Dr. Stephen Meyer and Dr. Douglas Axe were recently interviewed by author and radio host Frank Turek on the significance of November’s Royal Society Meeting on evolution, in London. The two Intelligent Design advocates discussed what they see as the top five problems for evolutionary theory:
(i) gaps in the fossil record (in particular, the Cambrian explosion);
(ii) the lack of a naturalistic explanation for the origin of biological information;
(iii) the necessity of early mutations during embryonic development (which are invariably either defective or lethal) in order to generate new animal body types;
(iv) the existence of non-DNA epigenetic information controlling development (which means that you can’t evolve new animal body plans simply by mutating DNA); and
(v) the universal design intuition that we all share: functional coherence makes accidental invention fantastically improbable and hence physically impossible.
In today’s post, I’d like to focus on the third argument, which I consider to be the best of the bunch. The others are far less compelling.
Over at the Sandwalk blog, Professor Larry Moran and his readers have done a pretty good job of rebutting most of these arguments, in their comments on Professor Moran’s recent post, The dynamic duo tell us about five problems with evolution (January 14, 2017). Larry Moran’s earlier 2015 post, Molecular evidence supports the evolution of the major animal phyla cites a paper by Mario dos Reis et al. in Current Biology (Volume 25, Issue 22, p2939–2950, 16 November 2015) titled, “Uncertainty in the Timing of Origin of Animals and the Limits of Precision in Molecular Timescales,” which convincingly rebuts Meyer and Axe’s first argument, by showing that animals probably originated in the Cryogenian period (720 to 635 million years ago) and diversified into various phyla during the Ediacaran period (635 to 542 million years ago), before the Cambrian. I might add that we now have strong evidence that anatomical and genetic evolution occurred five times faster during the early Cambrian, at least for arthropods – although as Intelligent Design advocates have pointed out, that still leaves unanswered the question of how animal body plans arose in the first place.
Meyer and Axe’s second argument asserts that natural processes are incapable (as far as we can tell) of creating significant quantities of biological information – and especially, new functions or new anatomical features. Much of the argument rests on the alleged rarity of functional proteins in amino acid sequence space – a claim that was crushingly refuted in Rumraket’s recent post on The Skeptical Zone titled, Axe, EN&W and protein sequence space (again, again, again) (October 12, 2016). As for the claim that natural processes can’t create new functions, it’s simply bogus. The following three papers should be sufficient to demonstrate its empirical falsity: Five classic examples of gene evolution by Michael Page (New Scientist Daily News, March 24, 2009), Evolution of colour vision in vertebrates by James K. Bowmaker (Eye (1998) 12, 541-547), and Adaptive evolution of complex innovations through stepwise metabolic niche expansion by Balazs Szappanos et al (Nature Communications 7, article number 11607 (2016), doi:10.1038/ncomms11607).
I’m not really qualified to discuss Meyer and Axe’s fourth argument, but it seems to me that Professor Larry Moran has addressed it more than adequately in his recent post, What the Heck is Epigenetics? (Sandwalk, January 7, 2017). The last four paragraphs are worth quoting (emphases mine):
The Dean and Maggert definition [of epigenetics] focuses attention on modification of DNA (e.g. methylation) and modification of histones (chromatin) that are passed from one cell to two daughter cells. That’s where the action is in terms of the debate over the importance of epigenetics.
Methylation is trivial. Following semi-conservative DNA replication the new DNA strand will be hemi-methylated because the old strand will still have a methyl group but the newly synthesized strand will not. Hemi-methylated sites are the substrates for methylases so the site will be rapidly converted to a fully methylated site. This phenomenon was fully characterized almost 40 years ago [Restriction, Modification, and Epigenetics]. There’s no mystery about the inheritance of DNA modifications and no threat to evolutionary theory.
