I recently attended the Discovery Institute event at Southern Methodist University in

Dallas, TX. It was titled: 4 Nails in Darwin's Coffin. What follows is the audio only of

the question I asked of the panel and the answers they gave. If you're hoping to see

blood, or a shouting match, or a witty retort, you're out of luck. I actually had some questions

prepared, specifically about the evolution of whales, but since they'd addressed that

point already, I ad libbed a question that had really been bothering me. It concerns

the limitation they placed on evolutionary change in development.

Before I play the clip, let me set the scene. For those of you unfamiliar with SMU's reputation,

it's affiliated with the United Methodist Church, but not overtly religious. It's a

very prestigious business school, very conservative, and the students have a reputation for coming

from wealthy families.

The event was planned to start at 7 PM, but they were 45 minutes late. We watched a 1

hour movie of DI Fellows saying incredibly stupid things about the Cambrian Radiation,

nothing new was presented. The most humorous comment was John Wells saying that we have

no idea how long the Explosion took... it might have happened overnight. Such comments

are obvious pandering to the Young Earth Creationists who fund the Discovery Institute. No mention

was made of the fact that the Cambrian Radiation did not give rise to a single vertebrate,

vascular plant or insect.

So it's almost 9 PM when they start the sessions, which lasted for about an hour. Steven Meyer

was the MC, Jonathan Wells was there, along with Doug Axe from the Biologic Institute,

a wholly owned subsidiary of DI, Paul Nelson, and Richard Sternberg. Meyer is a philosopher,

Wells has PhD's in biology and theology, but has never published a research paper, Paul

Nelson is a philosopher of biology, Sternberg is a theoretical biologist, which leaves only

Doug Axe as an actual research biologist. Doug has 9 papers in Medline, and Sternberg

has exactly 1, so the total number of peer-reviewed science papers published by the entire panel

is 10. That's about half of what Thunderf00t has published and a little less than I managed

before I went to industry. I'm not talking to equals, in other words.

The impression I got from the crowd is that many of them were part of youth groups or

campus groups at local churches. They moved in large crowds, and knew the sponsor well

enough to call him by first name.

Here's the clip. I'll pause it at several points to explain the questions and responses.

c0nc0rdance "So, this relates I think to several of the areas you talked about today, but one

concept I didn't hear discussed was gene duplication. Specifically, how that relates to mutations

resulting in lethality early in development. If there are multiple copies of a gene, and

they're less constrained, does that change your assessment of the possibility of mutations

[in genes expressed] during development?"

SC Meyer "...Or the probability.."

c0nc0rdance "or the probability..."

SC Meyer "It's a good question"

RV Sternberg "I did mention the topic of gene duplication as it relates to the model...

I presented. Certainly if you have extra copies of genes within the genotype... within the

genome. In theory, this provides the substrate for all kinds of innovative changes. In theory,

you should be able to relate gene duplications to innovations that have occurred, either

within the laboratory populations or along an evolutionary tree. The problem is that

whereas you find that a number of gene duplicates that are around, many of them are sub-functional;

those that we know in plants, those that we know in animals. So, it's still an open question

whether they do provide that substratum, but there's another aspect to it, and it's...

related to the figure that I showed. After a rather small number of changes, I mean you've

got this extra gene out there. Presumably, it's not..., the changes aren't being sieved

by natural selection. After 4... 5... 6 substitutions, it drifts into non-functionality. It... it...

More often than not, becomes a pseudogene. So, it remains a tantalizing hypothesis that's

constantly presented... as a...you know... covers, if you will, a multitude of theoretical

sins, but it's yet to be demonstrated that you really can find innovations for it."

I want to pause here, because I want to summarize what he just said. Gene duplications have

never been shown to generate new functions, and pseudogenes are irrelevant for evolution.

Remember that he just said that.

He also said that we aren't able to place gene duplications on a phylogenetic tree,

and I've been showing you papers published just in the last 3 months that put the lie

to that statement. It's well known that some plants are polyploid, that means they have

more than the standard number of chromosomes. These duplications change the way the plant

grows and what soil it can grow in, so that's a gain of function from gene duplication in

a laboratory model.

