I am working on a series of tutorials to cover the basics of Intelligent Design, especially the mathematics of it. This is my tutorial on Specified Complexity, and I would appreciate any thoughtful criticism of it.
Note that I am specifically requesting criticisms on the content of the video itself, not on applications of the concept that are outside the bounds of the video. This is both to help me (I’m trying to improve my presentation of ID) and to help clarify the conversation (is the criticism of *this* information or of some *other* information).
Allan Miller,
And your experimental support for this claim is?
Yet another logic fail right there from Bill, LMFAO
colewd,
What is your counter-claim, and what experimental support do you have for it?
I see no sound reason to suppose that LUCA had within it the genome of every modern organism, each modern lineage arising from a gradual whittling away of the things that were not it. It’s a bizarre notion. But, if you want to pursue it …
Allan Miller,
The argument is that the sequential space of the genome is too large and functional space is too small. I point to Axe’s penicillin experiment to support my claim.
The other claim you have not supported is that alpha helixes will gain selective advantage.
colewd,
We’ve been through this many times, but I don’t in any case see what that has to do with suppositions about the size of LUCA’s genome. You are surely not suggesting that it needed an actual universe of proteins in order to find one or two functional ones? Surely the others would somewhat get in the way? To say nothing of it being the size of a small galaxy.
I also feel the need to point out to you yet again that LUCA is not regarded as the first cell at the very origin of life. I repeat my claim: LUCA need not be furnished with any more genetic material than was necessary to support its immediate survival and reproduction. Your response does not go near that, and Axe’s fiddling with penicillin could not be much less relevant. One can produce dysfunctional enzymes? The hell you say.
Why not? Are we to suppose that the only possible advantageous arrangement of a protein is the one in which we find it today? On what grounds?
What are the constraints and capabilities of homo erectus or australopithecus afarensis?
It seems to me that we mostly discover the capabilities and constraints of individuals by studying what they have designed. Do you disagree?
peace
I would agree. However I don’t know of an entity that can do literally anything so I’m not sure what you bring this up.
God can’t make a square circle or a rock so heavy he can’t lift for example.
peace
I think I will put together a couple of OPs on just that topic as a follow up for the recent discussions here. We will see how it goes.
Yes, Do you?
peace
Such explanations are ad hoc. But if one doesn’t have actual calculations for the probability of such selection pressure existing, it’s just unproven speculation, it’s not at the level of highly verified science compared to other scientific disciplines like biochemistry. But what is a random alpha helix going to do when parked on membrane. It will take up space, and enough of those will block the membrane. Not good.
Anyway, some data on transmembrane proteins:
Thanks anyway for the comment.
Which I complete debunked in a large post on this very site.
Allan Miller,
What do you claim is the minimum cell configuration for life? Currently Ventner is down to 500 genes. Do you claim life before DNA, Ribosomes and ATP synthase. If so on what grounds can you translate chemical/solar energy to work continuously and maintain survival?
1. That depends on the definition of life you use.
2. Why is anyone required to know the minimum number of genes for a free living cell, in this context?
Given that this is entirely dependent on definition, the question is vacuous. For example, if I just define life as templated copying of polymers, then by definition there is life simpler than cells with DNA, ribosomes and ATP synthase. A thermal convective cycle can replicate DNA or RNA. Is that life? If you don’t think so, why not?
stcordova,
…? It is biochemistry! One can readily compute the amphipathic moment for a random helix. Fully radially-symmetrical helixes are likely to be rarer than those with an affinity on one side or the other. Membrane affinity will depend on the orientation of the helix wrt the rest of the protein. Point is, it is a perfectly realistic mechanism by which membrane location can be tuned.
Meantime you have just basically shot yourself in the foot. You reckon it should be possible to calculate the probability of a particular distribution of hydrophobic residues arising in one go. How do you propose that actually happens? What biological mechanism are you representing? Why are you ignoring the ones that actually happen?
