Link to my review of the whole book, written for Skeptic magazine

Fruitless Facts about
Four Winged Fruit Flies
and Evolution

I have to admit that I found the chapter on "Four Winged Fruit Flies" (chapter 9 in Icons of Evolution by Jonathan Wells) quite a bit different than I had expected. I was anticipating a more serious discussion of the science and genetics of one of the model organisms in genetics. Wells wants to claim that the mutation which results in flies having four wings instead of two is not quite what it's cracked up to be. Fine, let's see the evidence for what he says, and evaluate it accordingly. My friend told me this was a book written by a "noted developmental biologist", and the preface states that this chapter was reviewed by Ed Lewis, who won the Nobel prize in part for his work on four-winged flies. Based on this, I was looking forward to hearing a brief introduction into the molecular biology of the subject, followed by an outline of his arguments, and then a summary of the case. Instead I found a strange (in my opinion) useless collection of misinformation about Drosophila genetics, which, taken as a whole, left me quite bewildered as to what on earth Jonathan Wells is trying to say. In short, Wells had not done his homework, and is relying on an appeal to the ignorance of the readers, rather than trying to build up a logical, rational, compelling argument based on what is known about the subject. This was particularly evident in the bizarre tangent he takes towards the end of the chapter, where he seems to claim that the idea that genes play a role in development (or even that DNA makes RNA makes protein) is some sort of conspiracy amongst "Darwinians". I am left quite puzzled as to the real reasons why Wells wrote this chapter. In my opinion, it was certainly not to inform the reader, but more to try and pull the wool over the eyes of those who are not familiar with the recent developments in developmental biology, his alleged area expertise. Exactly WHY Wells would want to write such a deceptive chapter is not quite so clear to me, although I suspect it is due to his religious opposition to the "meaninglessness" of Darwinian evolution. Needless to say, this book is selling quite well in fundamentalist Creationist circles in the U.S.

I am willing to accept the premise that there are some commonly used examples of evolution which are more complicated in real life than is often portrayed. The case of the "Four-winged fruit fly" mutation is a good example. Although it has sometimes been held up by some as an example of a mutation which results in a gain of function, when one takes a larger perspective (compared to other insects) this mutation can be seen as a reversion. The reason for the additional wings is a mutation in the ubx gene (more on this will be given in the Background). Drosophila belongs to the Diptera order of insects, which have two wings, whilst most other insects have four wings. From an evolutionary perspective, the reason fruit flies have two wings (instead of four) is due to a LOSS of function present in its ancestors. Thus, if this were used as an example of a beneficial mutation, then great care must be taken to explain this in its proper context. I had anticipated that Wells was onto this, and would try and set the record straight, and then go on to talk about the importance of the hox genes (and the homeobox genes in general) in terms of developmental biology and the evolution of different types of body plans. However, Wells' agenda was a bit different from merely "informing" - he has stated clearly elsewhere that he has devoted his life to "destroying Darwinism" (see http://www.tparents.org/Library/Unification/Talks/Wells/DARWIN.htm) The reasoning in the chapter goes like this:

Preamble:

1. Nearly all mutations are bad, and neutral mutations are rare.
   No one has ever documented a "good mutation" in Drosophila.
   
2. Biochemical mutations in bacteria aren't really MUTATIONS after all.
   

   Main "Icon": Four winged fruit flies

3. The Four-winged fruit fly could never happen in the wild.
   
4. Four-winged fruit flies are reflections of an earlier ground state.
   
5. "Four-winged fruit flies are no better than a two-headed calf" in terms of providing evidence for evolution.
   

   Bizarre conclusion:

6. Mutations aren't REALLY the raw material of evolution
   
7. The idea that DNA makes mRNA makes proteins and that genetics plays an important role in development are part of a "Darwinist conspiracy" to try and cook up false evidence for evolution.
   

