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.
LoL. Except when it doesn’t.
After the famous Hashman Bombshell Miraclevolver anything looks pretty dim… lol
Mung,
His opinion on the age of the earth, I don’t know, but he’s very much Old Skool on Common Descent.
stcordova,
Huh? Sorry, I heard my name …
If I saw something created out of thin air, it would not be conclusive proof that this was the method by which all existing organisms had arisen. And I would still be very interested to know why there was all this apparent phylogeny all over the place. I can’t just unsee it, y’know.
Mung,
Preddymuchthesame. There’s a neat graphic somewhere, showing the Tree of Life, with multicellular organisms in a tiny corner, can’t be bothered to hunt for it now.
Maybe that’s why phylogenetics is so doggedly dismissed. We’re at the centre of the universe too, don’cha know.
Mung,
You think archaea aren’t related to bacteria? On what grounds?
Are any of you creationists ever going to tell us how design explains the objective nested hierarchy? (Rhetorical question. You won’t, because you can’t.)
The morphological and molecular trees of Theobald’s Figure 1 match to a precision of 1 in 10^38. Tell us why
Godthe Designer just happened to produce identical patterns for those two trees, out of the gazillions of possible combinations.Is it because God dislikes intelligent people, and wants to fool them into believing that common descent is true? Is it because he’s weak, and cannot operate except as an evolution mimic?
Why, if common design is true, does the evidence point so overwhelmingly to common descent?
Stop dodging the question.
John Harshman accuses me of Gish Gallop. So what? The facts remain.
Did he think I was making stuff up like say about miRNA’s constraint on nucleotide sequences? How about enhancer sites that sit on exons? How about binding sites for all sorts of histone modifying machinery?
I just provided a diagram of a micro RNA regulatory network. Did John Harshman think that was irrelevant to his belief that gene differences are created by random walks versus functional difference like say microRNA binding sites.
There are all sorts of binding motifs. The effect of a mutation might not be noticed immediately because the Eukaryotic genome is highly buffered. See Brenda Andrews work on this.
But anyway:
So Theobald is basing his random walks on limited data. In light of more modern data, the random walks don’t look so tenable because change in nucleotides that may seem superficially random turn out to have regulatory significance, and not necessarily for the gene in question but genes that are elsewhere.
A powerful example is the FIRRE lincRNA. Look at all the trans chromosomal interaction in the lower left corner of the following diagram. That’s made possible by binding sites. Binding sites can be on genes. That sort of orchestrated binding won’t come about by randomly changing genes that are required by Theobald’s model.
Is Escherichia coli a created kind? Enquiring minds want to know.
stcordova,
Skiddle-ump, skiddle-ump, skiddle-ump.
Corneel,
Flagellum-propelled, so yes, absolutely. Separately created in each pathogenic strain, too, seems to be the final destination of Sal’s train of thought. Thanks, God!
You don’t have any facts of interest here, all you have is really just your imagination. Some things are constrained, which really just means that not all changes are at any given moment possible, that doesn’t mean they’re immutable. Epistasis, look it up.
Constrained =/= immutable. Please attempt to grasp this elementary concept.
The genetic code has fourfold degeneracy for most codons.
No different than anyting else, there are some constraints on what can change at any given moment, but due to epistasis they still can.
I don’t know what John Harshman thinks, but I know I think your ability to attach a picture to your post doesn’t enhance your argument when it basically reduces to an unevidenced mere assertion that because some sites are constrained, they must be immutable.
No, Theobald is basing his conclusion on actual data, whereas you are just trying to handwave in the direction of your own incredulity.
There isn’t any difference between “modern” and older data on this point. Binding spots can change due to epistasis, and they can also do so in exons for the same reasons, and the fourfold degeneracy of codons.
They look entirely tenable. They look so manifestly tenable they have been experimentally tested and demonstrated to be changeable. Using ancestral sequence reconstruction, scientists have inferred the sequences of ancestral binding spots on both DNA and the protein transcription factors that bind to them, and have experimentally demonstrated how they have changed over time and what their ancestral functions were.