Histone modifications are never inherited through sperm because the chromatin is restructured during spermatogenesis. Modifications that are present in the oocyte can be passed down to the egg cell because some of the histones remain bound to DNA and pass from cell to cell during mitosis/meiosis. The only difference between this and inheritance of lac repressors is that the histones remain bound to the DNA at specific sites while the repressor molecules are released during DNA replication and re-bind to the lac operator in the daughter cells [Repression of the lac Operon].
Some people think this overthrows modern evolutionary theory.
So much for epigenetics, then.
The fifth and final argument discussed by Drs. Meyer and Axe relates to the universal design intuition. I’ve already amply covered both the merits and the mathematical and scientific flaws in Dr. Axe’s book, Undeniable, in my comprehensive review, so I won’t repeat myself here.
The “early embryo” argument, helpfully summarized by Dr. Paul Nelson
That leaves us with the third argument. Looking through the comments on Professor Moran’s latest post, it seems that very few readers bothered to address this argument. The only notable exception was lutesuite, who pointed out that examples of non-lethal mutation in regulatory DNA sequences are discussed in a paper titled, Functional analysis of eve stripe 2 enhancer evolution in Drosophila: rules governing conservation and change by M.Z. Ludwig et al. (Development 1998 125: 949-958). The paper looks interesting, but it’s clearly written for a specialist audience, and I don’t feel qualified to comment on it.
As it turns out, I wrote about the “early embryo” argument in a 2012 post, when it was being put forward by Dr. Paul Nelson. Nelson handily summarized the argument in a comment he made over at Professor Jerry Coyne’s Website, Why Evolution Is True:
Mutations that disrupt body plan formation are inevitably deleterious. (There’s only one class of exceptions; see below.) This is the main signal emerging from over 100 years of mutagenesis in Drosophila.
Text from one of my Saddleback slides:
1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
Obviously, loss of function is incapable of explaining the origin of new, viable body plans for animals.
A hole in the argument?
On the face of it, Nelson’s three-step argument certainly looks like a knock-down argument, assuming that the premises are factually true. But are they? A commenter named Born Right made the following response to Dr. Nelson over at Jerry Coyne’s Website (emphases mine):
Paul Nelson,
Lethal mutations will kill the embryo. But what you’re totally failing to understand is that not all mutations are lethal. Many are tolerated. I heard you cite the example of HOX gene mutations in flies and how altering them kills the embryos. You didn’t mention the entire story there. Do you know that there are wild populations of flies having HOX gene mutations? Even in the lab, you can create viable HOX-mutant flies that have, for example, two sets of wings. In fact, simple non-lethal mutations in HOX genes can profoundly alter the morphology. It is these non-lethal mutations that natural selection “cherry picks”, provided they confer a survival advantage on the organism.
Many mutations actually arise as recessive mutations, not as dominant ones. They spread through the population remaining dormant or having a mild effect, until there is a sufficient number of heterozygotes. Then, interbreeding between heterozygotes will cause homozygous mutations to arise suddenly throughout the population. If the new feature improves survival & reproductive success, it gets rapidly selected…
Macroevolution is a gradual response to climate change and other environmental pressures. Organisms accumulate non-lethal mutations that changes their body plan bit by bit until they are well adapted to their changing habitat.
However, a 2010 Evolution News and Views post co-authored by Dr. Paul Nelson, Dr. Stephen Meyer, Dr. Rick Sternberg and Dr. Jonathan Wells, contests the claim that Hox gene mutations are non-lethal. The authors assert that such mutations are, at the very least, defective:
Mutations to “genetic switches” involved in body plan formation … disrupt the normal development of animals. With the possible exception of the loss of structures (not a promising avenue for novelty-building evolution, in any case), these mutations either destroy the embryo in which they occur or render it gravely unfit as an adult. What the mutations do not provide are “many different variations in body plans.”…
… [T]here are solid empirical grounds for arguing that changes in DNA alone cannot produce new organs or body plans. A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12
None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
Indeed, the evidence justifies only one conclusion, which Wells summarized in his last slide at SMU:
“We can modify the DNA of a fruit fly embryo in any way we want, and there are only three possible outcomes:
A normal fruit fly;
A defective fruit fly; or
A dead fruit fly.”