Uh … yeah. I wonder what mechanism could possibly prevent that from happening? It’s like the wind always blows from the east with you guys. Why isn’t everything a giraffe?
colewd,
Pretty irrelevant to LUCA. It had about half a billion years’ worth of ancestors. I already said: LUCA was not the first cell.
Rumraket,
I have not seen any experimental evidence that you can sustain life in a simplified form. There is no logic to me where self replicating DNA turns into anything more on its own. The simple to complex by natural means is a story to try to explain what we have observed historically. In my mind its truth has no experimental back up or logic supporting it now that we are beginning to understand cell complexity.
One thing I agree with Allan’s approach is that if you cannot make sense of origin of life evolution does not make sense either.
Can I play this game?
ID is s phylosophy that has a disproportionate number of proponents who think that homosexuality is a sin that should be punished with the force of law. And the Turing test was developed by an individual who saved hundreds of thousands of people during the war, who was persecuted to the point of suicide for the sin of being homosexual.
What do I win?
I live in the buckle of the bible belt and I have never met a single person who thought that homosexuality should be punished with the force of law.
I’m not even sure how that would possibly work. You can’t effectively criminalize thought as far as I know.
I do know a few folks who think that sodomy should be illegal all most always these are the same folks who think that adultery,gambling and alcohol should be illegal. Those guys are generally equal opportunity litigators.
What happened to Turing was a terrible evil but he was not convicted of homosexuality or sodomy but of “gross indecency” a crime that IMO has more to do with prudish Victorian sensibilities in Britain than some sort of religious theonomy.
peace
Looks like johnnyb can’t think of any way for specified complexity to be applied to anything more that trivial combinational probability examples.
What a surprise.
the failure of ID continues year after year.
Neither have you seen evidence that an immortal Intelligent Designer has been fiddling with life for billions of years, yet you actually believe that.
How is this a response to my question? What definition of life are you using?
I dare say, there is no logic “to you” whatsoever.
Then whatever is “in your mind” is mistaken. I suspect it’s because you never understood the logic of phylogenetic inference. You still don’t.
That isn’t Allan’s “approach”. Do you want to know why? Because it wouldn’t make sense. Whether the origin of life was a physical/chemical process, or whether it was due to some sort of intelligent design, has no bearing on whether that first life subsequently evolved into all the life we see today (which it did).
How can it be possible for you to write so much wrong in so few words? There’s scarcely a single implied inference you concoct that isn’t a complete non-sequitur. It is astonishing.
IDiot logic:
“the size of genome that would be required to have a universal common ancestor so simple that it can’t sustain life, may be way too big”
So having selection scenarios that create extreme conditions far from the expected value of the binomial coin flip distribution is a little harder than just talking about having ampiphatic asymmetry that creates binding of a random helix. It’s way more complex than that.
Thank you for the comment but you misstate the problem.
If random alpha helices will bind to the membrane that is bad. One of the activities of the membrane is to allow only certain substances in or out and in the right amounts. Also if the otherwise functioning helix doesn’t bind because it lack insufficient hydrophobic/hydrophilic asymmetry (again the the extremes of binomial distribution) the cell could die.
Consider for example the GLU4 transmembrane protein or any functional equivalent that allows glucose in the cell as depicted below. Suppose the cell did not have a GLUT4 or equivalent, then glucose doesn’t enter the cell, the cell dies. If GLUT4 (or the equivalent) doesn’t exist, no life, not selection, no evolution. Dead things don’t evolve!
No point in talking about marginally binding GLUT4 if the marginally binding doesn’t bind enough and at the right time to keep the cell alive. Oh yeah, look at the other constrain on GLUT4 that interacts with insulin cascade — you need beta cells to make insulin (and that means lots of developmental complexity), you need the insulin gene, you need insulin regulation, you need receptor tyrosine kinases, etc. etc. and last but not least the transmembrane integral GLUT4 that interacts properly with the membrane when called upon. You improperly assume selection will act, when it won’t even get off the ground because the creature is dead!
