That’s another fine mess you’ve made Jonathan!

| 33 Comments

It has often been said that it takes two pages of science to correct all the misinformation an anti-evolutionist can pack into one sentence. A recent interview featuring Discovery Institute Fellow Jonathan Wells illustrates this rule of thumb. In a short space he makes numerous errors. For brevity I’d like to focus on two specific areas, but the rest of his pronouncements in this short piece are just as flawed.

Wells Wrote:

Dwarfing the resources wasted on phylogenetic trees and speciation have been the public resources devoted to finding the “gene for” this or that trait or disease.

Researchers are quite aware that many diseases are a complex interaction between the environment and multiple genes. Wells’s statement is a strawman. The idea is that the actual pathways of disease can be unravelled if the environmental and genetic factors can be distinguished, leading to preventative measures or therapies. Wells’s statement reflects his conviction that genes actually don’t do much, and that mutations in genes cannot play a significant role in evolution.

It takes some time between the identification of a gene involved in a disease to a clinical outcome, but already there are examples available. One is the gene BCRA2, involved in breast cancer. Breast cancer is considered to be a multi-stage, multi-factor process that involves genetic and non-genetic factors. However, women who have mutant BCRA2 genes are at much higher risk of developing breast cancer, and screening for this gene would result in careful monitoring and early intervention if cancer were to develop (early intervention being known to save lives).

Some diseases are due to mutations in a single gene, these include, Haemophillia A and B, muscular dystrophy, cystic fibrosis and severe combined immunodeficiency. All these diseases are amenable to gene therapy, and progress has been made in some of them.

Wells Wrote:

This approach is encouraged by neo-Darwinism (in which genetic changes are imagined to be the raw materials for evolution), but it has produced no real clinical benefits.

I’m sure the children with Severe Combined Immunodeficiency who have been successfully treated with gene therapy will disagree. SCID children are born without one of the critical genes for development of the immune system, and must spend their lives in an artifical germ free environment (the so-called “boy-in-the-bubble” syndrome). In France, 15 children with X-linked SCID, where a mutant receptor is responsible, have been treated for this disease, one child has died of leukaemia, but 14 are healthy [1]. The English cohort of children who have undergone gene therapy are all currently healthy.

One issue is the length of time it takes to develop a therapy (any therapy, gene or otherwise) once you understand the underlying cause. It may take up to 15 years of testing before approval for use is issued. Cystic fibrosis therapy is under development, and despite many advances and effective demonstrations in animal models it may take 5-10 years before gene therapy for cystic fibrosis is released.

Another ironic [2] example is mutants of the cytokine receptor CCR5. CCR5 is important for regulating the immune response. But in 1996 it was discovered that some people who were resistant to HIV infection had a mutant CCR5 receptor. From this it was discovered that CCR5 is part of the mechanism HIV uses to invade cells. Now drugs that act to block CCR5 are being developed as anti-HIV agents. ]. A really interesting application is make HIV-positive people “immune” to HIV by mutating the CCR5 gene in their stem cells. [3]

As noted above risk factor genes can also be screened for and coupled with preventative measures and early detection of disease can produce significant clinical benefits.

Wells Wrote:

For example, it is now known that the underlying cause of cancer is “chromosomal instability,” or damage to extra-genic structures – not mutations to individual genes.

Well, this knowledge seems to have eluded most researchers in the field (see this review and this comprehensive review as typical examples).

There are just so many things wrong with Wells’s statement that I will have to start with the very basics of cell growth.

All the cells of the body (with the exception of mature neurons) divide and grow during our lifetime; some such as blood cells divide often, others divide rarely. Growth and division are controlled by a number of genes and gene products: some stimulate cell division, some inhibit it, and others lead to programmed cell death. If you disturb the balance between growth promotion and growth inhibition pathways sufficiently, then the cells will grow out of control, and you have a cancerous cell (you need other changes for the transition to an invasive, malignant cell, but the primary change is a loss of growth control).

Because there are multiple pathways and multiple checkpoints, it often takes damage to several parts of the control pathway before a cell becomes cancerous. The damage can occur in many ways. For example, simple point mutations, insertions of viral genomes, or gene fusion or loss via chromosomal crossing over can all produce the genetic damage that results in cancer.

