCBI databases, and for that matter databases in the UK (the Sanger Wellcome Trust) and one in Japan (for the Sakiai Circular E. Coli). This can be done on the internet, you just have to be psycho enough to look at long strings of ACGTs…… and get some help with compters estimating the similarity. I was doing this because I was trying to get a feel for how representative any given E. Coli would be for the whole species.
But for me to just say, I think the E. Coli are conserved (highly similar) I get a flood of “you’re confused Sal, you don’t understand, yada yada yada.” I said lot’s of times I got no variation in my searches. 99.9% similarity seemed to show up.
But that doesn’t stop the flood of “sal you’re confused, you don’t understand.”
But then I cited this figure for E. Coli:
Just in line with what I’ve been saying. E. Coli are genetically similar to other E. Coli in the genes common to all E. Coli.
2. So I said, “if humans are so similar to each other, their most recent common ancestor must not be too far back in time” relative to the supposed time the ancestral line of humans and chimps went there separate ways 6 million years ago. A back of the envelope calculation was 375,000 years for that common ancestor of all humans.
The math guestimate goes like this:
humans and chimps took 6 million years to be 8% different, so how much time does it take for a humans to become 0.5% more different than each other?
6 million years * (0.5% / 8%) = 375,000 years
The actual figure provided by most evolutionists is:
But that estimate is based on how quickly genetic mutations enter each genome per person per generation. When the measurement was done right based on lab analysis of mothers and daughter’s DNA, the figure for mitochondrial Eve was 6,500 years! That figure was reported by Loewe and Scherer who were merely reporting the work of a real laboratory. The reasons for the discrepancy is the following.
We know there is a about 5% to 10% differences between chimps and humans. For shared genes like the cytochrome C (the one Denton cited) there is no difference. So we look at other genes, and the average difference in protein coding genes is 2%. So now we turn to the anthropologists who tell us, “the ancestral lines of chimps and humans split off 6 million years ago”. So now they use this “fact” (notice scare quotes) to calibrate the clock of how fast DNA mutates. It’s a bad approach because there is circular reasoning involved. That’s what I meant by the flaws in the clocks being used by evolutionary biologists vs. the ones the microbiologists are discovering in the study of diseases.
So the clock that the evolutionists used gave a date for Eve at 100,000-200,000 years, but the more accurate clock, the one free of circular reasoning gave a date for Eve at 6,500 years.
But as usual, a flood of “sal is confused, he doesn’t understand, he’s cherry picking, blah blah blah.” Pours in.
3. So I said, I think there must be plants called living fossils. One of them is the Cycad that supposedly popped up 300 million years ago. So I said, hey let’s look at such plants and see if they are similar to each other, and see if their similarity indicates their most recent common ancestor wasn’t 300 million years ago, but much more recent.
Sure enough, the figures returned were not greater than 12 million years.
And again I complained even those figures could be contested because the rate of change (the molecular clock) is calibrated with circular reasoning, not with direct techniques. It’s expensive to do it right using laboratory sequencers to calibrate the clocks by comparing parents and offspring, but it is cheap just to do arm-chair evolutionary reasoning with computers and off-the-shelf software and look like one is doing some high end science as long as there are lots of terms and vocabulary that next to know one understands.
But even with all the flawed methods, they had the embarrassing result the MRCA of Cycads was at most 12 million years ago not 300 million years ago as some were obviously hoping to find! They were disappointed, and hence reported Cycads today aren’t living fossils. Oh, but I suspect what those guys were thinking before they carried out the research, but it went bust.
That news report isn’t entirely accurate. What the researcher could have demonstrated was that the Cycads today were traceable to an ancestor 300 million years ago using their flawed molecular clocks. Even with broken clocks in their favor, they couldn’t even do that but returned a figure 288 million years off. 🙂
But that doesn’t stop the flood of “Sal you’re confused, you don’t understand, yada yada yada…” But I delivered with the data, and it just gets brushed aside.
