Philosopher Michael L. Peterson explains junk DNA for us at BioLogos in “Evolution and the Deep Resonances between Science and Theology, Part 5” (July 20, 2011):
Evolution is the only rational way to account for the molecular uniformity of all organisms, given that numerous alternative structures and fundamental processes are, in principle, equally likely. Moreover, the accumulation of damaged or “junk” DNA (mutations that do not affect function and thus are not subject to negative selection), passed on over time to species further down that branch of the Tree, makes the probability that evolution did not occur infinitesimally small.
Okay, so that means that if much that is thought junk turns out not to be, “the probability that evolution did occur infinitesimally small.” Right?
This is breathtaking. Here at UD, we never said it didn’t happen, or not as a dogma anyway; Many of us are just sick and tired of all the thuggery and bullshot around protecting Darwinism and Christian Darwinism, and would like to see an honest game for once. But if the prof wants to stake all on junk DNA … (shrug) …
See Also: The trailer for the Myth of Junk DNA film:
And the Darwin faithful know in their hearts that it’s still junk.
15 Replies to “Junk DNA: At Biologos, some keep the faith – it’s junk and that proves evolution”
Pardon my frustration, and Lord forgive me for what might seem like an ad hominem response.
Have any of these clowns ever considered the probabilistic resources that would be required?
Apparently not, otherwise they wouldn’t propose such transparently stupid stuff.
I love this. You have one group of Darwinists saying “junk? what junk? Who called it junk? It’s not a failed prediction!”
And then you have the other group still calling it junk and still acting as though it is a fulfilled prediction of the theory.
I have to say, my frustration is probably comparable, but for the opposite reasons 🙂
Firstly, Peterson is absolutely right: it is because there appears to be large amounts of DNA that accumulates heritable changes without phenotypic effect that we can trace genetic phylogenies so well. We can do this with segments that do have phenotypic effects as well, of course, but because they are subject to natural selection, we have a biased sampling (indeed that is what natural selection is, effectively). With DNA that does nothing, we have a non-biased sampling of mutations giving a rich dataset with which to construct phylogenies, and these tend (with certain interestinge exceptions) to confirm a tree.
Not that common descent depends on a tree, but natural selection i.e. does to a great extent. HGT doesn’t contradict natural selection on its own, but horizontal transfer of genetic material with the same phenotypic effects in both sender and receiver would be, if it was observed at all frequently (that’s where Gil’s probabilistic resources would be relevant.
Which brings me to my second point, those probabilistic resources! No, we aren’t “clowns” (and no offence taken, and it’s not, strictly, an ad hominem anyway)!
I hear constantly, from Gil and kairosfocus in particular, stuff about the huge improbability of useful sequences coming about “by chance”.
Yup. That is hugely improbable. Which is why no-one claims it, and why those probability calcs are a complete straw man.
Richard Dawkins frequently points out, somewhat misleadingly, that mutations are random but natural selection is not.
It’s badly put, but it’s essentially true. Nobody is claiming that the patterns we see in DNA are random, anymore than the fact that the exquisite sorting of pebbles by size along the 18 miles of Chesil Beach is random.
Stochastic, yes, but the probability distribution is a) gaussian, not flat and b) the mean of that gaussian varies systematically from Portland Bill to Bridport.
“Natural Selection” is a sorting mechanism, brought about by the fact that living things a) reproduce and b) do so with heritable variability in their ability to thrive in the current environment.
Any calculation of the probability resources needed to account for the observed patterns needs to account for the contingencies that follow, given those two requisites. If either fail (if there is no reproduction, or if their is no heritable variability in the capacity to thrive in a given environment) then the observed patterns would indeed have to be explained either by Design, or Chance, and we could rule out Chance on the basis of insufficient probabilistic resources.
But given those two requisites, far from requiring vast probabilistic resources, complex organisms well adapted to function (i.e. to thrive) in their environment become virtually inevitable.
So the remaining questions are: Where did self-replication come from, in the first place, and given that it did, where does heritable variation in phenotypic success come from?
If I were an ID proponent, that’s where I’d be concentrating my energies, not on dismissing Darwinian evolution as impossible given the probabilistic resources available!
As Behe has done, for the second, of course.
And as Meyer has done, for the first.
Elizabeth (though she knows better) states:
‘because there appears to be large amounts of DNA that accumulates heritable changes without phenotypic effect that we can trace genetic phylogenies so well.’
yet the actual evidence states:
A New Model for Evolution: A Rhizome – May 2010
Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations.
Why Darwin was wrong about the (genetic) tree of life: – 21 January 2009
Excerpt: Syvanen recently compared 2000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts – also known as tunicates – are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren’t chordates. “Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another,” Syvanen says. .”We’ve just annihilated the tree of life. It’s not a tree any more, it’s a different topology entirely,” says Syvanen. “What would Darwin have made of that?”