An example is chronic myeloid leukaemia (CML). At first sight it might appear to support Wells’s thesis. The disease is associated with a translocation of part of chromosome 22 to chromosome 9. But the translocation by itself is not enough. Unless a gene called c-ABL is fused to the gene BCR, producing the BCR-ABL fusion product, then CML does not develop. The cause of CML is a mutant gene, contrary to Wells’s claims. The anti-CML therapy, imatinib (Glivec or Gleevec, depending on which country you are in) acts by inhibiting the BCR-ABL gene product (a gain-of-function mutant which persistently activates growth pathways). It is spectacularly successful, with remission rates of between 80-90%.

Let’s look at that again, one of the most successful anti-cancer therapies known targets a mutant gene, one that Wells says is not the cause of cancer. And imatinib is not the only drug aimed at mutant genes. Iressa inhibits a mutant form of growth factor receptors. More of these kinds of drugs are being developed, targeting oncogenes such as c-Myc and c-Src.

But what about the actual translocation, surely that is the ultimate cause of the mutant gene and Wells is in part right? Chromosomal translocations do underlie several, but not all, cancers (translocations that cause mutation of the gene c-Myc for example, but remember translocation is not enough by itself, a gene must be mutated). What causes these chromosomal instabilities? We know that the incidence of CML is increased by exposure to radiation or benzene, known mutagens. Damage to the DNA is an important part of producing chromosomal instability, and inhibition of DNA topoisomerase II, a DNA repair enzyme, is implicated in the DNA damage which leads to chromosomal instability. Even worse for Wells thesis, BCRA2, a key gene in some breast cancers (see above), regulates a key recombinase (which is responsible for chromosomal integrity). So that chromosomal instability can be traced to a mutation in a single gene. A recent review of the genetic mutations that underlie chromosomal instability is in Nature (2004) 432, 338-341, doi 10.1038/nature03099 . [4]

Wells Wrote:

Although biologists steeped in neo-Darwinism discovered chromosomal instability, they did so NOT by being guided by neo-Darwinism, which had previously focused their attention on genetic mutations alone.

Biologists have known about chromosomal instability for almost as long as we have known about the existence of genes as discrete pieces of DNA, landmark work in the 1960’s on the Philadelphia chromosome led to the realization that a defective gene was at the heart of CML. Wells has the story exactly backwards. The work on chromosomal instability and mutation in cancer has been developing for a long time, it has long been known that chromosomal instability was one way (along with point mutations, viral gene disruption etc.) to generate mutant genes that will lead to cancer. And it has been realized for several years that genetic mutations underlie chromosomal instability (see also the review above).

The major proponent of the “Chromosomal Instability Only” theory is Dr. Peter Duesberg, better known as an HIV denier[2]. At a recent invitation-only conference, even Duesberg conceded that genetic mutation played a role in cancer.[5] Duesberg’s statement that targeting mutations “is probably useless.” is ironic, given the success of imatinib (iressa is less successful as it targets a fairly uncommon mutation, but it is successful in people with that mutation). Again, I will point people to this recent review of the role of gene mutations in producing genetic instability.

I hardly need to make the point that researchers were guided by experimental and observational evidence (such as experimental evidence of mutations, generation of tumours by transferring mutant genes, mouse transgenic models etc. etc.) rather than blind allegiance to Darwinist dogma.

Well, I’ve written four pages to cover just one paragraph. I have only briefly procised the mass of available data and haven’t covered the role of evolution in generating cancer drug resistance, or the evolutionary strategies people use to get around it. I think this more than demonstrates our rule of thumb, don’t you?

But this was just a short interview; does the interview really represent his views fairly? Are we worrying over a storm in a teacup? Sadly, the interview does represent his views. His paper on the “Theory of Organismal Problem-Solving” explicitly denies the role of mutations in genes as a cause of cancer [6]. In an ideological and political battle to supplant modern evolutionary theory, Wells is trying to place genes in a peripheral position in biology. One of the causalities is our understanding of cancer. To non-scientists, evolutionary theory is a peripheral issue, and the battles fought over teaching evolution is seen as academic. But ID has consequences beyond teaching evolution; it is an active threat to effective medical practice and health care. Surely, you might say, that the vast majority of knowledgeable active researchers and clinicians will not allow this anti-gene crack-pottery to affect our health care? Remember South Africa? Remember the health disaster there when HIV deniers arguments seduced the Health Minister? ID is a political movement, and as a political movement they can bypass the experts by seducing our lawmakers.