For example, the human TNF receptor is part of a superfamily of over 34 genes in our genome

each with different function, but only relatively minor differences in protein sequence.

This is a recurring theme in biology. A useful gene is co-opted for many different functions.

The way this happens is the gene is duplicated, drifts, and is activated with a new purpose.

Watch in the next clip as Richard Sternberg, Discovery Institute Fellow, confirms that

this is the case, in contrast to where he just said that gene duplication is NOT a source

of new functions.

RV Sternberg "You have a..."

c0nc0rdance "Just specifically on what you just said: Pseudogenes can also be reactivated."

RV Sternberg "That's true"

c0nc0rdance "Is that true?"

RV Sternberg "Well, pseudogenes, it depends. Often, when they are reactivated... I do not

know of an instance ... I mean, there may be one. The pseudogenes that have *supposedly*

adopted functionality are often performing a role in the cell in development that is

different from the putative ancestral sequence. So, if you have like a protein coding gene,

and you have an extra copy and it became a pseudogene, then the new role is often something

else. It does not go back to what it was doing. It... BUT! Nevertheless, it's very hard to

pin down a specific innovation where you can say...a-ha at this point...Give you an example:

bony fishes. You have anywhere from 22,000 plus species of bony fishes. A compelling

idea is that what happened is that the genome was duplicated... I mean the whole genome

is duplicated... they became effectively tetraploids for a while... or I mean at least part of

their genome became tetraploid. instead of two copies, you had four copies... and you

could explain pufferfishes, seahorses, flounders, etc. from this. But the problem is that when

you actually look at the many innovations you have, it's very difficult to tie them

to any of these extra copies you have lying around.

------- I'm going to pause again, and spare Rick his

misery. Steven Myer is about to step in to stop the travesty.

Did you follow where we've gone from? We started at gene duplication don't produce innovation,

we passed through pseudogenes producing new functions, and now we're at the point where

Rick admits he's observed developmental gene duplication in the evolutionary history of

his bony fish, but it's just really hard to tie the gene duplication to the innovation,

except in flounder and seahorses. Feel free to go back and see where he realizes his error

and starts correcting.

No wonder Steven is going to stop this and pass the ball to Doug Axe. Oh what fun I was

having at this point.

RV Sternberg "Again, because there seem to be..."

SC Meyers "Rick. Rick, can I get Doug to answer that as well? And just a sec, because I'd

like to point out that whereas the gene duplication .... operating as Rick does in his critique

still within the neo-Darwinian framework, accepting all the assumption that neo-Darwinism

asks you to uh... asks you to assume, you could entertain the gene duplication hypothesis

as a way of solving some of these problems, but when you get to the... the kind of things

that Jonathan and Paul are talking about, the problems of developing innovations at

the body plan level... So that adding extra copies of the DNA to help you, Even at the

level that Doug is addressing I don't think it solves the problem because you still have

this huge combinatorial space to search."

c0nc0rdance "Actually..."

SC Meyers "If you could speak to that Doug..."

c0nc0rdance "Can I restate the question for Dr. Axe?"

c0nc0rdance "Is the combinatorial space really all possible proteins that can be formed,

or is the current complement of proteins that exist? In other words, do cells try to invent

new proteins by randomly jamming the amino acids together, or do they modify existing

ones?

DD Axe "So, you're talking about new protein structures?"

c0nc0rdance "New protein functions, I thought, was the issue?"

DD Axe "Well, the fact is there are 2000 fundamentally different protein structures, so a Darwinist

has to explain how you get such different structures. So, often new functions require

new structures, because that's what we see when we see... new structures are often performing

new functions."

There are 55,000 proteins in the Protein Data Bank

There are only 80 fold families known, usually called domains.

Three of those folds: SH2, TIM, and B3B4 account for a high percent of all functional fold

domains. We call these the superfamilies or superfolds.