As the newspaper columnist Dave Berry would say, "I'm not making this up". This really is what Wells is saying in the chapter. I would strongly encourage the interested reader to have a look at some of the references given throughout this review to get a feel for what the evidence is for the issues, and then decide for themselves. My philosophy is one of trying as best as possible to get the current ideas explained, and letting one make an informed decision on their own. It is my own personal opinion that Wells' logic in this chapter is more of an appeal to the ignorance of the reader, and that they are not really encouraged to go out and read the literature on their own (despite references to a few technical articles in an appendix).

Background and Definitions.

Although the main subject for the chapter is the results of mutations in the Ultrabithorax (Ubx) gene, the context of this in terms of this and other Hox genes and development in Drosophila, is not presented. The Hox genes are never clearly defined by Wells. The interested reader can find much more detailed information in the introductory Molecular Biology texts mentioned in the references. In order to present clearer discussion of the topic, a few definitions are necessary.

Homeotic mutation. This refers to a mutation which transforms one part of the body into another. For example, in Drosophila, homeotic mutations (found in nature) include such things as a fly with a leg coming out of its head (instead of antennae), or a fly with eyes on its legs.

Homeobox. This refers to a 180 bp piece of DNA, which encodes a 60 amino-acid conserved domain which binds to DNA, found in all homeotic genes. The homeobox genes were first discovered and characterised in the fruit fly, Drosophila melanogaster, but have since been found in several hundred different organisms, including Plants, other Animals (including humans), and Fungi. That is, any organism with some sort of multicellular "body" has these genes.

Hox genes. This is a term referring to a family of clustered HOMEOBOX genes, which play a fundamental role in the morphogenesis of the vertebrate embryo, providing cells with regional information along the main body axis. One of the amazing things about the Hox genes is that they are expressed from "top to bottom" - for example, genes at the beginning of the cluster are expressed in the head, and genes at the other end are expressed in the tail. These genes are responsible in large part for the changes in morphology we see in evolution and thus are the reason for the importance of studying hox mutations in evolutionary biology.

Ubx gene. This is a hox gene in the fruit fly Drosophila melanogaster, which is involved in wing development (amongst other things). It is expressed in certain segments of the developing fly embryo, at certain times during development. Transcription of the gene results in an initial 77,000 nucleotides (nt) piece of RNA, which is then processed to a product of 4543 nt of mRNA, and the remaining RNA (roughly 73,000 nt) is spliced out and degraded. The processed 4543 nt mRNA is then translated into a protein which is a transcription factor (389 amino acids in length). As is often the case with eukaryotic genes, the gene is alternatively spliced, and only a fraction of the transcribed RNA actually codes for proteins. In this case, one would need only 1167 nt of mRNA to code for a 389 amino acid protein - that is, only 1.5% of the gene actually codes for protein. It seems likely much of the sequence (as well as regions upstream of the gene) is involved in the regulation of when (and where) the transcription factor protein is made.

     "Loss of homeotic genes by mutation or deletion causes the appearance of a normal appendage or body structure at an inappropriate body position. An important example is the ultrabithorax (ubx) gene. When Ubx function is lost, the first abdominal segment develops incorrectly, having the structure of the third thoracic segment. Other known homeotic mutations cause the formation of an extra set of wings (p. 1072), or two legs at positions in the head where the antennae are normally found (Figure 28-40).
     "The homeotic genes often span long regions of DNA. The Ubx gene, for example, is 77,000 base pairs in length and contains introns of up to 50,000 base pairs. Transcription of this gene can easily take nearly an hour. The delay this imposes on ubx gene expression is believed to be a timing mechanism involved in the temporal regulation of subsequent steps in development. The Ubx protein is yet another transcriptional activator with a homeodomain (Figure 28-13)." (from Lehninger, 2000, page 1114).