ID is not just bad biology; it is a health disaster waiting to happen.

[1] Three of the children developed leukaemia, and the trial was halted. Two children were cured. The reason for the development of the leukaemias was instructive. In these children the retroviral vector inserted next to an oncogene, activating it. Another blow against Wells’s thesis (as if we needed more). The children treated in the British trial used a different construct.

[2] Interestingly, Wells and other ID promoters appear on a list of HIV-denial supporters.

[3] I’ve only scratched the surface of the things that are going on here. There are two phase III clinical trials and three Phase II clinical trials for anti-sense oligonucleotides targeted to oncogenes going on at the moment. Novel “exon-skipping” anti-sense therapies are about to be trialed for Muscular Dystrophy. A gene-based medical revolution is creeping up on us.

[4] It is possible that non-genomic effects (eg protein cross linking in response to some mutagens, or excessive growth factor activation during long term inflammation) could lead to chromosomal instability in some cases. However, enough cases exist where we know that the primary lesion is a mutation in a gene to prove Wells wrong. A neat example is a family with a high incidence of aneuploidy and cancer, for which the key lesion is a mutation in a gene that helps guarantee that the right number of chromosomes are passed from cell to cell.

[5] A nice Duesbereg quote “Aneuploidy is thus a source of chromosomal variations from which, in classical Darwinian terms, selection would encourage the emergence of new cell “species” with neoplastic phenotypes and karyotypes.” The fact that cancer progression is a clear “Darwinian” process must irk Wells.

[6] Wells cannot have read the references he cites in this essay very closely. He cites 3 papers showing centriole dysfunction as leading to chromosomal instability, and hence cancer. Brinkley and Goepfert (1998) cite mutations in the tumor suppreor gene p53 as a cause of centriole dysfunction. Papers from Pihan and colleagues cite mutations in a number of genes, including p53 and our old friend BRCA2 as causes of centriole dysfunction. Once again Wells shows shoddy scholarship.

Acknowledgements: Many Thanks to the Panda’s Thumb Crew for helpful thoughts, useful papers and constructive criticism of this article.

33 Comments

Thank you, Ian, for a very well-written article. I learned several things I had not known about cancer biology from your explanation.

The ID people who would talk about time “wasted” on speciation and looking at genes, should be held in the same regard as Tom Cruise talking about the evils of psychiatry.

So John Wells and Philip Johnson deny that HIV causes AIDS?

I know someone who has taught about AIDS in the past, has no tolerance for AIDS skeptics, and yet is an avid fan of Intelligent Design. I clued her in to the fact that Phillip Johnson is deeply mired in the anti-AIDS movement, and that the arguments he made against AIDS were the same format and quality as the ones he made against the so-called evolution scam. I never got a reply.

Wells Wrote:

Although biologists steeped in neo-Darwinism discovered chromosomal instability, they did so NOT by being guided by neo-Darwinism, which had previously focused their attention on genetic mutations alone.

Actually, genes and genome rearrangements (chromosomal instabilities) were discovered at about the same time in Thomas H. Morgan’s lab. This was way before biomedical and cancer research had developed; the concept of chromosomal rearrangments have been around for nearly a century. The first rearrangements were characterized prior to the modern synthesis and played a major role in shaping the neo-Darwinian perspective (see the work by Dobzhanksy and Sturtevant).

Wells couldn’t be further from the truth if he tried – there was no neo-Darwinism when chromosomal instability was discovered.

Politically decreed biology is bad news. Just consider the victims of Lysenkoism in the former Soviet Union, which would not include just those folks Lysenko had executed or sent off to the gulags, but also the millions who experienced either hunger or starvation due to his failed agricultural policies.

The “intelligent design” movement not only brings us the opportunity to have a politically decreed form of biology right here, but also shares with Lysenko’s “Michurinism” a reliance upon teleological principles in biology. Historically, these fall into the “should be considered harmful” category. And the harm is not just that they put the advocates on the losing side of a philosophical tussle, but that their real-world application makes more people suffer more hardship. Until reading Ian’s article, I hadn’t realized that this new round of suffering could begin with cancer victims, who already have enough to worry about.

RPM Wrote:

Wells couldn’t be further from the truth if he tried — there was no neo-Darwinism when chromosomal instability was discovered.

