Over at Uncommon Descent, Jonathan McLatchie calls attention to an interview that Scottish Christian apologist David Robertson did with him. The 15-minute video is available there.
The issue is scientific evidence for intelligent design. As so often occurs, they very quickly ran off to the origin of life, and from there to the origin of the Universe. I was amused that from there they tried to answer the question of where God came from, by saying that it was unreasonable to push the origin issue quite that far back. There was also a lot of time spent being unhappy with the idea of a multiverse.
But for me the interesting bit was toward the beginning, where McLatchie argues that the evidence for ID is the observation of Specified Complexity, which he defines as complex patterns that conform to a prespecified pattern. He’s made that argument before, in a 2-minute-long video in a series on 1-minute apologetics. And I’ve complained about it before here. Perhaps he was just constrained by the time limit, and would have done a better job if he had more than 2 minutes.
Nope. It’s the same argument.
His Specified Complexity argument is William Dembski’s pre-2005 argument. It turned out that the argument required a conservation law to show that natural selection could not put this Specified Complexity into the genome. Dembski did have such an argument, but it turned out not to work (see my 2007 article for the details).
In 2005-2006 Dembski changed the argument, by redefining Specified Complexity to have an additional condition. Now you could only call a pattern Specified Complexity if it was not only complex and conformed to a prespecified pattern but also could not be brought about by natural evolutionary forces such as natural selection. A number of people here and at Panda’s Thumb pointed out that this fails to show us how this condition is to be evaluated. It makes SC something that comes in after one has somehow decided that an adaptation cannot have been achieved by natural selection. In short, it has been safeguarded against the criticism that evolution could bring about SC by defining the issue away. That makes SC a useless criterion.
But McLatchie has somehow missed all this history. He is back where Dembski was in the book No Free Lunch: Why Specified Complexity Cannot be Purchased Without Intelligence, published in 2002. McLatchie has totally missed both the refutations of Dembski’s original criterion, and the 2005-2006 fix that rendered the SC criterion useless. In spite of having 15 whole minutes to clean up the mess, McLatchie and Robertson preferred to spend the extra time back at the origin of the Universe.
Yes, why would it degrade? There is natural selection and trillions and trillions of cells.
.. proof of what? That you are vastly overestimating how rare functional sequences are in the space? Yes. Why do the numbers I have referenced here not suffice?
We are talking about how often we might discover a new function if we are randomly generating new protein sequences by complete sequence scrambling (which means we totally change the whole sequence, that is as random as it is possible to get). Right?
If we do it that way, we discover new functions at a rate of approximately 1 in 10^11 sequences. (And it’s not just for ATP binding, there are other similar studies out there that test other functions, but they roughly come up with the same number).
So what is the problem with this number do you think?
colewd,
Nah. Endosymbiosis is regularly observed. Secondary, quaternary and tertiary, like Russian dolls, with all the historic membranes still present. Of course these aren’t eukaryotic cells formed from prokaryotes. But there are also numerous systems such as the Ignicoccus/Nanoarchaeon archael system whereby ATP is passed from one cell to another in intimate association. (On probabilities, while we’re at it, what are the odds of that happening in the history of the planet? Why do we consider eukaryogenesis miraculous but not that particular association, which like endosymbiosis depended on the incalculable odds of two particular organisms living in the same place at the same time?).
colewd,
How? You must accept that the scenario I sketched is possible, surely? And therefore must be allowed as a possible explanation of any matching sequences?
And if you accept common descent in – say – Common and Spotted Sandpipers, do you do so circularly?
colewd, could you lay out the circularity of ‘UCD’, as succintly as possible?
Rumraket,
The number explains the probability to bind to ATP but that is just one function of proteins which I know you understand 🙂
Also if I assume the number for argument in order to make a spliceosome I need to make 500 proteins that bind together in shape and charge. Thats 1/10^550 chance of evolving 500 proteins that bind ATP that fit together to perform a higher level function. Your trillions and trillions of cell trials don’t help solve this. I think you are helping argue that the eukaryotic transition is the most difficult to explain.
Allan Miller,
If the sequences match exactly then your right common ancestry, in fact identical twins.
If there is an extremely close match like all dogs .15% or almost identical, (got that number from a paper John H recently sent on chimp to man genome comparison.) then common decent. At what point of dissimilarity does common decent go away. The argument is circular if you are assuming common decent among species with similar but not almost identical genomes unless you can demonstrate the relationship by some empirical means. The first transition to multicellular life is the eukaryotic cell. Can we demonstrate common ancestry with empirical evidence of the relationship? Is UCD still a reasonable hypothesis other than what else could it be?