For more details on the basics, I would encourage the interested reader to have a look at an introductory text, such as "Molecular Biology of the Cell, available on line, Link to section in "Molecular Biology of the Cell" about Drosophila and the Molecular Genetics of Pattern Formation One could also visit PubMed, and use something like the following key words, for example: "hox Drosophila review". (http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?db=PubMed)

A Brief Historical Background of Homeotic Mutations

Spontaneous homeotic mutations, while rare, have been recorded historically. Butterflies normally have 6 legs, but in homeotic mutants, they can have 8 legs. A 9th century bronze statue contains 8-legged butterflies in front of Budda (see Gehring, 1998). In 1894, William Bateson published a book which included drawings of three different, naturally occurring homeotic transformations: an antenna into legs in a beetle, hind legs into hind wings in a moth (similar to the mutation in Wells' famous Four Winged Fly), and a mutation resulting in an antenna instead of an eye in a crustacean. As Wells mentions, the first homeotic mutant in Drosophila was discovered by Calvin Bridges, in 1915 (only two years after Bateson published Mendel's work in English). This was a spontaneous mutation, in which the balancers are transformed into winglets; this mutation (bithorax) has been maintained continuously as a laboratory stock since then.

Jonathan Wells claims that four-winged fruit flies do not occur spontaneously. Perhaps he is right, but it is worth noting that similar spontaneous hox mutations have been found in other insects, such as those recorded more than a hundred years ago by Bateson. However, I really think that he's missing the point here. The significance of the discovery of the four-winged fly mutation (as well as the opposite - a fly with four halteres) is the implication that these genes play a role in specifying the body plan of the fly. Mutations in these genes results in different body plans - or so goes the prediction. Is there any evidence to confirm this? I think so - for example, the Hox gene cluster has undergone a gene duplication between invertebrates and vertebrates (this is a common occurrence in evolution - gene duplication which allows experimentation with the second copy). The evolution of the Hox genes in vertebrates has been detailed in a recent article in Nature magazine, entitled "Conservation and elaboration of Hox gene regulation during evolution of the vertebrate head" (Nature, 408:854-857, (2000)). In the abstract, the authors state "Here we present evidence for the conservation of cis-regulatory mechanisms controlling gene expression in the neural tube for half a billion years of evolution, including dependence of retinoic acid signalling." So Wells is correct that the four-winged fly is an interesting side show - but this is an example pointing to the hox genes, and the evolutionary significance lies in tracing the history of the genes themselves. To put this in perspective, Walter Gehring spends a single paragraph (out of more than 200 pages) describing the four-winged flies in his book on the homeobox genes (see Gehring, 1998).

The rest of this review will follow the same outline as laid out by Wells in chapter 9 of "Icons of Evolution".

The Origin of Variations from Darwin to DNA

As an aside, since I'm living in Denmark, I shouldn't pass this historical section without mentioning that Wilhelm Johannsen was Danish, working at the agricultural college in Copenhagen when he coined the word "gene". I was quite happy with the section on the history of the discovery of variations, although I think that Wells stops a bit short - he only brings the reader up to the 1970's - imagine someone giving a history of computers and stopping 30 years ago! A lot has happened in the field of molecular biology in the past 30 years.

There has been an explosion in the amount of sequence information. The "variations" talked about here are ultimately the result of variations in DNA sequences. The growth rate of biological sequences is breath-taking. For example, in 1970 we could only sequence very short pieces of DNA, and this took an enormous amount of time and effort. Even dreaming of sequencing the human genome was difficult. By 1980, it was possible to sequence tiny bacteriophages, and it would take more than a MILLION years to sequence the human genome, and perhaps a thousand years to even sequence a bacteria! By 1990, sequencing had improved (in large part by a very large investment of the human genome project - funded at $200,000,000 a year for 20 years!, and it would take a "mere" THOUSAND years to sequence the human genome. This month (January, 2001), a "draft" of the human genome will be published. We can now sequence the DNA from an entire bacterial genome in just a few hours! Of course, the problem comes in analysing all this amount of data. The point is, if Wells wants to talk about variations - which of course is variations in the DNA sequence - then he should take into account the explosion of information that is presently happening.

The information in GenBank is doubling every 10 7 months.

A look at genome sequencing over the past five years:

YEAR	# GENOMES Sequenced
1995	2
1996	4
1997	9
1998	17
1999	30
2000	53

Link to a table of sequenced genomes.        What does it all mean?