Sure there was. “Neo-Darwinism” was August Weismann’s reformulation of Darwinian principles, and the term is said to have been current by 1896. There was, however, no “modern synthesis” when Morgan corroborated the chromosomal theory of inheritance. Morgan is pretty famous for being a critic of natural selection as a mechanism of speciation. We don’t have to be as sloppy in use of terms as the ID advocates.

Wells is a despicable human being.

According to Wells:

Although evolutionary theory ultimately stands or falls on the proposition that one species can change into another through mutation and selection, this as never been demonstrated.

Of course it has been demonstrated. A lot of different data enables us to determine this. The fossil data is one part of the picture.

If he means that no human has observed rodent-like mammals evolve into gorillas, then sure. But that no person has seen an alleged event does not enable us to determine that the it is no more plausible than not that the event occurred. No person saw planet earth 65 million years ago, and I’m justifiably confident that it existed then. No person has seen the core of the moon, and I’m pretty sure it is not made out of cream cheese. No person has seen a living T-Rex, and I’m justifiably confident that some T-Rexes drank water.

The other day I was walking my dog. I made sure no other person was around. We came to a fire hydrant. Right after my dog lifted its leg, I closed my eyes. I kept them closed for about one minute. When I opened them, the fire hydrant was covered in dog pee. No person saw my dog pee on that hydrant. I’m justified in believing that it did. So, that no person has observed rodent-like mammals evolve into gorillas does not enable us to determine that it is no more plausible than not that it happened.

Besides, people have observed wolves evolve into dogs. I mean not every single reproductive event that resulted in wolves evolving into dogs was observed by at least one human. But some were. And it’s clear that wolves did evolve into chihuahuas, saint bernards, cocker spaniels, poodles, great danes and all the other dogs that have lived on earth.

According to Wells:

Although biologists steeped in neo-Darwinism discovered chromosomal instability, they did so NOT by being guided by neo-Darwinism, which had previously focused their attention on genetic mutations alone.

What does he mean by “neo-Darwinism?” He should say how he is using that term. It has a vague meaning for many people. What does Wells think happened? Does he think that a deity specifically intervened and – poof! – turned dust directly into two elephants (one male and one female)? That’s silly.

Many people influenced by Charles Darwin don’t just focus their attention on “genetic mutations.” For example, I’m interested in sexual reproduction, genetic reproduction and what happens when organisms sexually reproduce. Much of the difference between me and modern mice was caused by vast numbers of organisms sexually reproducing. One of my descendants is a little rodent-like mammal that lived on earth about 65 million years ago. Let’s call it a muskrat. Why am I so different than my ancestor the muskrat? Part of it is that massive numbers of organisms sexually reproduced with each other. Massive numbers of organisms sexually reproducing with each other contributed to my existing and being the way I am. Chihuahuas are fairly different from Saint Bernards. Their most recent common ancestor is less 100,000 years old, which is a blink of the eye in terms of geologic time. I don’t think that “genetic mutation” played that big a role in Chihuahuas and Saint Bernards being as different as they are. If woman X and I reproduce, my offspring will be different than they would be if woman Y and I reproduced.

According to Wells:

Although evolutionary theory ultimately stands or falls on the proposition that one species can change into another through mutation and selection, this as never been demonstrated.

I don’t know what Wells means by “mutation and selection.” But wolves didn’t evolve into dogs merely through “mutation and selection.” Genetic recombination and sexual reproduction were hugely important. They were the main factors.

Rodents didn’t evolve into gorillas merely “through mutation and selection.” Sexual reproduction and genetic recombination were hugely important. Organisms have been sexually reproducing at high rates for about 650 million years. Sexual reproduction always results in the offspring having a genotype and phenotype that are different than those of its parents. I exist because my parents chose to sexually reproduce.

Some people are focusing too much on “mutation” and not enough on genetic recombination and sexual reproduction.

Wells also failed to mention lateral gene transfer and genetic drift.

He’s starting sound sound like Jeremy “Kitchen-sink” Rifkin.

Wesley R. Elsberry Wrote:

Sure there was. “Neo-Darwinism” was August Weismann’s reformulation of Darwinian principles, and the term is said to have been current by 1896. There was, however, no “modern synthesis” when Morgan corroborated the chromosomal theory of inheritance.