In other words, most proteins re-use what already works, they don't go searching for

new ways to fold proteins very often.

So, Doug made a terrible analogy of optimal fitness searches in protein domains to Google

queries. I'd like to modify it. Suppose you wanted to generate functional webpages that

would draw visitors. Would you have to invent fantastical animals and clever stories, or

would you just cut and paste porn, fail jokes, and pictures of cute cats into a random generator

and spit out 90% of the Internet? Here on Youtube, you'd just need a steady stream of

make-up advice, licensed music videos, and cute things sneezing.

Proteins are more like the Internet than a well-written novel. The same motifs are re-used

over and over, and only sometimes do we see the emergence of some new successful meme,

which is quickly seized upon and adapted into thousands of other cross-over innovations.

AN example is the ABC transporter, which is shorter for ATP binding casette transporter.

It's a modular unit recombination can plop down into any gene and turn it into something

that moves molecules in and out of the cell against a gradient. It's part of everything

from antibiotic resistance in bacteria to human cystic fibrosis. We call it a cassette

because it's more or less self-contained information about how to do something. We know it's ancient

because it's highly conserved.

I'll deal with where domains come from in just a minute, after Doug has a chance to

be interrupted by Steve Meyer yet again.

SC Meyer "But the space that has to be searched isn't just the 2000 possibilities, it's..."

DD Axe "Those are the things that we see out there, doing the job.... How that happens,

nobody knows has a clue, but presumably it would have to involve extensive cutting and

pasting and mutating. And effectively, if you look at the... sequence... divergence...

difference between a novel structure, and the closest sequence you can find, the sequences

are so wildly different that you're effectively... as I try to give in my simple example, having

to search the whole space. You basically have to be able to pull things out that are so

remote in the space that it makes no difference what you started with.

SC Meyer "So effectively in that case, having a second copy of the same gene isn't going

to help you solve..."

DD Axe "Let me clarify that... when I say search the whole space, I do not mean you

have to have tried all possibilities, what I mean is you have to wander so far in the

space, that the starting point is irrelevant."

New folds, and therefore new domains, arise very rarely, but they aren't impossible as

Doug thinks. That's because to get from A to B, as I show in the diagram on the right,

you have to have a version of A that is pretty bad at its job. That's only possible if there's

a duplicate copy that's good, or if A isn't a critical fold. Then the bad form of A finds

that it can do the job of fold B, but only very poorly. But that poor version that can

do both A and B has a selective advantage. Further evolution will result in stepwise

movements up that shallow hill to the fitness peak for fold B.

What Doug has done is to imagine a fitness landscape where there can be no overlap between

A and B, no gentle slope to climb between them. The good news, at least for me, is that

several papers in the last few years have shown that the model on the right is more

accurate. My message to Doug is that whenever you and the rest of the scientific world disagree,

sometimes it's healthy to question your own conclusions rather than everyone else's.

c0nc0rdance "I don't mean to monopolize time, but I know that there are literally hundreds

of thousands of different sequences that all do the same function in different organisms,

right? For example, a jellyfish adenine... whatever reductase...

DD Axe "homologous..."

c0nc0rdance "homologous, right, but doing the same function, so there must be hundreds

of thousands of possible functional proteins accomplishing the same purpose in different

organisms. Is that true?"

DD Axe "Sure. And you can go a lot higher than that, but... the JMB 2004 paper, which

I can give you the reference for, carefully examined the prevalence of those functional

variants, and there's trillions of them, but the thing is you have to divide by 20 raised

to the 150th power, which is ?shockingly? large. So, it doesn't matter that you have

trillions of functional sequences, the denominator is so large, it becomes an impossibility,

virtually."

I'd say of the three people I interacted with, Doug gets a small measure of grudging respect.

Sternberg was a buffoon, and Meyer was a slimy weasel who could only recite mantras.

To all the panelists, I want to say thank you for being such good sports, and providing

us with such great entertainment!

Thanks for watching.