In all fairness to Darwin, he carried out quite a bit of correspondence with animal breeders, and was convinced that whatever the source of variation, it was not directional, but was random, and traits could be selected for in many different possible directions. Many contemporary "Darwinians" believed strongly in the idea of progression - that nature has some sort of direction, and is headed towards some goal. In contrast, Darwin thought that variation was random.

But there is a difference between "random" mutations and extremely rare chance events. Wells certainly leaves one with the impression that mutations are rare events, and that beneficial mutations are so rare as to be considered extremely unlikely. There are some scientists who believe this, but, to be honest, I have never been very happy with Jacque Monod's view that evolution is the result of some sort of rare freak accident (see Monod, 1971). I much prefer the view of Monod's colleague at the Institut Pasteur and fellow Nobel Prize winner, François Jacob (see Jacob, 1976). I think that Kuppers makes a very good and clear distinction (see Kuppers, 1986). He asks the question, "where does biological information come from?", and offers three possibilities:

1. The chance hypothesis (he cites Jacque Monod's "Chance and Necessity").
2. The teleological approach (a miracle - God supersedes the laws of nature.).
3. The molecular-Darwinistic approach (which takes into account information theory and far-from-equilibrium chemistry).

In this chapter, Wells seems to imply that the ONLY option for evolutionists is the first, or alternatively they could renounce their "faith" in evolution and believe in the second. In the book as a whole, it is this third hypothesis which Wells excludes from discussion, and really, in my opinion, it is the third option which makes the most sense here.

The question is fairly simple: what types of variation do we see in the world around us? Is it REALLY true (as Wells seems to think) that most mutations are bad, and if they are neutral, they would be simply ignored? What types of levels of variation exist in nature? So what is the evidence? What is the level of variation within Drosophila, at the level of DNA?

There are many different species of the genus Drosophila. Listed below are the sizes of several different Drosophila genomes. Note that most of the species have larger genome sizes than Drosophila melanogaster, and there's easily enough room for complete duplication of the smallest genome in many of the other organisms - in fact the genome of D. nasutoides is more than FOUR times as large.

In summary, the genome sizes of the Drosophila species that have been examined so far range from about 127 million bp to about 800 million bp. But of course at present we SUSPECT that they contain roughly the same number of genes, although it is possible (likely) that they contain duplicated regions (or perhaps even entire chromosomes; there is ample space to have an entire extra copy (or two or more) of the entire genome). In addition, they also contain various types of repeats, known as "selfish DNA". The point is that, even just looking at the SIZE of the genomes, there is an enormous amount of variation from one genome to another. Within a given species, there is also an extraordinary amount of variation - at least a lot more than was once thought. It is this large variation within different organisms of a population that is the pool for selection. There is a considerable amount of variation out there, and all that is required is some reason to select particular traits. On average, there is a mutation every third time the genome is replicated. That might sound pretty low, but consider how many copies are necessary in order to make a fly - and how short the life span of a fly is, compared to hundreds of millions of years of insect evolution, this is a tremendous amount of variation.

Beneficial biochemical mutations

Wells claims that most of the cases of "medically significant" antibiotic resistance genes are not due to mutations, but rather the acquisition of complex enzymes from other sources. I tend to disagree with him on this point - this is of interest to me because it is related to my own research, and I have just recently published a paper on this very subject. (Genetica, 108:47-51, 2000.) I apologise for going off on such a tangent, but I think I can make an important point or two, relevant to this discussion. Consider two examples:

1.The antibiotic resistance cluster found in Salmonella DT104, which contains a cluster of genes giving resistance to nearly all known antibiotics as well as disinfectants. Several of the genes are flanked by direct repeats, which imply they could have been inserted by homologous recombination. It is certainly obvious that this island is flanked by transposable elements, and is inserted into the main genome. Hence, this event in itself is a change in DNA sequence, and a "mutation". Furthermore, these genes (as well as toxin genes) often contain DNA sequences which can mutate much more readily than other "housekeeping" genes.