I would like to point out that this, ‘annihilation’ of Darwin’s genetic tree of life, article came out on the very day that Dr. Hillis, a self-proclaimed ‘world leading expert’ on the genetic tree of life, testified before the Texas State Board Of Education that the genetic tree of life overwhelmingly confirmed gradual Darwinian evolution. One could almost argue it was ‘Intelligently Designed’ for him to exposed as a fraud on that particular day of his testimony instead of just any other day of the year.
Since evolutionists, like Elizabeth, continually misrepresent the true state of the evidence for molecular sequences, here are several more comments and articles, by leading experts, on the inconsistency of molecular sequences to Darwin’s theory:
Hillsong: “Lord Of Lords” Worship and Praise Song featuring Brooke Fraser (HQ)
With DNA that does nothing, we have a non-biased sampling of mutations giving a rich dataset with which to construct phylogenies, and these tend (with certain interestinge exceptions) to confirm a tree.
How does anyone know that any DNA does nothing?
Well, one way of finding out is to remove lots of it and see if you get any phenotypic effects.
Another is to look at lots of variants and see if there are any phenotypic effects.
Another is to look at how highly conserved certain sequences are.
Then you’re really only looking in a few places to see whether it does nothing. What if it does something under only very specific circumstances? What if it needs to be triggered?
It’s quite a leap from ‘we don’t know what it does’ to ‘it does nothing.’ That could be called an argument from ignorance.
Well, if it did something it wouldn’t be junk DNA, would it?
But you just did say that.
You just said that the reason you can construct phylogenies is because there are patterns in DNA that are not biased by natural selection.
Yet you apparently approve of Peterson, who himself writes:
Well, it would be if that was the argument. But the way you find out, in science, whether something has an effect (it’s the basis of the experimental method) is to change it and see what effects changing it has.
You can also do this observationally. And if something has high genetic variance in a population with little phenotypic variance attributable to it, then you can at least raise your priors that it doesn’t do much. And if you can see that it is related to some gene that does do something in some related species (synthesise Vitamin C for instance) and is highly conserved in those species, but, in a particular branch of the family does not do that something (that branch cannot synthesis vitamin C) and we can see that why (there’s an obvious glitch in the sequence) and then that broken sequence acquires mutations in a manner that matches the phylogenetic tree of the branch (because, unlike mutations in a functioning gene, they won’t be weeded out by selection) then we have nice evidence for natural selection as well as confirmatory evidence for the phylogeny.
Junk DNA Is Junk. What they try to do is find out how life works – how the data are distributed, what patterns there are in those data, what mechanisms might account for those patterns, what coding genes do, what non-coding genes do, what the acquistion of mutations in certain sequences might tell us about the lineage etc.
As for your suggestion of “triggering” – that’s problematic, because not only does Darwinian theory predict that mutations will tend to accumulate in non-functional sequences (providing that they are not costly, which seems to be the case) it’s hard to see why this would not happen whether ID is true or not.
How would the sequences that are inert while not “triggered” be protected from accumulated mutations?
However, if you could come up with a mechanism, then your idea would predict highly conserved sequences, found across lineages, but with no known function.
You might be interested in this paper:
Mung, you really aren’t trying.
Seems like the geneticist is playing the part of a cryptanalyst in all these scenarios. Partly, they are looking for pattern and repetition in the genome, am I right? You identify a pattern and it indicates that there is something interesting lurking in the genome. Now, to identify a pattern is one thing, but to decipher its meaning is a whole other thing. I am not a geneticist, but these are the sorts of questions that I think about when I consider a strand of DNA are these: (feel free to answer them if you know the answers!)
1)Can a pattern be identified?
2)How many times does it repeat?
3)Is a pattern dependent upon another pattern?
4)Is the order of repetition significant?
5)Is the order of pattern occurrence significant?
But the way you find out, in science, whether something has an effect (it’s the basis of the experimental method) is to change it and see what effects changing it has.
There’s this pink soapy stuff in the engine compartment of my car. I threw it away, and the car still starts and drives like before. The gas mileage is unchanged. I guess it was junk attached to my car.
That’s the faulty reasoning that occurs when I start up front assuming that everything attached to my car relates directly to driving.
You don’t know whether certain DNA has a function or not. You know of certain functions DNA can have, and assume that it has one of those functions or none. That’s a huge assumption. Is biology such a closed book that we can say there’s nothing going on in cells or organisms that we don’t know about yet?
I’m curious to know what the author’s basis is for concluding “that numerous alternative structures and fundamental processes are, in principle, equally likely.” What principle is he referring to? What data can be brought to bear to determine the liklihood of what he’s talking about?
Bridges and buildings conform to uniform engineering principles; aircraft conform to uniform principles of aerodynamics; and yes, organisms to uniform molecular structures and fundamental processes, according to the author. What’s so unreasonable—in principle—about at least considering the possibility that such homogeneity points to uniformity of design—especially when the person making the argument (a biologos commentator) is a professing xian theist?
I note Elizabeth tried to use the vitamin C argument, yet Jonathan Wells refutes the vitamin C argument here:
Vitamin C pseudogene refutation By Jonathan Wells – from appendix of ‘The Myth Of Junk DNA’ pages 109-114 by Jonathan Wells