The Wikipedia article on Drosophila embryogenesis may interest some readers.
What I would like to know is: are the Hox mutations in fruitflies mentioned by Born Right in his comment above neutral or deleterious – and if the latter, are they only slightly deleterious or highly deleterious?
A follow-up comment by Born Right
In a subsequent comment over at Why Evolution Is True, Born Right cited two scientific references in support of his claims:
Paul Nelson,
Fantastic new research shows how fish developed limbs and moved onto land. Boosting the expression of Hoxd13a gene in zebrafish transforms their fins into limb-like structures that develop more cartilage tissue and less fin tissue!
http://www.sciencedaily.com/releases/2012/12/121210124521.htm
http://www.sciencedirect.com/science/article/pii/S1534580712004789
Importantly, the overexpression of Hoxd13a in zebrafish was driven by a mouse-specific enhancer. This shows that the regulatory elements acting on the enhancer are present in both fishes and distantly-related mammals!
The first paper, titled, From fish to human: Research reveals how fins became legs (Science Daily, December 10, 2012) is written in a style that laypeople can readily understand. I’ll quote a brief excerpt (emphases mine):
In order to understand how fins may have evolved into limbs, researchers led by Dr. Gómez-Skarmeta and his colleague Dr. Fernando Casares at the same institute introduced extra Hoxd13, a gene known to play a role in distinguishing body parts, at the tip of a zebrafish embryo’s fin. Surprisingly, this led to the generation of new cartilage tissue and the reduction of fin tissue — changes that strikingly recapitulate key aspects of land-animal limb development. The researchers wondered whether novel Hoxd13 control elements may have increased Hoxd13 gene expression in the past to cause similar effects during limb evolution. They turned to a DNA control element that is known to regulate the activation of Hoxd13 in mouse embryonic limbs and that is absent in fish.
“We found that in the zebrafish, the mouse Hoxd13 control element was capable of driving gene expression in the distal fin rudiment. This result indicates that molecular machinery capable of activating this control element was also present in the last common ancestor of finned and legged animals and is proven by its remnants in zebrafish,” says Dr. Casares.
This sounds fascinating, and to me it constitutes powerful evidence for common ancestry, but the real question we need to address is; exactly how early in the course of the zebrafish’s embryonic development did these mutations take effect?
The second paper cited by Born Right (“Hoxd13 Contribution to the Evolution of Vertebrate Appendages” by Renata Freitas et al. in Developmental Cell, Volume 23, Issue 6, pp. 1219–1229, 11 December 2012) is much meatier, because it’s the original papaer on which the Science Daily report was based. The authors contend that “modulation of 5′ Hoxd transcription, through the addition of novel enhancer elements to its regulatory machinery, was a key evolutionary mechanism for the distal elaboration of vertebrate appendages,” and they conclude:
Within the developmental constraints imposed by a highly derived teleost fin, our results suggest that modulation of Hoxd13 results in downstream developmental changes expected to have happened during fin evolution. This, together with the evidence we provide that the upstream regulators of CsC were also present prior to tetrapod radiation, makes us favor an evolutionary scenario in which gain of extra 5′ Hoxd enhancers might have allowed the developmental changes necessary for the elaboration of distal bones in fishes that evolved, ultimately, into the tetrapod hand.
This sounds a lot more promising, but after having a look at it, I’m still rather unclear about exactly how early these hypothesized mutations would have had to have occurred, in the course of vertebrate embryonic development. Perhaps some reader can enlighten me.
Well, that’s about as far as my digging and delving has taken me. I’d like to throw the discussion open at this point. Are there any known examples of early embryonic mutations which are not deleterious, and do they shed any light on how new animal body plans might have evolved? Over to you.
(Note: the image at the top [courtesy of Wikipedia] shows the ventral view of repeating denticle bands on the cuticle of a 22-hour-old Drosophila embryo. The head is on the left.)