Even more impressively, they have experimentally demonstrated that there were HUNDREDS of additional possible way that the binding interactions we see today could have evolved from ancestral transcription factors with different regulatory functions.
See for example this “peer reviewed research article by PhD researchers, published in the prestigious scientific journal nature“:
Tyler N. Starr et al. Alternative evolutionary histories in the sequence space of an ancient protein, Nature (2017). DOI: 10.1038/nature23902
My bolds.
Conclusion: Everything you say is demonstrably false.
Thank you for this counter-factual blind assertion. When all else fails, just assert what you are trying to prove.
Yes, not completely unexpected. For what it’s worth; I admire your perseverance. But it should be clear by now that Sal is incapable of following what it is that common descent explains, and how that explanation works. He is just so happy with the good ol’ argument from design analogy that he is unwilling to let go of that argument in a discussion where that no longer has any relevance.
Haha, mysterious ways and all that I suppose.
I still hope he answers, because it is interesting that Sal actually brings up an example from the microbial world for once. E. coli has, by his own admission, excessive polymorphism within the species. There is even considerable polymorphism for gene presence / absence. How does that rhyme with that exquisitely fine-tuned and immutable design?
I’d suggest “not interested”. I think Sal’s agenda is to road-test his strawmen and make improvements as needed in preparation for the larger battle for hearts and minds. I bet Betsy will be proud!
Yep, I have had the same suspicion for a long time.
It is very ironic that Sal is in a sense evolving his creationism by artificial selection. By throwing out a lot of crap and selecting the shit that sticks for further rounds of change and testing. 😀
Sal is open about the fact that he uses TSZ as a testing ground, but remember that it was also him who wrote the OP “Common Design vs. Common Descent”. Why would he do that if he has no interest in the matter whatsoever? No, it runs deeper than that. I think that he is so absorbed by the design argument that he perceives every evolutionary topic where it is irrelevant as a diversion attempt.
ETA: corrected typo
Suppose that’s true.
What explanation do you have for the data he did use? Whim of God? Deception? Desire to destroy people for believing the evidence God left behind?
We know that you don’t and won’t explain anything at all, since this isn’t actually about science or evidence, merely about your preferences. But we still have a lot of evidence that evolution explains, nothing that design explains, and no interest from you in getting to an explanation.
Other than avoiding and denying evidence, what’s your point?
Glen Davidson
At least it’s not the same picture over and over.
To try to save face.
Sal at some point said he would do an OP.
He was chided for not doing so. (Some people just don’t know when to keep their yap shut).
So now we have an OP on it.
He should try harder then
Rumraket,
You might not find this interesting but there is an issue with complex regulatory networks being originated by random change. A protein ancestral history has very little to do with how these complex networks arose. I cited a paper previously to Allan Miller that showed a mutation to the mouse apoptosis complex stopped proper skull development and the mouse was still born.
He may also realize deep down that he has nothing to say about common descent, no hypothesis to explain the evidence, and so he concentrates on the spots where he imagines he has an advantage.
So why did he ever promise a post on common descent vs. common design, and even deliver at least as far as the title? Now that’s a mystery.
colewd,
Let me repeat this, since you are conveniently ignoring it:
Are any of you creationists ever going to tell us how design explains the objective nested hierarchy? (Rhetorical question. You won’t, because you can’t.)
The morphological and molecular trees of Theobald’s Figure 1 match to a precision of 1 in 10^38. Tell us why
Godthe Designer just happened to produce identical patterns for those two trees, out of the gazillions of possible combinations.Is it because God dislikes intelligent people, and wants to fool them into believing that common descent is true? Is it because he’s weak, and cannot operate except as an evolution mimic?
Why, if common design is true, does the evidence point so overwhelmingly to common descent?
Stop dodging the question.
But was it born dead?
Tell us again why it must be either one or the other?
If you mean Betsy DeVos, dang right.