But not evolution of anything on the scale of things like spliceosomes, spliceosomal introns, nucleosomes, chromatin remodelers, histone signaling management, etc. from prokaryotic forms. Even Lenski’s long term evolution confirmed the absence of such transformations.
Half-implemented chromatin remodeling managed by half-implemented inter-histone signaling is worse than just keeping the prokaryotic DNA repair.
When half-baked mechanisms are lethal, this prevents evolution of the full-baked mechanisms that are not lethal. Thus natural selection prevents evolution of such Rube Goldberg novelty (like Eukaryotic DNA repair mechanisms), it doesn’t facilitates it. Darwin was dead wrong in his understanding of what natural selection does. If he properly titled his book, “Origin of Species by Means of Non-Existent, Un-Natrual Selection” the absurdity of his views would have been readily apparent, because the sort of selection that he claims exists in nature, only exists in his imagination, not in reality.
No, the numbers are not multiplicative in this way. For every protein, the number would roughly correspond to 1 in 10^11, you can’t just multiply them all together. That would imply you think the spliceosome originated as one giant chance event of 500 proteins all evolving simultaneously (which I agree would be absurd), rather than a sequential addition. Not sure where you get the 500 number either, but regardless of whether it is 200 or 500 I agree it would absurd to think they all evolved simultaneously.
I agree that if you assume the spliceosome had to evolve in one step, all 500 proteins simultaneously, that would be an absurdity. But why would you ever assume this? Phylogenetic evidence implies this is false.
Why? Why is it circular to take nesting patterns of similarity as indicative of common descent, when we (both you and us) take it indicative of common descent between human individuals? Or [all canines], or [all felines] etc. ?
Have you ever witnessed your great great great great grandmother give birth? No. Have you seen wolves give birth to the first dogs? No. So it is an inference in both cases that your far removed family members (or dogs and wolves) share common descent. Yet this is reasonable to you and you don’t think it’s circular. But press the relationship a bit further back and you suddenly think it’s “circular”. Why?
It confirmed no such absense. How do you know what the genome rearrangements happening in that experiment will ultimately result in, say, a million generations down the line? Regardless, the experiment is a synthetic and simple environment where the only form of competition is basically replication speed. Under such a scenario the one major hurdle is genome replication during cell division, which would massively favor deletions and shortening of the genome.
Even so, a gene duplication still happened that formed an active association between two genes that were previously unrelated. Looked at in isolation that is an increase in complexity, not a reduction.
Well doh, why didn’t you just tell us. If it won’t work it won’t evolve. Somebody stop the press!
When you can just sit there and declare that these systems MUST have gone through stages of being “half baked” that are lethal, then you have assumed what you should be trying to prove.
Rumraket,
Mikkel
You believe in some type intermittery co option and I know this argument was also made for the flagellum. You need to organize the genome to express 500 proteins that fit together. You also need to be able to build the machine any time a cell replicates. So they need to bind by shape charge and have to form a collective function. 1/10^550 is a ridiculously conservative estimate for this problem. Lets agree to disagree at this point.
colewd,
For a modern eukaryote with lots of different introns and a complete modern spliceosome. Why do you assume this all appeared at once?
.. if you assume the whole thing appeared overnight. Why would you assume that? Such a view is flatly contradicted by the evidence.
Again, the origin of eukaryotes is proposed to be a bacterium becoming the endosymbiont of an achaeal cell. Do archaea or bacteria have a spliceosome and dusins of different introns? No they don’t. So there’s simply no good reason to think the spliceosomal complex we see today in eukaryotes must have been there right from the beginning at the moment one cell invaded another. This is when looked at from the bottom-up approach (as in, what would a bacterium invading a archaeal cell imply?).
At most there are a few types of rare, self-splicing bacterial introns. Self-splicing. As in they splice themselves out and are not dependent on external protein machinery to accomplish this. And a couple of splicing RNA’s (that deal with non-self-splicing introns), homologoues of which are found in the core of the spliceosome.
If these invaded the host archaeal cell’s nucleus at the endosymbiotic event, that would be the beginning of the evolution of the spliceosome. A few introns came with the symbiosis event, and a few splicing RNA’s. That’s it, that’s how it would have started (at least, if we allow evidence from phylogenetics to guide out speculations). Those 500 proteins or however many it is, they came later, gradually, one or a few at a time. That would be the evolutionary model.
