Pseudogenes, Intelligent Design, and Kitzmiller - Part 2

(system) #1
As we saw in yesterday’s post, the 2005 Kitzmiller case was a watershed for the ID movement. Central to the case was demonstrating to Judge Jones that evolution, in contrast to ID, was a productive scientific theory.
This is a companion discussion topic for the original entry at

(Dcscccc) #2

hey prof venema. the main argument is that share mutations between pseudogenes is evidence for a commondescent. this claim is actually falsified by the fact that we can find share mutations without a commondescent. one example is the prestin protein. some dolphin and bat species share in this protein 14 amino acid without a commondescent (another example may include even 29 amino acid) . so this fact alone refute any argument for a share mutations as evidence for a commondescent. even more-its also disprove the phylogeny of this specific group because according to the prestin phylogeny some bats are colser to some dolphins then those bats to other bats!

yours sincerely

(Dennis Venema) #3

Hi dcscccc,

You’ve made a very similar comment before, and there was a number of replies made to it - did you read the materials suggested to you in that thread?

(Dcscccc) #4

hey again dennis. your main claim is that a shared muations in pseudogenes are evidence for a commondescent. so i simply showed that its possible without a commondescent- and therefore a shared muations in pseudogenes cant be evidence for a commondescent more then an evidence for a commondesigner.

sure. i also make a simple calculation that make this point valid (again the chance to get 14 shared mutations in a sequence space of 20^14 compare to 12 mutations in a sequence space of 4^12).

(Nuno) #5


Excellent reasoning and very clear and succint presentation of the facts. I can only hope you will find the time to address their other top claims on biological “evidence”. Thank you for your consistently valuable contributions.

(Patrick ) #6

Your calculations are bogus. These mutations happened so they have a probability of 1 of occurring.
You would really benefit from a study of Bayesian Probabilities. For example, what is the probability of a certain mutation occurring given all these other HAVE already occurred. You will find that your numbers come down considerably.

Here is a simple example: What is the probability that a couple will have eight sons in eight pregnancies? 0.5^8 or 1 chance in 512

What is the probability that a couple will have eight sons given that they already have seven sons? 0.5

The second example is Bayesian probability. That’s what you should be looking at when you discuss mutations. Given all the other mutations have already occurred, what is the probability of the mutation that you are interested in.


Great series, @DennisVenema!

(Patrick ) #8

Yes, Dennis excellent. Also did you see my posting of the Ancient Irish DNA? The migration of Europe over the past 30,000 years is getting rapidly filled in detail. It is amazing how much process in genome sequencing technology has made in the past five years!

(Dennis Venema) #9

Thank you!

(Richard Wright) #10

Continue to love your stuff Dennis.

(Philip Cunningham) #11

Should not the ‘bottom up’ genetic reductionism model be shown to be true before you presuppose that genetic similarity proves common ancestry as true? Moreover, Is it not the differences that need an explanation not the similarities? To approach the topic as you have done is to presuppose your preferred conclusion of common ancestry into your argument.
I listened to a lecture by Dr. Sternberg on the subject and it turns out that the higher level regulatory regions, which are far more resistant to change than the protein coding regions are, are far more different than the protein coding regions are. It is the second lecture in this series if you are interested:

Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? part 1
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 2 (Major Differences in higher level chromosome spatial organization between even supposedly closely related species)
Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? Part 3

Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 4
In the following podcast, Dr. Sternberg’s emphasis is on ENCODE research, and how that research overturned the ‘central’ importance of the gene as a unit of inheritance. As well he reflects on how that loss of the term ‘gene’ as an accurate description in biology completely undermines the modern synthesis, (i.e. central dogma), of neo-Darwinism as a rational explanation for biology.
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 5

(Dcscccc) #12

not at all. they base on fact and not an assumption (14 amino acid have a sequence space of 20^14- its a fact). and the fact is that we can find shared mutations without a commondescent. so shared mutations cant be evidence for a commondescent. simple logic.

(Steve Schaffner) #13

No. The argument depends on the fact that DNA is inherited, and that pseudogenes no longer function as protein-coding genes. Nothing to do with genetic reductionism.

I’m not sure what you mean. The differences are the signal of common ancestry: they form a nested, tree-like pattern, which is what we would expect if DNA were inherited between species, with changes caused by mutation. That applies both to the appearance of duplicate genes and to the mutations that disable them.

No, the argument is this: if common descent is correct, then we should see a tree-like pattern in genetic differences between species. We observe that kind of pattern (over and over again), confirming the prediction.

Could you summarize the argument? On the face of it, your statement is incorrect. Protein-coding genes are in general much more resistant to functional change than regulatory regions. Chromosome spatial organization is known to vary within species, and there’s nothing particularly surprising about the degree to which it varies between species. Closely related species, like humans and chimpanzees, have very similar large scale organization, while more distantly related species have less similar organization. There are very few places in the genome where the detailed organization seems to matter very much.

It was known long before ENCODE that focusing solely on genes misses a lot of stuff: regulatory DNA has been known for decades. It’s been known at least since the sequencing of the mouse genome that the majority of functional DNA lies outside of protein-coding regions. This fact has done nothing at all to undermine the continuing importance of genes – which are the only parts of the genome that actually produce anything, whether RNA or protein – or the modern synthesis. (And yes, our genomes are full of junk DNA, in case Sternberg argues otherwise.)