Yes, I meant the modern synthesis. I was using the terms interchangibly, which I shouldn’t have been doing. I think my point is still valid – that the field of genetics and our understanding of genome rearrangements developed simultaneously, prior to (and during the initial stages of) the modern synthesis, and played a major role in shaping modern evolutionary theory. Wells’s chronology is totally off.

Wesley R. Elsberry Wrote:

Sure there was. “Neo-Darwinism” was August Weismann’s reformulation of Darwinian principles, and the term is said to have been current by 1896. There was, however, no “modern synthesis” when Morgan corroborated the chromosomal theory of inheritance.

Yes, I meant the modern synthesis. I was using the terms interchangibly, which I shouldn’t have been doing. I think my point is still valid – that the field of genetics and our understanding of genome rearrangements developed simultaneously, prior to (and during the initial stages of) the modern synthesis, and played a major role in shaping modern evolutionary theory. Wells’s chronology is totally off.

Funny, I remember when Carl Zimmerman discussed how genetics and evolution help advance medical research, Answers in Genesis announced that this was all covered by “micro evolution.” Guess Wells missed the memo.

Let’s look at this sentence by Wells one more time:

Although evolutionary theory ultimately stands or falls on the proposition that one species can change into another through mutation and selection, this as never been demonstrated.

No dog has given birth to an armadillo. No offspring is massively different than its parents. I mean maybe the Elephant Man is an exception. But essentially offspring are quite similar to their parents. However, self-replicating molecules evolved (through reproduction) into all the organisms that have lived on earth. Wells is saying this hasn’t been demonstrated? What is he talking about? It is a basic scientific fact. What does he have in mind?

I mean “demonstrated” is sometimes used in terms of logical algorithms or systems of mathematical thought. And it is not a necessary truth that humans and bacteria share common ancestors. But it is, for lack of a better expression, a scientific fact. Does he not realize that? I don’t understand what he is getting at.

Like I said, no person has seen reptiles evolve into mammals. It took place over millions of years. Humans weren’t even around back then.

I’m not sure how Wells is using the word “species.” But does he think it has not been “demonstrated” that humans and chimps share common ancestors? Of course they do. I mean I guess there is the issue of Cartesian certainty. But let’s put that aside and talk in normal language. Humans and chimps share common ancestors. Does he think that it has not been “demonstrated” that wolves and chihuahuahs share common ancestors? Of course they do. I mean that is not even an issue.

Hawks and eagles share common ancestors. That’s not even an issue. If Wells thinks they don’t, then how they heck did hawks an eagles get here. Did they just poof into existence? Give me a break.

No person saw every single reproductive event where a homo erectus evolved into me. But so what that no one saw it? I’ve never seen an electron. I’ve never seen a planet outside our solar system. No person saw my dog pee on that fire hydrant. No person’s having seen an alleged event does not enable us to determine that it is no more plausible than not that the event occurred.

“One of my descendants is a little rodent-like mammal that lived on earth about 65 million years ago.”

Wow. I’d love to see your family tree! :)

He’s starting sound sound like Jeremy “Kitchen-sink” Rifkin.

Isn’t that the guy who wrote that awful book ‘Algeny’, or something like that?

Longhorn:

Wells is saying this hasn’t been demonstrated? What is he talking about? It is a basic scientific fact. What does he have in mind?

Wells is not making a statement of fact, observation, or evidence. He is stating a policy position. Wells’s target audience is not anyone who knows or is interested in evidence, or in learning anything. His target audiences is anyone who feels comfortable sharing the same policy.

Remember that his target audience doesn’t feel comfortable contemplating Deep Time. To them, those species around us are all that has ever existed, created that way in a day to stay that way forever. “One species changing into another” is intended to be understood as one current, visible, easily identified species suddenly transforming into another current, visible, easily identified species. And sure enough, this is exactly how it’s interpreted. Dawkins has written several times of his professors identifying Cambrian phyla by classifying them into current categories, none of which existed or were even remotely meaningful at the time. What we see around us today is what we assume has always been, and even Dawkins’s professors assumed this, giving the development of life over the past half billion years no more than intellectual lip service.

Does Wells himself know better? Why should he care? That’s not his job.

How do Wells and other evolution deniers account for the fact that we share 99% of our genetic makeup with other hominid apes? And if I remember correctly, cladistic studies largely confirm previous assumptions about evolutionary relationships; to me, this suggests rather strongly that evolution worked just we all believe it did. How do they respond to this?