If you insist on trying to calculate the odds of the whole thing assembling itself simultaneously, you are emphatically NOT calculating the odds of the evolutionary postulate. You are actually calculating the odds of the CREATIONIST postulate, since THAT is the one that says the whole thing had to appear at the same time.
Disagree on what point, specifically? That the whole thing had to appear simultaneously? Yes, we disagree on that being relevant to evolution.
Well, actually it’s really you disagreeing with reality! Nobody proposes anything like what you are saying actually happens. So all it is is your insistence on keeping your misunderstanding intact rather than a disagreement.
If it was a disagreement, you could point to actual biologists who make claims that involve probabilities of 1/10^550 and lower. But you can’t. But I doubt that’ll matter eh?
Rumraket,
I think you believe this because you underestimate badly the statistical problem of the genome forming or changing sequences. Sequences get a lot more precise when they make up nuclear proteins. I think this assumption is based on faulty analysis of how new sequences are formed. IMHO we have no idea, and so the a priori assumption of universal common decent is way ahead of the new molecular evidence. IMHO it is time for science to embrace the new evidence and take a step back from old paradigms. You, John Harshman and Joe Felsenstein are talented scientists and there is no limit to how you can help science if we just retire the common ancestor for now. We have clear common biochemistry. Lets focus on analyzing how the relationships can help science. I could use all of your help showing how blood vitamin d levels are critical for health and cancer prevention.
The ID inference is remarkable:
It all had to appear at once, but that is so improbable as to be impossible, therefore it all appeared at once.
Brilliant deduction!
Rumraket,
So what were these proteins doing before they became components of a macro molecular machine that can cut and past to atomic precision? How is it they went form individual proteins to components of a bigger complex?
When have we ever see individual components designed for a stand alone purpose and then become part of different bigger system?
This is why IMHO the evolutionary model needs a re think 🙂
Do you have any evidence for this interesting claim? Nobody is talking here about “the genome forming”, only about changing sequences. We call those mutations. They happen frequently, so I don’t see why you consider it a problem. Nor are we talking just about proteins. The main evidence of phylogeny is the nested hierarchy of similarities, not just similarity. This hierarchy is displayed in proteins and protein-coding DNA sequences, RNA-coding sequences, introns, transposons, and all the random junk in a genome.
What do you mean “we”? You have no idea, because you haven’t bothered to look at the literature. New sequences are formed almost entirely from old sequences by the well-understood processes of point mutation, insertion and deletion, duplication, and inversion.
What new evidence do you have? I don’t recall you presenting any theory of the formation of new sequences, much less any evidence for that theory.
I don’t think you know what you mean by that.
So all scientists should abandon basic research and go into medical research, specifically on your particular obsession? Doesn’t that sound the least bit arrogant to you?
Incidentally, you got that number wrong. The correct figure from that paper would be 1.3%. Is that almost identical? Where is the line between almost identical and not so identical? What do you think is the line between “same kind” and “different kind”?
John Harshman,
Pulled from your paper.
You mean all of the new evidence that also supports common descent? I think it has been embraced.
You have it completely backward. God could open up the skies and tell us that, notwithstanding the evidence we have, almost no evolution has occurred, it was all created to look like it did. What we’d have to do then is continue to use common descent as if it had occurred, because that is the only pattern that makes any sense of the data. Sure, it would then have to be taken as a heuristic device and not as what actually happened, but what choice does anyone have but to use the pattern that exists, the one coming from UCD, as the guide to future discovery?
Mere similarity tells us nothing. Manufactured items have mere similarity, but they don’t have the sort of similarity that occurs from the constraints of reproduction plus mutation (plus a few other mechanisms that factor in, but don’t wreck the overall hereditary pattern).
ID can do nothing but try to ruin actual science, because the latter tells against ID.
Glen Davidson
First, not my paper. It belongs to the chimp genome consortium, and I’m not a member.
Second, my bad; I see you were referring to dogs, not the chimp/human divergence.
Third, wait: the divergence among dog breeds is all you get from a paper that was intended to show you some of the evidence for the relationship between humans and chimps? Talk about wearing creation-glasses.
You use the word “system” here Allan.
What do you mean by that word in biology? Its really just a euphemism isn’t it?
Because you don’t actually believe a system exists do you? How could one believe in a system, if one believes in Darwinian evolution? The theory provides that all of the aspects of evolution are really just a meaningless set of accidents, that happen to form things that survive.