Deliver little by your definition, not mine. I delivered the goods, you haven’t, according to my definition. So who is right?
So we had different ideas about what we would actually be talking about. I talked about what I believes makes my case, you talk about how you think I didn’t make my case.
In any case, I’m not even half done making my case against common descent.
If you don’t want to participate anymore, I respect that. I’ve been appreciative of you and most everyone’s participation here.
I’ll try not to put up too many OP’s. I’ve said I’ll try to abide by the 2 OP’s a month guideline, and I see no need to even make too many OP’s at TSZ.
I’ll just blast away in the comment section. People that don’t want to read can put me on ignore.
Really? Look for example at some of the first things we are learning about transcromosomal control of gene sets or stretches of DNA. We do a ChiRP-Seq experiment and find 832 locations where the HOTAIR lncRNA parks itself on a variety of spots on different chromosomes. This illustrates what is true about a lot of other molecular machines. DNA serves as movable parking lots and road signs for molecular machines to park and work…
We find a binding motif in all sorts of places and associated histone changes. How did that binding motif get there. You think they evolved. Ok, consider the difficulty….
As depicted in one of the diagrams provided, many times the biding motif works well within a 3D framework. That is a binding motif on one Chromosome works if the binding site on the chromosome is located so the molecular machine parked on it can service another chromosome. I showed a conceptual illustration with the FIRRE lncRNA. This works provided the chromatin can be properly oriented to take advantage of the positioning of the binding site.
Oh, not to mention that’s just the constraint on the DNA, there is also constraint on the corresponding RNA that is regulated by micro-RNAs and who knows what other constraints there are on the RNA. And then if the DNA codes for something there are even more constraints!
This requires 3D coordination. How the heck does that happen without some foresight?
I’m not pumping out imagination, this is cutting edge understanding of higher order chromatin structures.
See the NIH 4D nucleome project for starters.
For a website that promotes itself as being pro-science, I seem to be posting a larger proportion of stuff that actually gleans from recent papers on molecular biology. There is more to biology than evolutionary biology fer cryin’ out loud.
https://commonfund.nih.gov/4dnucleome
When I posted this OP I was expecting to eventually talk about stuff like this because it is dang interesting. Much more interesting than theories that don’t make much mechanistic sense like how a fish evolves into a giraffe over several million years.
I am, clearly. You’re talking about the supposed inability of mutation and natural selection to produce complex adaptations, while I’m talking about common descent vs. common design as explanation for the nested hierarchy of life. The latter is what I asked for and you promised to provide.
Not quite. I talk about how you didn’t even try to make your case and don’t seem to know what you’re making a case for. You aren’t even making a case for intelligent design, much less common design. All you’re doing is attacking the standard mechanisms of evolution, as if that would support ID by default.
On that we can agree, since you have not yet begun.
If you’re so respectful and appreciative, and this whole thread is supposedly for me, why won’t you even try to do what I asked you to do in the first place? Disappointing.
Good question.
I believe that in living systems the parts reflect the whole and I have no problem believing in common design (of sorts) and common descent.
If we focus on the development of an individual human we can see that all the body cells form a nested hierarchy with the zygote at the root. But we also know that the development of the individual follows a regulated, pattern to a predestined outcome under normal circumstances. It is a process of increasing autonomy of the individual from the mother.
Living nature follows the same general direction where increasingly autonomy is a recognised feature. And increasing autonomy leads to greater self awareness and the flexibility to consciously begin to take control of ones own actions and destiny.
Below is a reference to a book by Bernd Rosslenbroich
One example of this pattern is the development of endothermy as witnessed in the bodily processes and integumentary systems in birds and mammals.
Sorry but not really, no.
That’s just incorrect I’m afraid. The paper I linked is just the latest in a long line of articles detailing the proliferation of a whole family of steroid hormone regulated transcription factors, from their common ancestor which was a transcription factor that existed before the origin of vertebrates, more than 450 million years ago. This ancestral steroid hormone transcription factor has diverged into dusins of steroid hormone transcription factors involved in all sorts of complex gene-regulatory networks related to development and gender-based gene-expression.