You don’t have any evidence for common design, nor any entailed prediction of it.
It’s just a dimwitted excuse creationists use to avoid dealing with the evidence for common descent.
Glen Davidson
Larry argues that microRNAs are functional? Good for him. But why are they functional? They regulate genes.
But what is one of the ways microRNAs regulate genes? Through pseudogenes! Yay! Larry may have to revise his 10% figure of junkDNA and add pseudogenes to his tally of functional.
Supporting my claim the pseudogenes regulate real genes through microRNAs:
From the prestigious scientific journal Nature
http://www.nature.com/nrg/journal/v11/n8/full/nrg2835.html
You see, the authors at the prestigious scientific journal can revise their views on pseudogenes (that was 2010), so why can’t Larry?
Will you be supporting this conclusion formally?
Presumably they should accept your conclusion of common design for the reasons just quoted?
Here is an excellent article on insulators? You know, “insulators”, a term which Larry was not familiar with, but was quick to write off. 🙂
http://www.sciencedirect.com/science/article/pii/S0959437X11001894
I think it’s time you moved on from your Dan Graur-obsession.
Do you know everything then?
I belive Larry agrees the siRNAs are functional. He better since Nobel Prizes were awarded for their discovery.
Here is a description:
https://en.wikipedia.org/wiki/Small_interfering_RNA
But where do siRNAs come from? Well some come from (TADA) pseudogenes!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981145/
Also some miRNAs come from pseudogenes:
https://academic.oup.com/jhered/article/97/2/186/2187653/Primate-MicroRNAs-miR-220-and-miR-492-Lie-within
From the prestigious scientific journal Nature: A thousand empirical adaptive landscapes and their navigability
Oh look, the prestigious journal nature published a prestigious publication by esteemed gentlemen, scholars and professional research-scientists working at prestigious scientific institutions, that concludes transcription factors and their binding sites are the result of the evolutionary process.
Seriously Sal, this level of used-car-salesmanism and specious cherrypicking of publications you like because you can misconstrue them to fit your preconceptions, complete with fake appraisal of the particular journal, is truly pathetic.
Some, a subset? Oh no! So they found one that had a function. Shieeeeeet.
multiple non-linear feedback control regulatory? As opposed to multiple non-linear feedback control only?
You forgot to say they biocybernetically info-regulate and with multi-level switching-controlled crossdimensional 3D regulation, on-site, real-time. Delivery within 24hrs.
Do anyone even buy this bullshit he’s spamming? Who’s actually impressed by this galloping technobabble?
stcordova,
How could you distinguish the same pseudogenes appearing separately in two lineages from both inheriting them from a common ancestor?
If you freaking studied classical systems and control theory (as you might have if you studied electrical engineering), you might actually understand the significance and the interdisciplinary application of control theory to miRNA regulatory networks.
Gene networks to first approximation are likened to single input single output linear systems as evidenced by this:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940894/
But that was a linear simplification of feed back loops which avoided the problems of non-linear feedback loops.
But the better picture is this that actually deals with multiple non-linear feedback miRNA regulatory circuits!
Oh, I guess Rumraket, you’re just not up-to-date on the latest stuff.
Look at the diagram below. You should recognize P53 right? You know, that protein involved in cell-cycle checkpoints?
An FBL is a feed-back loop. The relationship of the output fed back to the input of the control circuit is defined by differential equations with non-linear solutions. This feed back loop shows how the protein P53 is feedback regulated by the microRNA miR-34.
But this is a single-feed back loop system. The paper shows multi-feed back loop systems, and they are non-linear as well.
Hence my description is not babble as you assert. If you actually knew what you were presuming to talk about, you might not have bloviated what you just did. Let the readers look at the actual paper!
https://academic.oup.com/nar/article/44/13/6019/2457646/Understanding-microRNA-mediated-gene-regulatory
Rumraket,
Everyone on his ‘side’, I guess …
Sal, you are doing the same thing the you condemned Patrick for doing. He has said he did not accuse your father of child abuse.