4. I then said, how about E. Coli’s ancestor. Well there isn’t a study that comes out and gives a figure that I’ve found, but there was one that was close, and the MRCA for E. Coli by Lenski and friends 2005:
But it’s unclear if Lenski had a good clock or not. An updated clock was reported in 2010:
I merely pointed out, if lenski had the same order of magnitude error in his 2005 paper that was later corrected in 2010 research, Lenski’s figures, could be revised from 1.5 million years to 8,500 years.
I wasn’t being that serious except to point out the absurdity in the range of evolutionary speculation passed on as God’s truth.
Note from that 2010 paper:
Traditional rates? As in the the ones that came from evolutionary biologists not micro biologists?
The correct re-calibration came from microbiologists looking at changes in diseases — they did it right! The recalibration paper is here:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0004053
Note, “62-312K” was even yet another figure based on an flawed clock used by evolutionary biologists.
312,000 / 400 = 780
The clocks provided by evolutionary biologists are up to 780 times SLOWER than the clocks provided by micro biologists and epidemiologists.
I alluded to the somewhat chilly relations between the medical community (as represented by the NIH) and the community of evolutionary biologists. This is an example of the reasons why.
Nevertheless there’s a flood of “sal doesn’t understand, sal is confused, sal is cherry picking anomalies, blah blah blah.”
I don’t mind it too much anymore, I find it entertaining because I know I’m more right than wrong because I now have citations in hand which I didn’t have 10 years ago. And now I’m more confident than ever future lab experiments and real field observations vs. evolutionary speculations will confirm what I’ve been claiming.
I’ve gone out on a limb on 2 things:
1. MRCA off most species will be indicated to be relatively recent (around 10 million years or less) even using flawed (too slow) molecular clocks published by evolutionary biologists
2. molecular clocks published by evolutionary biologists over the years will be in conflict with molecular clocks inferred by micro biologists and epidemiologists
[And now I add a 3rd.]
3. Use of re-calibrated clocks (done the right way by using lab data not evolutionary speculations) will show the MRCA will even be on shorter timescales! If revisions of clocks come in on the order of 100-1000, the revised MRCA should be really close in time. As I showed, even lenski’s figures could be revised to under 10,000 years for one strain of E. Coli. Hehehe!
stcordova,
Oh dear. Looks as if Sal is now so confident in his skills that he’s prepared to ignore all criticism. Nothing anyone has said to him has sunk in. Complete waste of everyone’s time.
Allan Miller,
Why not ask Ayala? 😉
BTW Allan – I just referenced you to quite some extent on the AP Teachers’ forum. Courtesy dictates that you should be informed thereof.
Your status as an educator confers privileged and restricted access.
Would love to see your reaction thereto.
Nugatory Nitpicking & Bob Kuhn’s grasp of sex with leaping lesbian lizards
found on
https://apcommunity.collegeboard.org/group/apbiology/discussion-boards/-/message_boards/view_message/80661545
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best regards
Why should this latest goat rope be any different than the last ten years?
Convictions not based on evidence, cannot be dislodged by evidence.
petrushka,
Thanks. Here is a recent article from the Lenski website that forms hypothesis that mutations are linear across E. Coli gene. Also great deal of mutations occur when DNA repair mechanism genes mutate. Is not relevant to Sal’s argument but interesting Mol Biol Evol (2015)
doi: 10.1093/molbev/msu405
I find Sal’s argument interesting but agree with the criticism that he has yet to get back up data in a way that promises testability. Intuitively I can think of many conditions that could create variation in divergence rates yet I would like to see his argument developed as a possible way to sanitize date claims. This blog has interesting potential as hopefully the diverse thinkers can work together better with time. My experience is that strong disagreements are normal with new diverse groups.
stcordova,
Thanks so much for the detailed summary. I think your argument is interesting and potentially quite useful in specific applications. I see it as a method to potentially sanitize specific dating mechanisms. I think John Harshman Dave Carleson and Allan Miller have relevant criticisms that point to testability and repeatability. Can genetic divergence be repeatable. From looking at the Lenski data it initially looks tough. The hope may be sorting out the mutations caused by broken DNA repair. Here is the latest paper.