Conversely suppose any random dang thing binds to the membrane and lets any random dang thing go in or out of the membrane. Too many potassium ions flowing through a transmembrane protein that implements an ion channel in the wrong direction. Oops. Too many sodium ions passing through a transmembrane protein that implements a transporter. Oops.
Your selection scenario generously assumes it the trait of hydrophobic/hydrophilic asymmetry (aka amphiphatic characteristics) is easily selectable in the first place based solely on hydrophobic/hydrophilic asymmetry alone, but selection must be more targeted than that and it must exist in the first place. If the organism is dead, it’s rather pointless to talk about selection isn’t it?
I’ve shown two reasons why the organism could be dead. If the transmembrane protein is necessary for life, and it doesn’t exist, the organism is dead. If any random polypeptide starts providing random channels through the membrane, then stuff that should stay in the cell leaks out and membrane potential and concentration gradients are gone — or just as bad things leak in that should stay out. The thing dies.
Or just as badly, the membrane is clogged with an abundance of non-functioning poly peptides with alpha helicies. Does the cell look like it’s full of non-functioning alpha helicies to you from which selection can experiment and create new functioning transmembrane proteins? And if a transmembrane protein isn’t necessary, why will it be selected for? It’s silly to assume poking random holes in the cell membrane to with randomly formed proteins will do anything good.
Your selection scenario runs into challenges when confronted with more realistic scenarios and actual data.
And speaking of poking random hole in a cell:
Every time a creationist argues that cells must have self-assembled on their own, the Flying Spaghetti Monster kills a kitten
Pretty sure colewd thinks the Intelligent Designer has been fiddling for 6000 years.
Similar to those of early humans, which is why we can distinguish between artifacts they may have produced and those they could not have.
You’re confusing the issue. You claimed that sciences like archaeology and forensics demonstrate that we can detect design scientifically. My point is that such detection is only possible because we know the capabilities and constraints under which humans operate.
You can’t make design claims about an omnipotent entity because it could do literally anything. And we all know that IDCists mean their particular god when they say “Designer”.
So, you don’t know of anyone who is opposed to same sex marriage? Or anyone opposed to same sex couples adopting?
In many of the bible-belt states it required the Supreme Court to remove sodomy from the books. The same is true for same sex-sex marriage.
Homosexuality was considered gross indecency. They didn’t charge him with sodomy because they didn’t catch him in the act.
Substantive critique from Wes @ AtBC
http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?act=ST;f=14;t=7304;st=810#entry255928
Logic Fail.
If only God can create a universe from nothing then that pretty much narrows things down.
Spot the difference:
Entity “E” can only do “X”
Only entity “E” can do “X”
colewd,
I don’t recognise the position being attributed to me.
Evolution occurs whatever the origin of the replicating entities. I have in fact strived to put substantial distance between LUCA and the origin – an effort that is clearly in vain.
My original statement was that LUCA – merely our most recent common ancestor – would need only those genes necessary for its immediate survival and reproduction, in contrast to jonnyb’s strange suggestion that its genome would be too big if it was a common ancestor. You challenged that (on spurious ‘experimental evidence’ grounds) but have spent the rest of the time talking of something else entirely.
stcordova,
I still have no idea what biological process you are representing with coin flips.
You are misstating the problem. Random helices really do have differential asymmetry with respect to hydrophobic moment. It’s unavoidable, but is hardly the all-or-nothing cartoon that you spin. If such a helix arises and that is detrimental, the organism dies. That leaves the field open to all the organisms that are not dead. Perturbations from symmetry are not favoured if they cause damage. The fact that you can cook up some particular scenario does not mean ALL perturbations from symmetry will ALWAYS be damaging, or that the slightest hint of a change in moment will cause all proteins to gum up the works. It’s the classic ‘some-therefore-all, few-therefore-none’ dodge of Creationism.