Go ahead and show your spin of the events are true, I would be interested.
What you don’t like that I’m pounding most every class of RNA that Larry declared as junk?
The only one I really have problems with is ERVs. He wins the day on ERVs, so far.
Charlie M, being involved in missile guidance engineering might actually recognized the terms and feedback loops from electrical engineering.
stcordova,
What percentage of junk have you reclassified, then?
Of course. Don’t ask a biologist, ask an engineer. Better yet one who thinks there is a mysterious undetectable ‘field’ surrounding biological molecules as a way out of the wholly imaginary ‘DNA problem’.
What doesn’t, so long as it’s anti-evolution?
Glen Davidson
Then it is strange that we have produced both.
And again, how how you defining common descent? Human family trees are an example of common descent. But that doesn’t support the claim that chimps and humans share a common ancestor
The target audience for his upcoming book. I expect a lot of what he posts here to make it in. Hopefully he’ll learn the hard way that if there were any more money left to make, Dembski would still be writing ID books.
GlenDavidson,
It is indeed a big tent. The YEC may lay down with the New Age Chopraite. All Is One. Potential is the driver of curiosity. This life is nothing short of a condensing quantum shift of cosmic complexity. Consciousness consists of electromagnetic resonance of quantum energy. “Quantum” means a blossoming of the unlimited.
Refute that!
Hey, great question! If I can beg your assistance, do you have a link to Larry’s infamous tally’s of functional and non functional? I had a hard time googling the one you used (it was pretty good).
We can visit the list line by line.
Thanks in advance.
http://sandwalk.blogspot.com.es/2011/05/whats-in-your-genome.html
stcordova,
I don’t recall ever having discussed that with you, but try this:
http://sandwalk.blogspot.co.uk/2008/02/theme-genomes-junk-dna.html
But, you are aware that finding a function for a member of a class does not give that function to the entire class, I hope?
I didn’t accuse his father of child abuse for raising him in the Catholic church, as Sal claimed.
What Sal is upset about is some flaming armchair psychoanalysis I perpetrated on him in Noyau some time ago, speculating about the root causes of his mommy and daddy issues. It was venting on my part after reading too much of his nonsense.
The conclusion that his admitted behavior “teaching” kids constitutes child abuse is separate and much more serious than that.
Of course not, I’m merely pointing out Larry is premature and totally unhelpful. The working hypothesis however is that most of it is functional, and that’s good enough for most researchers.
Thanks for the link. Maybe it was Petrushka who gave the list.
L1’s are recently indicated to create genomic diversity in somatic (not germline) cells for the Brain giving each nerve cell a unique genome and transcriptome. Research is early, but that’s good enough to say Larry is premature to write them off and is not being very helpful to researcher who actually research L1 that have interest in treating neuro degenerative disease. So that 16% right there.
Press release only a few months ago:
So I’m merely showing Larry is jumping the gun and not helping research into an important area.
Next are SINES. The most prominent SINE is the Alu SINE which is about 10-11% of the genome.
I posted at length on the Alu here, and Larry had some responses, but the good stuff is toward the end of the discussion:
So I wanted to cast reasonable doubt that one can’t unequivocally assert L1s and Alus are non functional. Adding this change:
L1s + Alus = 11% + 16% = 27%
The rest of the discussion so far is on the smaller stuff like insulators, lncRNAs, pseudogenes.
I think you are depending on that tendency ,Sal.
On one side it seems the inefficency of junk DNA is evidence against your unknown position considering how hard as you objecting to it but then you seem to think the inefficiency of Rube Goldberg mechanisms is support for it.
So far the best explanation is that this has nothing to do with creationism at all. It is all about the competition. Showing who is smarter
I fail to see how the science you have presented so far could convince anyone, its value seems to be to reinforce an existing belief with sciencey pictures.
stcordova,
You’ve just imported the entirety of a class to ‘functional’ based on a few instances. It doesn’t work like that, as I said.