You would be well served by finding other sources of information about biology than marginal figures like Sternberg.


@DennisVenema thanks for the post, very interesting. It seems to me that common descent is the most fitting explanation here, and that this is a sensible rebuttal to the ID argument.

I will betray my ignorance of genetics here, but I’m curious, is this discovered functionality always a theoretical possibility? Are there any genetic markers that are open and shut, no possible function by any reasonable standard? Not that I think this is required in order to make conclusions, but I am wondering if there are other genetic candidates that are more undeniable than the beta globin pseudogene? Could Ken Miller have originally chosen a more ironclad example in the court case?

(Dcscccc) #15

actually there is one example of the makorin 1 pseudogene:

and like the beta globin example in this article its indeed have a function. so its not a realy rare case.

again- the main point is that share mutations=commondescent. but we can find share mutations without a comondescent. so share mutations cant be evidence for a commondescent.

(Dennis Venema) #16

Hi @Josh,

Any sequence in our genome could potentially be exapted to have some function, so any example chosen could be shown, later to have some role. The point is that the original function is lost, and we are confident of that: this pseudogene is not a translated beta globin, the GULO pseudogene cannot be translated to make the enzyme required for making vitamin C, and so on. Even small fragments of transposons and retroviruses have been exapted into regulatory DNA (and thus gained a function).


(Philip Cunningham) #17

Of related note:
Evolutionists Lay an Egg: Vitellogenin Pseudogene Debunked
by Jeffrey P. Tomkins, Ph.D.
Excerpt: One study claimed to have found genetic evidence of an ancient vtg gene in the human genome.2 Because the actual data for this discovery were questionable, the evolutionary community in general did not actively popularize the alleged finding. However, BioLogos, a religious group of evolutionary scientists and liberal Christian theologians, has been promoting the so-called egg-laying pseudogene3 discovery as evidence of evolution.4-6 Because this type of propaganda is targeted to the Christian community,7 the claim should be more thoroughly investigated.

The main piece of evidence for the vtg pseudogene is the presence of a 150-base human DNA sequence that shares a low level of similarity (62%) to a tiny portion of the chicken vitellogenin (vtg1) gene.8 However, the chicken vtg1 gene is actually quite large at 42,637 bases long, so a 150-base fragment of 62% similarity represents less than 0.4% of the original gene if the evolutionary story were true! But this miniscule amount of questionable data isn’t the only problem for the evolutionary egg-laying fable.

In a detailed research report recently published in a technical journal, I show that the alleged vtg fragment in humans is not a pseudogene remnant but rather a functional feature called an enhancer element toward the end (fifth intron) of a genomic address messenger (GAM) gene.8 This GAM gene produces long non-coding RNAs that have been experimentally shown to control the function of other genes, a majority of which have been implicated in a variety of human diseases. The RNA products from this GAM gene are also known to be expressed in a variety of human brain tissues that span from infant to adult.8

As an enhancer element, the 150-base alleged vtg sequence contains a variety of highly specialized sequences that enable the binding of specific protein machinery that controls the activity and function of the GAM gene.8 These specialized sequences are also associated with a wide variety of epigenetic marks—chemical modifications in the DNA. The specific types of biochemical data associated with these marks also tells us that this DNA feature is not only active but important to the overall three-dimensional structure and function of the GAM gene in a process called long-range chromatin interaction.8,9

Upon investigation, we see that this 150-base sequence is not an ancient egg-laying “fossil” in the human genome. It’s a functional enhancer element in a GAM gene expressed in brain tissues. Once again, when we examine the genetic data more closely, the evolutionary scoreboard shows nothing but a big zero—a “goose egg,” as the saying goes.

(Philip Cunningham) #18

glipsnort, your arguments all boil down to denials without evidence and ad hominem. Is this the type of shoddy argumentation that Darwinian Christians rely on? For instance, when I asked for you guys to prove your ‘bottom up’ materialistic model true, you simply say “No” (it does not need to be shown to be true) and then just automatically assume your flawed ‘bottom up’ model is correct. Contrary to what you may believe, I can find no empirical evidence that your reductive materialistic model is correct, and indeed find much evidence against it being correct. i.e. Your base assumption in your ‘bottom up’ evolutionary hypothesis is flawed and unwarranted!

(Steve Schaffner) #19

You didn’t present any evidence to refute – which is why I asked you to summarize the argument. You haven’t done so. Much of what you did write was incorrect, and I told you so. If you want to discuss details, we can certainly go into them. But you’ll have to present something concrete first.

You asked me to prove a bottom-up genetic reductionism model true. Since nothing written by me here (or by anyone else here, for that matter) has anything to do with genetic reductionism, there was nothing to defend. Do you know what genetic reductionism is?

(Philip Cunningham) #20

glipsnort, you don’t even know your base philosophical assumption? as well much of what you asserted was incorrect.
My advice for anyone reading this is to ignore what these guys are asserting. They are not even on the right playing field as far a real science is concerned.