Mol Biol Evol (2015)
doi: 10.1093/molbev/msu405
Those who have been exposed to Sal for a long time are less interested. Basically, when you start to clear away the noise, the red herrings, the misdirections, the misunderstandings, and the like, you find that Sal actually believes that there MUST be a bottleneck for ALL species, which was Noah’s Ark. If the evidence can be twisted to support a single gene as having a MRCA recently enough for him, he’ll use that as a proxy for the entire species. Similarly, if he can find individuals within a population without many differences (pick among DNA, genes, body plans, whatever comes closest), this indicates the species hasn’t had time to diverge much since the Ark. If he can’t make it work for sexual species, he’ll use bacterial strains. And so on.
What he can NOT do is consider ALL of the evidence together – morphological, molecular, genetic, fossil, etc. – because these lead directly to an unacceptable conclusion. Nor can he use ANY sort of evidence across species, for the same reason. Nor can he afford to grasp any of the criticisms of his meanderings, for the same reason.
So you need to understand, this is not a disagreement about biology. It’s a disagreement about the ethics of trying to force biology to fit a religious doctrine that it universally refutes. This same effort has been ongoing, from various angles, for over a decade. As you can see, it has been completely ineffective.
Flint’s a “Jesus Myther.” ’nuff said.
stcordova,
Yeah, everyone else was wrong; you sure showed ’em! Or … I see the term ‘unembarrassable’ used occasionally; it seems apposite.
I’m not going to wade through it all again, but if I had to pick I’d vote this the densest thing you’ve said, and the one I’m most disappointed to see you just repeating:
Mung,
So he can’t be right about anything. ’nuff said.
colewd,
Refinement of date estimates and inferential methods has been an active topic for many years. That, indeed, is where Sal gets all his info from. What he appears unable to do is evaluate competing hypotheses.
It should be a very simple matter to find the Ark bottleneck in genomic data of animals and their obligate parasites, for the scientifically diligent Creationist. They should have a different pattern to plants, fungi, unicellular non-parasitic organisms, marine creatures, and so on.
Why do you think that?
We have 3 general scenarios:
1. We were more diverse before as a population and then became nearly identical (99.5% identical)
2. or we were even more identical than we are now (practically clonal) and then later diversified.
3. diversity was 0.5% and stayed that way with mutants drifting in and out of the population
I chose option 2. Hope that clarifies the initial conditions I was working from to get the increasing diversity to 0.5%, I was assuming a clonal situation at one point.
I suppose even under evolutionary assumptions, near clonal populations are possible.
Chromosome 2 is a distinguishing feature of humans vs. chimps. How did it become the same in most humans. How about human-to-human synteny and layout of genes on chromosomes?
Seems to me there was a point when the human population was nearly clonal, after which it diversified. That resolves a lot of paradoxes if we make that assumption.
FWIW, humans are very similar:
http://news.bbc.co.uk/2/hi/science/nature/2975862.stm
I should add one detractor at UD said the difference between any given human is as big as any difference between chimps and humans. I wish he’d show up here now, and get set straight in light of the above article from the BBC.
I guess some evolutionists don’t like evidence that isolates humans from other species.
I think so because we see some evidence in anti-biotic resistance studies. That is we’re able to repeat evolution of anti-biotic resistance in the lab to some extent and get about the same mutations to re-emerge that cause resistance.
The medical community has some vested interest in computing the speed of evolution since it has bearing on evolution of germs that cause diseases.
Many of the evolutionary studies conducted by the medical community have less ideological commitment to traditional evolutionary ideas since the medical community is thinking about finding cures. I find them to be more impartial in their research — they have to be, lives count on them being right.
I’ve asserted my belief that mutations happen at a much faster rate than what evolutionary biologists suppose. I provided one paper that argues this, but it is only one paper. I expect the medical community to revisit the issue since it appears we are seen surprisingly rapid evolution of germs that hurt human health. Also the mutation rates in humans also affect human health. So the question of the molecular clock rates is not settled, and revised rates (which I expect to be revised to faster rates) will not sit well with evolutionary biologists who have sworn by much slower rates of mutation.