Bill, you can’t extract a trend from a single mutation. That’s silly and you could have worked this out yourself.
I think you’re not understanding the difference between mutations that HAPPEN and mutations that get fixed. Deleterious and lethal mutations happen, but nevertheless during adaptive evolution, most mutations that are fixed are neutral or beneficial.
You like graphs? Here’s one for you (from Barrick & Lenski. Genome dynamics during experimental evolution. Nat Rev Genet. 2013 Dec;14(12):827-39. doi: 10.1038/nrg3564:
And if there is inability, then common descent can’t be an explanation for the patterns of similarity unless one invokes miracles to make common descent feasible. Therefore common descent by ordinary means is falsified.
You don’t seem to count that as evidence for common design. I do. We have different criteria for what counts as evidence.
By the way, can an intelligent designer in principle create nested taxnomic hierarchies if he wanted to, like say the nested molecular taxonomy one would find for cytochrome-C or aaRS or whatever.
Yes, and it can also cause all crystallization, plate tectonics, thermonuclear reactions, and ecological interactions.
What of that? If God is all about faking things, we’re pretty much screwed in understanding the world.
If you’re willing to hang your eternal soul on something that ridiculous, clearly there’s not much of a discussion to be had.
Glen Davidson
Can an intelligent designer created nested hierarchies defined by Taxonomically Restricted Features or Orphan Systems. For example mammals nest within vertebrates. Their salient Taxonomically Restricted Feature is the mammary gland which helps create their nested taxonomic position within vertebrates.
How does common descent explain the existence of the mammary gland except to say, “evolution did it” which isn’t much of a mechanistic explanation is it? Common descent only pretends to invoke natural mechanisms but is actually quite sketchy on details as would be found in other mechanistic theories like celestial mechanics. Common design by miracle isn’t a mechanistic theory, nor does it even pretend to be. No explanations in terms of mechanics is therefore needed if one is willing to accept miracles that are beyond our comprehension as explanations.
Now, if one will say one won’t believe unless one has an mechanistic explanation, then why do evolutionists blindly believe mammary glands evolved without a mechanistic explanation? “Evolution did it” isn’t a mechanistic explanation, it is a statement of faith without facts.
Yes. Read the papers. Transcription factor binding sites can and do evolve. You’re just in denial. History actually took place. Again, they have reconstructed the evolutionary history of an entire family of steroid hormone receptors that control developmental genes. They know what hormones that used to control it, they know what hormones the many different and specialized members of the family respond to now today. They know what DNA sequences it used to bind to, and what DNA sequences the many different specialized descendants bind to, today. They know how it evolved and they know that there are HUNDREDS of additional ways it could have evolved also. Your difficulty is, again, entirely imaginary. No amount of stuffing your post with text and inconsequential factoids is going to make it go away.
Are you saying you don’t know? Isn’t that an appeal to ignorance fallacy?
I did, the difficulty is imaginary. Epistasis. Permissive mutations allow later mutations to change residues that initially look “immutable”. Turns out they aren’t. Read the papers. All the papers, not just the ones you think you can spin into your creationism. Stop ignoring the evolution-related papers just because they say things you find threatening.
This is just filler-talk. There is no substance here. You are just listing a bunch of facts that move us no closer to your sought conclusion. The more you smear this butter the thinner it gets.
Yes who knows, and better yet, does it prevent the evolution of regulation due to epistasis? Nope.
Oh would you look at all these constraints. And yet they can still evolve and change, due to epistasis.
3D coordination you say? Holy moly, that sounds Soooooo fancy.
Is that not an argument from ignorance?
It can happen as described now multiple times. Epistatic interactions between different residues in both the DNA and the regulatory elements, allow new binding spots to emerge and old binding spots to change. Binding spots get duplicated, or they emerge by accumulation of point mutations. The transcription factors that bind to them get duplicated too, and these in turn also change by accumulations of point mutations.