Real amendments to hydrophobic moment happen by small degrees, and they can lead in either direction. They do not automatically mean that membranes are always clogged with asymmetric helix! An absurd reduction.
Are you proposing that it is flat-out impossible for such a helix to improve function in any protein by increasing or decreasing its affinity with membrane or cytosol? Instead you argue for the ridiculous and non-biological mechanism of drawing a few hundred acids from a bag with the hydrophobic residues already exactly where they need to be, with no possibility of any less specific precursor state.
Of course, the probabilities are easier, because they are independent, and you get what you really want: BigNumbers. But the result is meaningless. 10 to the hundred million. 300 to the squillion. It’s enormous, and totally irrelevant.
I actually agree with Salvador on this one. What good is half a membrane?
I can hear some evolutionist now. Well, maybe first it just sort of helped keep off the rain. And then it evolved a bit from that. Until eventually, a modern membrane!
What good is half retard? Go full on!
Unless, of course, the membrane prior to the evolution of GLUT4 was semipermeable, because it was made of simpler fatty acids, instead of phospholipids.
Things are a certain way now =/= they must have always been like that.
E coli seems to be doing quite fine without insulin. Have you spent even a single minute looking at the comparative genetics of insulin and related regulatory pathways? I haven’t, but I predict it’s not universally conserved. Test me!
But is it? How do you know?
I agree. Which is why nobody believes or suggests such a preposterous scenario.
Sure, if the universe came from nothing, and the only possible way that could happen is if God made it so, then God would have to have made the universe. Yes, it follows.
Now, time to substantiate the premises:
1. The universe came from nothing.
2. The only possible way this could happen is if God made it so.
Impress me.
Turns out it’s better than no membrane at all.
Physical effects underlying the transition from primitive to modern cell membranes.
Budin I, Szostak JW.
Pay special attention to reference 3: Template-directed synthesis of a genetic polymer in a model protocell.
Rumraket,
Hah, yes, I’d missed the fact that Sal was talking about multicellular creatures! The only kind worth talking about. I think we can all agree that membrane-protein associations did not originate in multicellular organisms.
Mung,
OK, let’s allow that membranes were magicked up by pixies or something, does that mean that you agree with Sal on the consequences of amphipathic asymmetry, and his deduction on the resultant impossibility of all pathways by which protein/membrane associations can be tuned?
I’d agree with that. But Salvador’s essential point still remains.
Mung,
What, that it is impossible for selection to tune protein-membrane affinity, in either a positive or negative direction?
I know he went a bit Gish-gallop, so it’s hard to pin down what specific point you might mean. But he was, at least initially, responding to my point about tuning.
I provided an example of algorithmic specified complexity a while back: hermit crabs forming a conga line to exchange shells. The simplest approach (contrived, as is the norm in ID examples) to calculating the ASC is similar to what he did in the presentation. That is, it takes a lot more bits to describe an arbitrary permutation of
shells than to describe a size-descending sequence of 
shells. The log-ratio of those quantities qualifies as ASC. I’m sure Jonathan is capable of setting up the model, and doing the calculation. I’m not so sure he’s prepared to deal with the result. Make a large number distinguishable copies of a system operating according to very simple rules, and the collective can generate large amounts of ASC, even though none of the individuals can.
Are you trying to say something?
Mung,
Yes, we got the memo, and saw the picture. There is no question that the amount and location of hydrophobic and hydrophilic residues affects the general locale in which a protein is found (though not as rigidly as people with any kind of ‘plastic-sheet-and-velcro’ model in their minds may think). If that was Sal’s ‘essential point’, I won’t argue with it. The point I was responding to, though, was the relevance of independent-probability computations for the pattern observed in any given protein – Hoyle’s Fallacy, yet agin. Substitution, selection, domain donation, excision and migration, tandem duplication – do they not happen?