But now the molecular clocks are becoming a question of medical significance, so it can’t be ignored, and I think finally we’ll start get a lot better answers that aren’t driven by ideological beliefs.
The MRCA questions might arise in terms of the microbes as well as it does have relevance to disease control. We have to characterize MRCAs of germs and then estimate how quickly their descendants can become the sort of germs that cause an epidemic. So the data will keep being gathered and I’ve offered predictions of what the future observations will uncover.
1. molecular clocks (mutation rates) will be revised to tick faster
2. MRCAs will be found to be relatively recent for most species.
Thanks for the Lenski paper.
NOTES:
This talks about some of the repeating of evolution in the lab.
http://gbe.oxfordjournals.org/content/6/6/1287.full
Why not design an experement?
Sal, I don’t have time for extensive replies at the moment but can you clarify this for me:
I imagine that what you mean by “relatively recent” might be very, very different from what others might mean. How old is too old for your prediction to be correct?
stcordova,
Because there is no reason to suppose that our population was 100% identical at any point in the past, let alone ‘a sixteenth of a chimp ago’.
Imagine taking a single population, ancestral to humans and chimps. Now imaging dividing it, stemming gene flow. Now allow those separate populations to diverge, without the ‘anchor’ of mating and meiosis. You will get approx 4% of the difference between those two populations in each line through to now.
You have designated a time T at which we were supposedly homogenous – a large inbred population, a genome-wide selective sweep, or a bottleneck. Why? What persuades us that diversity nose-dived then, at a time consistent with the wider pattern of divergence going on between us and chimps? That total divergence, after all, accumulated both before and after T. I am having a hard time envisioning a series of mutational fixations diverging us from chimps, and yet leaving us necessarily homogeneous at a time T which is derivable from the rate of that longer series that passes right through it. Surely, if we were diverging, we must also have been diverse. Divergence implies intervening polymorphism, as the divergent alleles move towards fixation from initial rarity.
There actually is a bottleneck of sorts in the human population, given present diversity, but you can’t derive its time from the rate of the human-chimp divergence, only from the within-population diversity, and a bit of population genetics.
For this you break your long silence on a thread you started yourself? Not helpful.
Mung has pimples, so we can’t believe anything he says. Nuff said.
stcordova,
How about anything? If you require a bottleneck before the fixation of every change, you are not going to get much divergence between two lines. Effectively, at a bottleneck, variation stops, or at least slows to a trickle, because the population is too small to throw up many mutations. I don’t see much more reason to suppose a bottleneck at the fixation of Chromosome 2 than that of any other change. Fixations don’t require bottlenecks at all, apart from very deleterious ones, and there is no particular reason to suppose a fusion/break to be substantially deleterious. If it can get above 50% frequency, it’s the ‘new normal’.
Your solution introduces more problems than it removes. You would resolve a lot more paradoxes by taking population genetics on board.
Is that a unit of time?
What makes you think I am a creationist and that I don’t know what a homolog is? Not helpful.
Well there isn’t much divergence is there 0.5%.
Lots of things could get fixed into the population through a bottle neck. I should point out, there are limits to how fast either selection (Haldane’s Dilemma) or neutral traits can get fixed (4Ne generations). If the population is large the neutral won’t get fixed in geological time and during the fixation time as mutants drift in and out, there will be substantial divergence in the genome between individuals.
If in each generation we introduce 2N novel mutations into a population of N individuals by distributing each randomly to individuals to random locations in the genome, only 1 mutation on average will eventually get fixed on average, so in the mean time we have all these variants floating around before they drift out of the population — ergo the genome looks increasingly divergent.
If the mutation rate, as Larry Moran supposes, is on the order of 100 per generation per individual, and we have an effective population of N = 10,000, the mutation introduced into the population are 100 * 10,000 = 1,000,000 per generation. The divergence will just keep increasing practically speaking until the population is dead or the genomes are all random because the time to fixation is 4Ne = 40,000 generations.