Jon A. Pastor wrote:

How do Wells and other evolution deniers account for the fact that we share 99% of our genetic makeup with other hominid apes? And if I remember correctly, cladistic studies largely confirm previous assumptions about evolutionary relationships; to me, this suggests rather strongly that evolution worked just we all believe it did. How do they respond to this?

They say that the Creator aka Intillegent Designer used similar techniques in creating similar organisms. An unassailable argument (i.e. isn’t falsifiable.)

Behe, on the other hand, has (sometimes) allowed for natural evolution to operate ever since the first cell was designed by the Intelligent Designer.

It’s interesting how people whose arguments for their own positions are based in various types of complexity will rely on gross oversimplification of the evolutionary position in order to try and discredit it.

How do Wells and other evolution deniers account for the fact that we share 99% of our genetic makeup with other hominid apes

I assume he would say that a good designer will reuse a design to create similar beings. A Volvo has more parts in common with a Peugeot than, say, an army tank.

Creationism vs. Evolution?

Of course devout people hate to admit that they are closely related to apes; however, I’ve noticed that pride is the one sin everyone seems to cling to when they’ve ostentatiously given up all the others.

Re “I assume he would say that a good designer will reuse a design to create similar beings.” Yeah, that’s probably what an ID advocate would say. But a human engineer wouldn’t make random changes to the parts (dna) being “reused”, he/she would simply copy it exactly except for where changes are actually needed for function. So imo changes that don’t actually change anything would be evidence against that hypothesis. And for those no-change changes to be (more or less) randomly distributed among all the dna would be even stronger evidence against it. And I gather that those two points are what is observed.

Re “closely related to apes;” and “pride” - What I wonder about when somebody seems to think that relation to apes hurts their pride, is why is an intentional sharing of 99% of dna somehow less hurtful to pride than an unintentional (i.e. by evolution) sharing of that same amount? I’d think for the “designer” to have chosen to make us so much like apes would be worse for that kind of pride than the evolutionary explanation.

Henry

In Comment #37181

Jon A. Pastor Wrote:

How do Wells and other evolution deniers account for the fact that we share 99% of our genetic makeup with other hominid apes? And if I remember correctly, cladistic studies largely confirm previous assumptions about evolutionary relationships; to me, this suggests rather strongly that evolution worked just we all believe it did. How do they respond to this?

Well, you’ve seen how Wells handles it, he denies DNA has any major role in development or body plans or anything. If humans and chimps have 99% similar genes, so what, DNA doesn’t actually do much, says Wells.

Wells Wrote:

“So DNA does not program the development of the embryo. As an analogy, consider a house: the builder needs materials (such as pieces of lumber cut to the right lengths, cement, nails, piping, wiring, etc.), but he also needs a floor plan (since any given pile of materials could be assembled into several different houses) and he needs a set of assembly instructions (since assembling the roof before the foundation and walls would pose a serious problem). In a developing organism, the DNA contains templates for producing proteins-the building materials.

To a very limited extent, it also contains information about the order in which those proteins should be produced-assembly instructions. But it does not contain the basic floor plan. The floor plan and many of the assembly instructions reside elsewhere (nobody yet knows where). Since development of the embryo is not programmed by the DNA, the Darwinian view of evolution as the differential survival of DNA mutations misses the point. At most, Darwin’s theory may explain “microevolution” within established lineages-such as minor differences among closely related species of salamanders. But it cannot account for “macroevolution,” - the large-scale differences between shellfish and insects, or between birds and mammals.”

And from his TOPS paper:

Wells Wrote:

“TOPS then explicitly rejects several implications of Darwinian evolution. These include: (1a) The implication that living things are best understood from the bottom up, in terms of their molecular constituents. (1b) The implications that DNA mutations are the raw materials of macroevolution, that embryo development is controlled by a genetic program, that cancer is a genetic disease, etc.

Dembski tries to relegate the similarities to irrelevance, and, for example, concentrates on changes in gene expression. Unfortunaely for him, chimps are closest to us in gene expression as well. See here and here for essays where I analyse the errors in his essay.

Behe accepts common descent, and the idea that chimps and humans share a common ancestor. He seeks deisgn futher back in time (where exactly he is not clear. He thinks the clotting system is designed, but is on record as saying the last design event was around 300 million years ago).

Jon A. Pastor asked:

How do Wells and other evolution deniers account for the fact that we share 99% of our genetic makeup with other hominid apes?