Take Alu. Some of these things are still actively transposing. They provide the basis of genealogical tests. That does not speak strongly of global function – the idea that wherever you find an Alu, you have found a functional Alu.
If an Alu copy ends up in a gene or promoter, that is at best a function for that Alu copy. If an Alu has lost even the ability to transpose, it can’t even do that – end up in a gene.
Sal’s strategy consists in finding some instance of function to then affirm that the null hypothesis must be function, because showing something in particular has no function is a lot harder.
He can’t do that without ignoring the positive evidence, of course.
In addition to spliced out introns, there are intron lncRNAs and Alus create circular dsRNAs that include introns. Given we’re just beginning to research Alu functionality, it is way too premature to say introns have no function. What Larry said of introns “littered with defective transposable elements ” is not unequivocal given the Alus are mirror-image paired and are the delimiting points from which dsRNA with intron sequences are made. These dsRNA are involved in inducing alternative splicing. Larry is way premature to write these off.
What to do with that 30% figure? Say he’s premature. Right now all he has is his interpretation of evolutionary theory and incredulity, not actually lab experiments demonstrating unequivocal non-function (if such a thing is even possible).
Now regarding intronic lncRNAs (not to be confused with lincRNAs!), I know a researcher at NIH who studies the circular intronic RNAs in relation to aging. But anyway:
http://www.sciencedirect.com/science/article/pii/S109727651300590X
One should go back to the exchanges between Sterngerg, Wells, and Meyer against Moran, Matheson and Hunt. Matheson’s criteria for non-function of introns was that introns didn’t leave the nucleus. I wanted to say, “duh, that suggests they have function in the nucleus, you just don’t know what it is yet!”
Now we have a better idea, but we won’t have a clearer picture if we just keep writing it off as junk and then not studying them. So take some of that 30% that Larry wrote off as junk and add it to the tally.
L1s: 16%
Alus: 11%
Introns: 30,20,10% whatever
That’s a lot of active research in real labs that Larry is writing off.
But this is the real thing that grabs my attention, a paper co-authored by Francis Collins, the director of the NIH himself says 88% of SNP indicated in disease are from non-coding regions. Correlation doesn’t imply causation, but it would be negligent not to notice and consider the possibilities.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687147/
43% + 45% = 88%
!!!!!
So that basically flips Larry’s figures around to over 88% potential function (including the coding regions).
You’ll complain that’s not proof. That’s not my point. It would be irresponsible for medical researchers to write off research of 88% of the genome because Larry (or Graur or any other nay-saying evolutionary biologist) says it’s junk, especially in light of this study by Collins and so much other data.
We can see that by applying the working assumption 100% could be functional, progress has been made in finding function. The noise coming from the junk DNA advocates is not contributing at all to scientific understanding, it’s a hindrance.
My goal is to provide credible evidence that we can’t unequivocally write all this off as junk. It is way too early.
And please, don’t confuse my position with other IDists or the Discovery Institute that say junkDNA has to be functional because ID theory predicted it.
That was never a prediction of ID, imho. Both I and Michael Behe don’t agree with the Discovery Institute’s position as articulated by my friend Casey Luskin that this was a prediction of ID theory. It was not, it was a prediction by some IDists, but it doesn’t proceed from ID theory. And I don’t agree with this prediction. We simply don’t know.
The point is to show that the enemy is wrong. Never mind that the enemy never said that every last Alu or what-not is nonfunctional, the literalism common among creationists/IDists can readily lead them to assume that they did.
Now, show that the enemy is wrong, therefore unworthy of consideration.
It’s warfare with the devil, nothing to do with learning what actually is going on. None of the creationist/IDist regulars has shown any interest in finding out what’s going on, rather than fighting the devil.
Glen Davidson
I didn’t insist it did, it opened the possibility. You’re not accurately representing the point I’m making.
No, it doesn’t, and if I understand the argument you’re without excuse.