But if one doesn’t like the math laid out, consider we have a population now that is 7 billion spread out globally. Does anyone seriously think any novel trait is going to get fixed any time soon by selection and/or drift? Maybe not in the life of the Solar system, and given the mutation rate is on the order of 10^-8 per nucleotide per generation, if we have 10^8 generations to fixation, there is little point in assuming fixation since every nucleotide position will have been mutated before fixation!
I hope that illustrates the point of the value of supposing a founder couple, a bottle neck, a special creation event, a whatever — to get a near clonal ancestor set.
In light of these considerations, I think your comment about me saying supposedly dense stuff may have been a little misplaced.
I have to agree with Salvador here, “dense” would seem to indicate some sort of cohesiveness.
Are you an ID supporter?
stcordova,
1. molecular clocks (mutation rates) will be revised to tick faster
2. MRCAs will be found to be relatively recent for most species.
Thanks for the Lenski paper. Thanks for the oxford paper.
Point 2, I have know idea but interested to look at further. Point 1. Do you think this might be different depending on the specie? In the oxford paper the fast resistance appeared to come from gene amplification vs. random mutation. The mutation rates seem to vary depending on the environment. The mutation rates in primates would appear to come particularly from the accuracy of DNA repair which interestingly enough adds repeatability to the process.
Flint,
I sympathize that it is difficult to sort through evidence if you think the opposition is trying to spin the data. Some of that is certainly going on with both sides of the argument. On the other hand, without opposition these blogs get very boring. Sal’s last post had 775 comments. The most I have ever seen on this type of blog.
Uh, colewd, Sal is a YEC! His goal is to make entirely coherent, consistent, consiliant evidence fit a young earth and Noah’s Ark. To do this, he is reduced to what you have seen here – no coherent hypothesis, no attention paid to anything anyone else presents, switching both subject and object with every post, abject refusal to understand what “MRCA” means in any context, and so on.
And sure, with Sal dodging both facts and theory, and thus jumping around like a drunken cricket, you are going to see long threads of efforts to chase him around in circles, trying to pin him down to a single testable claim. You aren’t seeing “opposition” in the sense of any real scientific dispute, you are seeing nearly everyone correcting everything he posts.
I remember another long thread, on another site, where some ninny was defending a flat earth. He filled his posts with nonsense equations, jumped from gravitation to astronomy history to the physics of optics, talked about what the earth rests on and why the water doesn’t drain off, and on and on and on. Please understand that this thread was no sort of healthy argument. Yet a flat earth is no less plausible than a young earth.
(And I should mention that the flat earth guy was sincere because his interpretation of the WORD OF GOD, don’t you know, SAID SO.)
Dave Carlson,
First, I think we can have far less contentious discussion on the lncRNA thread. I think their is stuff there for our mutual interest.
Regarding your question:
Around 10 million years ago using the accepted evolutionary molecular clock rates give or take.
Where all this got started was regarding the candida vs. baker’s yeast split hundreds of millions of years ago and yet Denton’s dayhoff diagram indicated a divergence of only 25 for yeasts that diverged supposedly 300 million years ago. Yeast have a fast generation time, that would be on the order of 90 billion generations ago!
I would be interested to see the MRCAs of the baker’s yeast speices and the candida species. Hardly anyone does this sort of work, they are obsessed with the data of splitting, not the MRCAs.
But even with a split, here is one of the baker’s yeast MRCA
So S. cerevisiae will probably have an even closer MRCA if we did the study with INTRA-specific variation, not the phylogenetic date of split as above.
So all of this last round of exchange was sparked by the Yeast MRCA, and so far, so good for my hypothesis!
With respect to a candida species (not one that Denton listed, but one available for study):
http://www.sciencedirect.com/science/article/pii/S1087184505000204
But as mentioned, revised clocks have been provided orders of magnitude speed corrections from 35-780.