So when you say system, it is sort of a borrowed word from the real meaning of system, because you can’t have system if their is no intelligence or plan can you?
Its another one of those phrases, sort of like what KN and others uses, when he says that an animal developed intelligence as a way to better find food. You side hates the word accidents, but a ‘random mutation” is an accident, and if that is what is forming your so called ‘system, I don’t think system is the proper word. “Fortunate random mutations” perhaps, if one considers life fortunate?
I confess I don’t see why not. I think of a system as an arrangement whereby multiple parts work together in some coordinated fashion. And such an arrangement might be said to have a “plan” (in the sense of a layout), but no intelligence is necessarily involved.
Where I think the confusion comes in, is where mutation (which can be regarded as accidental) is sorted by selection (which is most definitely NOT accidental), resulting over time in an interconnected system of selected accidents. Much as one might build a very tightly constructed stone wall out of stones which have been shaped purely by accident, but very carefully selected to fit. Each individual stone is an accident, but the wall is not.
colewd,
The papers that try to model this fail because of the vast sequential space of the genome especially long sequences. I have read the literature on this, and all support large populations and time for only a few mutational adaptions. This is part of Lynch’s paper I already sent you. The paper you sent me said that 69% of human genes have 1 or more substitutions vs chimps. Per your paper:
So 71% have an average of 2 substitutions so assume around 30000 genes. According to the math of neutral theory that Joe educated us on in a prior post 50% should be advantageous:
So by the math you should expect 15000 advantageous nucleotide changes from the common ancestor. To be advantageous they would have to occur on the same condon and force a helpful amino acid change. Per your paper many of the changes occur in the transcription area which is not forgiving of mutations. The math does not work here if takes all the probabilistic problems in account of working through the sequence get to 15000 advantageous mutation fixed in the population. This is one of 6 areas of problems I see with this transition.
You are indulging in word salad again, probably occasioned by your many misunderstandings of the literature. First, there are only about 20,000 genes. 70% of that would be 14,000. But of course not all sequences under selection are protein-coding. You should also note that about half the differences would have arisen in the chimp lineage and half in the human. I have no good estimate for how many of them are advantageous. Joe’s example appears to be strictly hypothetical, and I would expect that the majority are neutral. Still, if one takes his notion, that’s actually around 7,000 advantageous mutations in protein sequences in the human lineage.
Not sure what “would have to occur on the same condon” means. Same codon? No, that makes no sense. But I can’t think of another interpretation. “…in the transcription area which is not forgiving of mutations”? No clue at all.
Also no idea what problems you think “the math” would cause for an evolutionary scenario. All that stuff about sequence space is nonsense, as it assumes you’re starting from a random point in sequence space. You are not; you are starting from very close to the end point, as the bit about 30% of proteins being identical and the other 70% differing only in an average of 2 residues should make clear. You also seem to imagine that each of the advantageous mutations must be both specific and necessary, and there’s no reason to suppose that either. Of all the mutations that could possibly occur, some do occur. Of all the mutations that could possibly occur, some are advantageous. The set of those that are both advantageous and do occur is drawn from a much bigger pool of potential advantageous mutations, and you forget that.
colewd,
Did you ever actually read Andreas Wagner’s Arrival of the Fittest? You said you were going to, as I recall.
keiths,
He doesn’t so much read as search for little bits he can object to in order to maintain his creationism.
Why, this genetic accident resulted in a slightly better reproduction rate? How so?
That is complete speculation, for which you have zero evidence of. You have no idea If any one small mutation (a mutation that never existed in the population before) ever caused enough biological change in a species to cause it to increase its reproduction significantly to THEN allow it to get a second mutation (to that same gene!) to allow it to increase its usefulness even more.
That whole fairytale is completely unsupported by real evidence. All you side can ever really say is, “can you prove it couldn’t have happened?”
Bad science.
Flint,
But you wouldn’t call a wall a system, now would you? If a bunch of rocks accidentally fell down a hill, which caused them to block a bunch of water, that is not a system. It is just a block of rocks that so happens to clog things up.
Now when you say “plan” I have no idea what that means, if it doesn’t mean designed. If it is not designed, there is no plan. A plan by definition means a design.
Allan Miller,
How many would many be?
Other than actual experiments performed in a lab on E Coli by Dr Lenski, etc etc.