So for the emptieth time, until you address the positive arguments for 90% junk, you don’t get to claim that the null hypothesis is function for the rest of L1’s, and there’s no reason to doubt the vast majority of them are junk
I believe you. The Catholic Church’s guilt in that area is does not stem from teaching children about Hell.
It seems Sal appreciates its value as a distraction.
Right,it belonged in Noyau as well. At the minimum you should have been clearer about the nature and relevance of the abuse.
If Sal explanation is correct( I vaguely recall Sal saying something different which became the genesis of the charge) using child abuse in that context diminishes by overuse the abhorrent nature of the action. In my opinion.
By pounding you mean committing the fallacy of hasty generalization in like every imaginable way?
A piece of RNA has been found to be functional does not entail, it doesn’t even indicate, that all RNA is functional. Can you say “it doesn’t follow”?
“If all RNAs were functional, they could function in this way that this particular one does”, is not proof that all RNAs are functional.
Basically all the papers you keep quoting are of that type: They find some particular stretch of RNA (or another molecule or structure) and elucidate some biochemical activity that goes on. Then they speculate that’s how all functional RNAs(or whatever it is) of that type might function.
That’s it. That’s what they all do. Yet you cite these papers as if they constitute evidence that all RNAs of that type is functional. Finding a functional RNA, and then suggesting other RNAs of that type might also function like that, isn’t evidence that they do all function like that.
It doesn’t follow. Can you say it? Do you understand it? Logic?
It is really just a completely hypothetical suggestion.
It’s one of those dreaded just-so stories I’ve heard you all hate so much. Except, of course, if it’s a just-so story you can fit into your pre-conceived notions. Then you’re basically presenting it as if it was an unassailable fact and anyone who dares suggest the conclusion you seek is premature and unwarranted… well, they’re stifling research, it’s dangerous, they’re nay-sayers, evolutionary biologists as opposed to those hard-working research scientists, they’re behind the times bla bla bla que an endless stream of substance-less rhetoric, brainless declarations of faith in some particular christian denomination, testimonials of how sad your obviously fake but former atheistic life made you, how “mind boggling” biochemistry is, and lots and lots of pretty graphs with fancy technical abbreviations and jargon.
No amount of fancy-sounding technical jargon haphazardly sprinkled with metaphors about Rube Goldberg machines, schematics of chromatin-mediated DNA methylations and obsessive name-dropping of famous and “prestigious”* institutions and journals (including the NIH and how much funding they get), is going to magically convert RNA predicted to be mostly junk, of which there’s no doubt still fragments that isn’t, become entirely RNA that is functional. Not even close.
Seriously, you wrote “prestigious” about the journal nature. A publisher the majority of the output of which you’d reject (and basically perpetually ignore) because it conflicts with your young Earth creationism.
Text and subtext.
No, he’s not. That’s basically his whole problem. Sal loves himself a nice fat just-so story though. If an author of a paper that elucidates a function for some intronic sequence, or an alternatively spliced protein, or an ORFan, or a lncRNA or what have you, suggests in the discussion part of the paper that other such molecules might also function in that way, Sal’s right there having bought into it with warm abiding, lubricated faith. Drooling and puppy-eyed.
Particularly if it’s been published in the “prestigious” scientific journal nature, by an esteemed laboratory researcher working at Harvard or Cold Spring Harbor, and funded by the NIH, (who, by the way, has a lot more money than Dan Graur). Also, Rube Goldberg machines! And did you see this diagram? It’s mind-boggling.
LOL. He’s the director of the NIH himself. Fuck me, what are we to do?
Sal, you know that mutations (that’s what single-nucleotide polymorphisms are) can cause junk DNA to become active, right? The fact that it can cause disease isn’t evidence for or against junk. At all. Again, it doesn’t follow.
And you know that we already know non-coding DNA isn’t thought to be junk-DNA and never was, just becaust it is non-coding, right? I know you know this, because you’ve been told.