Many residues can change with nearly neutral effects, which in turn allow other mutations that previously were strongly deleterious or even lethal, to happen, because the combination is permissive.
It is an observed fact. It has been verified in experiments. The historical changes by which the mechanisms we see today came to exist through evolution, has been elucidated with phylogenetic methods and tested in the laboratory. It really is how it happened in actual history.
And the work on the reconstructed evolutionary history of the origin and diversification of a whole family of developmental transcription factors is cutting edge too. The paper I linked is from september 2017. Not that it being “cutting edge” is what matters here.
4D now? Why didn’t you just say so. Oh well then I guess a MAGIC MAN must be required. Did he buy his wand in Diagonalley too?
The problem isn’t the facts, it’s your entirely IMAGINED interpretation of what those facts entail.
So chromatin can form in many places on chromosomal DNA? So miRNA must match the sequence of the DNA it binds? So one thing is constrained by another?
Look Sal, these vacuous handwavings in the direction of “constraints” get you nowhere. None of the articles you link, or the nice pictures you post, come with any information that says there are no possible epistatic interactions that would allow chromatin binding interactions to evolve or change. You have got no closer to where you wanted to go with all this.
I’m quite certain that nowhere in all the NIH-4D-coordinations-miRNA-hotair-chromatin-nucleosome-binding-regulatory-wibble-wabble-how-many-fancy-words-do-you-even-need papers that you link, will I find even a single sentence that says that there is no possibility of change or evolution of any of these entities. There will not be a conclusion found that they are immutable.
You’re trying to make it appear as if they are immutable, by spending a lot of time making the constraints sound big and fancy. And you fail, because despite all the …well, hot air you exhale, the conclusion still doens’t follow. Even more importantly, real world experiments with phylogenetically reconstructed ancestors and intermediates, the results of which should not be possible if they are truly “immutable”, say otherwise.
Nobody claims otherwise. But that mere factoid is not a barrier to evolution. At all. It doesn’t even hint or indicate any such thing. It’s not only a false dichotomy to put it like that, they’re not even mutually exclusive options. Both molecular AND evolutionary biology can be and IS true at the same time.
That just shows you didn’t even know what the hell this Op was even supposed to be about.
There is in fact no other way to create a nested hierarchy than by “Taxonomically Restricted Features”, though we tend to call them by another name, synapomorphies.
Common descent doesn’t explain the existence of the mammary gland or any other synapomorphy. That isn’t the sort of thing common descent explains. How many times do you have to be told that? Common descent explains the pattern, not the individual elements that make up the pattern. Common descent explains the distribution of characters, not their origins.
Common descent invokes natural mechanisms, but since they aren’t the mechanisms you think and aren’t the things to be explained you think, you don’t notice.
Convenient, eh? But still irrelevant to the subject you claim to be discussing.
Who ever said that? And of course we have good evidence of how mammary glands evolved. We even have intermediate conditions in monotremes. Still irrelevant to common descent vs. common design.
if there is? Turns out there isn’t.
It is certainly conceivable that there is an extremely deliberately deceptive intelligent designer that wants us to think life evolved, yes. But that can never amount to a scientific hypothesis, that’s just an insane ad-hoc rationalization you’re forced to bring up. Why the hell would anyone ever believe that a designer deliberately designed life to look like it evolved? It’s not like you just mentioning a mere in principle concievability somehow makes it rationally compelling to believe.
colewd,
I have no idea what that is supposed to show, other than mutations can be harmful. You still haven’t established a causal link between the cytochrome c isoform and the pattern of apoptosis in the organism. Till you do, there isn’t one. Apoptosis is not regulated at the level of cytochrome c binding. I can’t even see how the form of the organism could possibly be encoded in this way. Especially in a molecule that has a vital respiratory function, and can’t easily be retuned to do something unrelated as well.
Do you have any kind of evidence for that happening? Do you even have a clue what sort of evidence would exist for it?