Please make an effort, Phoodoo. You assert what you want to be true and are always wrong. Learning to research / read articles in full will help you in life – people will find you more informed and interesting.
You appear not to know that natural selection works on individuals within populations, not species as a whole. Now, as for evidence, are you claiming that there are no known cases of advantageous mutations? Are you claiming that all alleles were present in every population from the beginning? That seems to be an unusually expensive pair of blinders, even for a creationist.
Richardthughes,
You mean we have to base the assumption that some human type form got a slight mutation which caused a new gene, and which caused a noticeable difference in its form to give it an increase in its reproductive rates to such an extent, that it then out-survived all those without the slight mutation (for which we have no evidence), and then it got another and another (for which we also have no evidence), ALL on the fact that lenski put bacteria in a petri dish and they are still bacteria in a petri dish?
THAT’S what we have to use as the only basis for this fairytale?
Holy shit its worse than I thought!
Oh you’re right: Evolutionary theory predicts bacteria will become pigeons in a maximum of 3 months. Dang. Design it is!
You read, but don’t participate at UD for ‘educational purposes’, you say?
Richardthughes,
Evolutionary theory makes up a lot of fairytales, is that what you meant to write, but your wife refused to show you the keys?
phoodoo,
No it isn’t Phoodoo. You’re embarrassing yourself again.You’re incredibly opinionated yet either lack the intellect or application to actually research the material you (think you are) so upset about. You post about articles when have only read the abstracts. The tragedy is that the education system has failed you and you don’t have it within yourself to fix that.
OK, time to put phoodoo on the “ignore” list.
That might well be true 🙂 but on the evidence shown so far it won’t be you doing that rethink. Nor will any of your objections be part of that rethink as they’ve all be comprehensively dismantled. Not that you’ve noticed that.
But the proof is there. For example, you can point to any such ‘re-think’ in the next 50 years or so and point out how your ideas have influenced it. Or not. We shall see!
Odd how there seem to be many books and papers published daily that talk about ‘non-designed evolution’ that seem to be full of words not arranged in that particular order.
Yeah, I mean who has ever heard of a scientific discovery that involves a petri dish!
The funny thing it’s it’s one more petri dish then has even been involved in any ID experiment!
John:
As important as religion is to guys like colewd and Sal, you might think they’d be eager to know whether their beliefs are true (including creationism).
It’s just the opposite. They are so afraid that their beliefs might be false that they’re scared to test them. I suspect that colewd’s refusal to read Theobald and Wagner has far more to do with fear than it does with laziness.
Don’t look too close, guys. That diamond ring might turn out to be a cubic zirconia — or a Cracker Jack prize.
A mutation has to be big enough to cause an advantage, and yet small enough not to destroy the individual. You can give no examples of these in higher primates.
All you can really point to are different frequencies of alleles.
You don’t stand up to scrutiny very well. I thought you were supposed to know some things about this topic.
keiths,
Giant vacuous handwave alert.
Giant vacuous surrender alert.
phoodoo,
You describe yourself as a “giant vacuous handwave”? Hmmm… that’s pretty accurate, actually.
OMagain,
“There are lots of books about evolution”
Yes there sure are.
And yet all your side can tell us for evidence is all those petri dishes still full of the same dam bacteria.
How many new genes did they create all in those pertri dishes.
phoodoo,
Oh dear. I used the term as I might in the word ‘ecosystem’ – interactions between organisms, not as one might in ‘system of government’ or ‘the payroll system’. Or system of a down, or whatever the hell else you might imagine.
colewd,
Good grief! Not the first time I’ve noticed this habit. Unless it’s a typo.
colewd,
I’m not sure you’re really following this. I started with a common ancestor, then through a series of generations in 2 separate lineages, the common ancestral sequence gradually changed, independently. When we come to compare 2 descendant sequences many generations later, there is a degree of similarity and a degree of difference. Inevitably.
Thus, if we find 2 sequences with some degree of identity on alignment, we must allow the possibility that they arose by that mechanism. Do you agree?
If the sequences remain identical, we are NOT justified in saying they must therefore be identical twins! Note that I’m not talking about entire genomes here. I’m talking about pairwise comparisons of shorter sequence, typically 1 or more ‘genes’.
Allan Miller,
I think there is a reason why ecosystem is one word, because it refers to a set, not a system. Its not eco system.
Ignicoccus/Nanoarchaeon archael system whereby ATP is passed from one cell to another in intimate association is nothing akin to an ecosystem is it?