Mike Walker replied:

I assume he would say that a good designer will reuse a design to create similar beings.

Henry J added:

Yeah, that’s probably what an ID advocate would say. But a human engineer wouldn’t make random changes to the parts (dna) being “reused”, he/she would simply copy it exactly except for where changes are actually needed for function.

Let’s take this a step further, shall we?

As I recall, vertebrate and cephalopod eyes have some striking structural similarities. Evolution explains this as convergence. IDers scoff, saying it’s much too improbable that such similarities evolved independently, right? They argue there must have been a common Designer for both structures.

In that case, wouldn’t we expect the Designer to use some of the same genes? It should be a relatively simple matter to identify various genes involved in eye development in squids and mice, and show that they’re much more homologous than predicted by evolution.

;-)

Re “Evolution explains this as convergence. IDers scoff, saying it’s much too improbable that such similarities evolved independently, right?”

It doesn’t seem all that improbable to me, since the basic shape (spherical with a single small hole in one place) isn’t that complicated.

Re “It should be a relatively simple matter to identify various genes involved in eye development in squids and mice,”

Good point. Not just genes though - also check for subtle differences in the structure. Like where the nerves and blood vessels are relative to the light sensing cells.

Henry

Of course devout people hate to admit that they are closely related to apes; however, I’ve noticed that pride is the one sin everyone seems to cling to when they’ve ostentatiously given up all the others.

Indeed. Want to see prideful self-righteous arrogance at its finest? Just ask a fundie why HIS religious opinions are any more authoritative than anyone ELSE’s are.

The “holier-than-thou” (literally) crap will start flying before you know it.

Behe accepts common descent, and the idea that chimps and humans share a common ancestor. He seeks deisgn futher back in time (where exactly he is not clear. He thinks the clotting system is designed, but is on record as saying the last design event was around 300 million years ago).

Is that when the designer decided to take a nice long vacation or something?

Regarding the eyeball posts:

Without pretending to any expertise, my understanding is that this has been a fruitful area of evo-devo inquiry over the past few years (obviously it can’t have been a fruitful area of IDiot inquiry, since they have no research program), with the sequence going somewhat like this–

1. Because of the difference in detail, the assumption for a while was that this was an example of independent evolution converging on a sensible visual “solution.”

2. Then, as the Hox etc. genes were discovered and their functions in development across the animal kingdom elucidated, the thinking was that perhaps the ur-bilaterian might have had visual (or at least photoreceptor) capability, with this rudimentary visual system evolving divergently in most of the lineages.

3. The latest thinking seems to suggest that the shared developmental genes may have had something to do with specifying photoreceptive cell types, rather than fully-developed (or even rudimentary) visual apparatus in ur-bilateria. The ancestral photoreceptive cells may have been used for something else, like harmonizing Circadian rhythms. The photoreceptor cell lines have developed different detailed uses in the different lineages, which brings us at least partway back around to independent evolution and, in some lineages, convergence on similarly high-tech (but different in detail) optical instruments.

PZ Myers had a good post on this area a while back: http://pharyngula.org/index/weblog/[…]iliary_eyes/ I’m certain his explanation is a good deal more rigorous than my sketch above.

None of this thinking or research, again, was performed or inspired by any of the IDiots or their sycophants, so what they would have to “scoff” about beats the heck out of me.

None of this thinking or research, again, was performed or inspired by any of the IDiots or their sycophants, so what they would have to “scoff” about beats the heck out of me.None of this thinking or research, again, was performed or inspired by any of the IDiots or their sycophants, so what they would have to “scoff” about beats the heck out of me.

They are all about posteuring and making themselves bigger than they really are. If you want an analogy, picture a baleen whale encountering a puffer fish. Try as hard as he might, that little puffer fish just can’t get as big as that whale, which moves on and pretty much ignores him.

Joseph O’Donnell wrote

If you want an analogy, picture a baleen whale encountering a puffer fish. Try as hard as he might, that little puffer fish just can’t get as big as that whale, which moves on and pretty much ignores him.

I love that image! Perhaps Dembski can add it to his wrestling imagery: the brave little puffer fish, puffing himself up as far as he can, facing down the monstrous whale about to chomp him!

RBH

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This page contains a single entry by Ian Musgrave published on July 6, 2005 9:30 PM.

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