Above all, why don’t other organisms lactate? It could be quite useful, but evolutionary mechanisms in eukaryotes don’t generally allow for transference of even simple traits across separate lines, let alone complex ones.
No, of course it doesn’t only “explain” with something as dumb as the design “explanation.” First off, the distribution of mammary glands specifically fits common design with its limitations alone. You have absolutely no explanation for why only mammals lactate.
You have no explanation for why humans develop many nipples, like our ancestors would be presumed to have, and then end up with only two nipples apiece. Usually.
Secondly, evolutionary theory opens up possibilities for research into the origin of mammary glands, with some reasonable possibilities. I haven’t really gone through the linked speech, as I have things I must get done before the end of tomorrow, but it’s absurd for you to repeat the old creationist BS that states that evolution just says “it evolved.” Wrong, that’s just projection of ID’s non-explanation.
Pretty sketchy on the details of Rodinia as well. Nonetheless, it is an important continent in explaining the past. I suppose I could just be a mythicist on the existence of Jesus, too, if I thought that sketchiness on reliable details ruined the usefulness of historic reconstruction, but I don’t go for such a pro-ignorance position.
No, it’s just an anthropomorphic assertion.
Then you can take your pick of whose made-up “causes” you want to believe in. Do we believe Hindu miracles, ancient Greek miracles, or sheer animism?
We have a mechanistic explanation, mammary glands likely evolved other skin glands. That’s the beauty of a real explanation, it can be researched. You certainly haven’t explained anything, nor have you bothered to understand evolutionary explanations.
No wonder it’s a creationist strawman.
Glen Davidson
stcordova,
What I still don’t get is why ‘common design’ looks like common descent. And, the less ‘common’ there is, the more ‘design’ there is. I realise I will never get answers to these – just a repeat of the naive question on introns you have taken to putting in every other post.
Of course! Who needs ID now? You were right to ditch Arrington!
Only better.
So convincing.
Glen Davidson
Hey Sal and Bill Cole, read this paper:
McKeown AN, Bridgham JT, Anderson DW, Murphy MN, Ortlund EA, Thornton JW.
Evolution of DNA specificity in a transcription factor family produced a new gene regulatory module.
Cell. 2014 Sep 25;159(1):58-68. doi: 10.1016/j.cell.2014.09.003
This is just the summary and introduction. Read the whole paper, it’s open access. No excuses. Then ask yourself this question: If the phylogenetic methods that you both reject and claim are just some similarity-based fantasy, are not actually correctly inferring historical events, why do they consistently manage to infer functional intermediate and ancestral molecules? How is that even possible if a phylogeny is just some tree with no relation to real historical events and entities?
Oh by the way, this study was funded in part by NIH grants. You know the NIH right sal?
The other oddity I notice – in a nutshell, common descent ‘explains the similarities’. The ritual challenge is ‘explain the differences!’. But, that’s not common descent’s job. If you have 90% similarity and (inevitably) 10% difference, the existence of the 10% does not make the 90% magically disappear. It’s still there, to be explained.
So, the ‘common designers’ are concentrating on the bit that’s not even ‘common’ – the 10%. They seem to be perennially missing the point.
Hear! Hear!
Rumraket,
I am not trying to extract a trend. I am showing how single mutations can be delirious to complex regulatory structures such as apoptosis. This is evidence against its evolvability by random change.
These are complex structures that are unlikely built by mutation at all. This is the hurdle from a single cell to multicellular organisms that bacterial experiments fall short as adequate supporting evidence.
colewd,
“Some mutations are bad therefore all mutations are bad” is up there with “why are there still monkeys?” in the list of Nonsense Creationist Arguments.
Allan Miller,
I think you need re look at this. It has shown a causal link between the cc isoform and the action of the apoptosis mechanism especially rate and initiation.
The God-guided mutations are the good ones. When God stops guiding, then you get he bad ones, like CF.
keiths:
Mung:
Tell us again why you are unable to read a series of comments and figure out what people mean by ‘common design’ in this context. It isn’t difficult.
Reading comprehension, Mung. You lack it.