Flint,
If this is truly the case then facts and evidence will pin him down. I believe the YEC case is very difficult to support but I am interested in any aspect of his argument that may bring new insight. “drunken cricket” good one:-)
You’re new, aren’t you? YEC nitwits have been utterly unbudged by entire LIBRARIES of fact and evidence, and by the entire output of every peer reviewed journal for at least a century, and by every research study eligible for such a review. And you seriously propose that facts and evidence will pin down Sal?
News flash: convictions not based on evidence, cannot be dislodged by evidence. In the words of Richard Dawkins, “no evidence, no matter how overwhelming, no matter how all-embracing, no matter how devastatingly convincing, can ever make any difference.”
We have seen it all before. If you are truly interested in any of this, you can get a much more organized, more clearly presented picture from any freshman-level biology textbook. Otherwise, eventually even you will grow tired of Sal’s incessant “well, look over there” technique for avoiding any and all facts and evidence.
Flint,
I just provided 3, and they will be tested and observed not because of me, but because the medical community has a vested interest in these question either directly or indirectly. I gave them:
The figure of 10 million was ball park and these must be MRCA based on INTRA-species comparisons, not inter-species phylogenetic trees calibrated by the fossil record.
I wouldn’t bet on the evolutionary molecular clock rates, even the mainstream is starting to acknowledge they clocks are broken!
and
Allan Miller,
What tools would you suggest to help him here?
stcordova,
You misunderstand. And this is a big part of the problem talking to you: terminology. Divergence is what takes place between two non-interbreeding lines. So yes, there is more than 0.5%, there is (on your figures) 8%. ie, the divergence between human and chimp after 6 million years.
Ain’t gonna happen. Sal’s been running from the facts and evidence for more than 10 years. His goal isn’t to learn what actually happened concerning the history of life on the planet. His goal is to do whatever is necessary to ignore the facts and evidence so he can hang on to his YEC beliefs.
Honesty would be an invaluable start. This might influence him to ponder “I wonder whether there ARE competing hypotheses? I wonder if there are different kinds of clocks or dating methodologies? I wonder if molecular methods dovetail with any independent methods? You know, things like that.
This is suggested INSTEAD of “I wonder how I can selectively pluck and misinterpret a datum here and a datum there, from different studies and methods over the last 20 years or more, so as to support my religious requirements?”
colewd,
The tools are present in his own intellect. It is currently bent towards picking only those conceptions that allow his YEC to be maintained, from among the many that come his way. That includes a conviction he is right even in discussions with both a professional phylogeneticist and one of the founders of the field. I can’t do much about that.
Flint,
Yes, I have never found any arguments of a YEC interesting prior to Sal. I am interested if you can argue the points he just challenged you on. Again, Sal is a long way away from convincing me that the YEC view is accurate.
Allan Miller,
I am thinking of using the scientific method as a standard. If his point can form a mathematical model and be verified through experiment then I think we should be convinced of a reasonable hypothesis being formed. Thoughts?
stcordova,
And lots of things could get fixed without. So why suppose them? As I say, there was one – down to about 10,000 or so – but that’s still not 100% similarity, and your ‘human-chimp’ calculation cannot possibly locate its time.
I don’t mean to be unkind, but it is dense to continue to use the divergence rate between two reproductively isolated populations to infer a time when one of them went through a bottleneck and recovered to a present level of variation.
If nothing else, you must agree that you were out by a factor of two? 8% difference means average 4% in each line. But more importantly, it’s a bogus calculation.
We aren’t talking about populations with 7 billion members, and Haldane’s supposed dilemma is irrelevant. You fail to see how a population with (say) 1% diversity could become two populations with (say) 0.5% in one and 1.5% in the other but 8% difference between them, without ever going through a ‘micro’-bottleneck or period of zero variation. I certainly can’t make you. But it is entirely possible, and requires nothing unusual to happen at all. Just mutations in 2 populations with mating in each but reproductive isolation between.
stcordova,
You mean diversity not divergence, but no, because of gene flow and meiosis. Either random mating will keep its genomes anchored around a single drifting mean, or the population will fragment into separate subpopulations with their own diverging means. You can’t increase the diversity of a random-mating sexual population indefinitely.