But you get that nobody actually does this, right? There isn’t actually anyone who advocates that we stop trying to find out exactly which pieces of the genome are functional and what they actually do, right?
This is a strawman you are working day and night to keep standing.
Please cite a single fucking example of a researcher deciding not to do research because he was hindered by junk-DNA advocates.
That’s not my position, you aren’t representing it accurately. Larry’s being premature. Pointing to examples of function should be helpful in showing he’s premature.
I didn’t say, “all RNAs are functional”. Show me where I said that verbatim? You can’t because I never said it. You’re attributing a statement to me I didn’t make.
What’s the matter, you can’t contest the arguments I’m actually making so you contest arguments I didn’t make? That’s kind of comical.
Here we go again! LMFAO, No one could make this shit up
You aren’t making any actual arguments. You’re 100% weaselly insinuation and handwaving. Even God could not extract a quantifiable prediction from you.
Your whole “case” amounts to trying to manufacture a controversy between evolutionary biology and functional genomics, without ever being explicit or bold enough to dare make any testable claims. Which is of course the whole point, to construct this false picture that evolutionary theory is somehow a hinderance to science.
On the one hand you’re all too happy to leave your gullible sycophants with the impression that pretty much the entire genome, perfectly designed by God (Halleluja!), has subsequently deteriorated a little bit since “the fall”.
Not that you’ve ever put any numbers on it. But evolutionary theory, and inter-species genome-size comparisons, together with knowing the actual gene-contents and sequences of the genome, strongly indicate it’s mostly junk.
But the evolution-part of it, that’s what really bugs you. So whatever fraction it is evolution predicts is junk, is wrong. You don’t know how wrong, but if evolution predicts it, it’s wrong. You’re quite sure of that. So you’ve of course covered your ass by just vaguely handwaving in the direction of “of course there’s going to be some junk, it happened after the fall”, you haven’t put any numbers on it. And rather than test your own “prediction” (haha, as if you had made any), you’re much more interested in trying to find ways to insinuate that the theoretical prediction from genetic load is wrong. And a hinderance to science. Those nasty evolutionary biologists prevented medical researchers from curing grand-ma.
I’m going to take a wiiiiiiiiiiild stab in the dark and guess you’ve spend exactly no time at all correcting fellow creationists and ID-proponents who’ve suggested the genome is entirely functional. Or if one of your sycophant cohorts took your words and cherrypicked quotes from hypothetical suggestions in the discussions of papers, to imply the entire genome was shown to be functional, or that all lncRNA, or intronic sequence, or whatever, is functional, then.. well who has the time to correct that totally accidental misapprehension you unintentionally through no fault of your own, left them with?
No no, you’re all about having a correct understanding of what the data shows. We shouldn’t jump to conclusions. Nooooo (C14 in coal? Young Earth!). Oh did I tell you about this new study where someone who is a director at some prestigious institute with lots of funding indicated function for L1’s in brains? They could all be functional!
But not the entire genome of course, now that you ask. I forgot to say, of course not the entire genome. But thank you so much for bringing it up. You’ve taught me so much. Some of it deteriorated after the fall. How much? Oh well you see I have no idea, it’s just a different fraction than what the genetic load-calculation predicts. I’m pretty sure of that.
As we all know, Larry Moran has repeatedly claimed that all non-coding DNA is junk, as are all SINEs, LINEs, pseudogenes, lncRNAs, lincRNAs, and every part of every intron. Ask Sal. He will gladly quote the places where Larry has said all these things. Right, Sal?
Oh but you see John, of course Sal never said explicitly, that Larry said, that all lncRNA, lincRNA, all SINEs, LINEs and pseudogenes are junk. So why would you ever think that?
How oh how did we ever get that impression?
Your projection is duly noted. IDists know what is going on and that is why ID exists.
So here comes J-mac, who clearly got the point Sal never tried to make:
And here we have Sal, working hard to disabuse J-mac of his mistaken and not at all intended impression:
R O F L
So does everyone agree with:
How about without the (which are invariably either defective or lethal)?