Here is a table of the genes encoded in the antibiotic resistance cluster in Salmonella DT104:

Now I assume that Wells means that antibiotic resistance is not due to a mutation in the function of a HOST bacterial protein, but rather results from the importation of a new protein from outside. However, if one actually examines the genes in the table above, which confer resistance to antibiotics and disinfectants, the genes appear as though they were derived from (mutated from) other genes of related function - often from within the same bacteria. You can see this from comparing the sequences of the genes in this cluster to everything in GenBank. To me, this sounds typical for what happens in evolution - you have duplication of a gene, and one copy of the original is kept, whilst the second copy can be varied with relative impunity. You see this sort of thing happen often in bacteria, as well as in eukaryotes.

I also want to mention two other examples of beneficial mutations. Perhaps it is most easy to consider mutations in the human genome which are beneficial. One example is a case in Italy, where a family has the ability to maintain very low levels of cholesterol in the blood (the mutational event has been dated back to around 1923). This is a mutation that in our sedentary society would be considered "beneficial" by many. Another example is people who can see in FOUR colours, rather than the three that many people have (or the two and a half or so that some men have). This is due to a simple duplication and mutation event in the colour rod receptor genes.

It is possible to design better enzymes in the laboratory. Most of the enzymes in nature do not have optimal activity - certainly not for most of our in vitro applications. Recently, there has been an entire sub-discipline develop around the idea of using directed evolution to select for enhanced activity for particular enzymes. I have listed below several review articles on this subject for those who are interested in reading more about this. The point is that we don't live in the "best of all possible worlds" (in the words of Voltaire's Dr. Pangloss). Enzymes can be improved, and there's no reason to believe that it is not possible for the activity of an enzyme to be selected for under some circumstances. (It seems very likely that there are conflicting sets of selective pressures - yes, it would be nice to have a better enzyme, but there are lots of other competing demands which might dampen the direction towards improvement of a particular activity.)

2. Toxin genes in Escherichia coli pO157, as shown in the figure below. In this plasmid, the genes which code for the toxin genes have a much higher AT content, and are also flanked by inverted repeats which are Insersetion Sequence (IS) elements. The higher AT content means that the genes will mutate at a higher frequency than other genomic DNA, and the IS elements encode a transposase gene which will help the genes to "splice out" and form a small circlular piece of DNA, which can then find another piece of DNA to splice itself into. This is a classic example of evolution in action - you have a copy of a gene, which can randomly place itself into (more or less) anywhere in the genome. Actually, there are some regions of the genome where it can more readily integrate, but the point is that the DNA sequences are not at all as stable as they are often presented in textbooks. For example, the Escherichia coli genome of the pathogenic strain from which this plasmid came, has a genome with an extra MILLION bp of DNA - that is, it is 25% larger than the common laboratory Escherichia coli strain that has been sequenced. The mutational frequencies of specific regions (such as for the toxin genes shown in the figure below) can be measured experimentally, and it is possible to watch the bacteria mutating within a single experiment. So is Wells saying that what I see in the laboratory not real?

I think it is a play on words to say that the introduction of a new gene in an organism is not an example of a mutation, and to pretend that it does not have anything to do with evolution. In short, I think that his statements are simply false. At this stage, it is not my intention to engage in speculation on whether this dishonesty is intentional or just simply a mistake. But nonetheless, it is my opinion that the statements in this section are simply wrong and misleading.

The Four-Winged Fruit Fly

Wells speculates (but doesn't really prove, in my opinion) that the ONLY way one could obtain a four-winged fly is by the same method of three mutations that Lewis used, and that it is impossible for a single mutation to result in the same phenotypic effect. However, I suspect that it IS indeed possible for a single mutation, in the right spot to result in a four-winged fly. There are known, spontaneous mutations resulting in the transition from two-wings to four-wings in other Dipteria, for example. Perhaps a mutation within the regulatory binding sequences upstream of the target genes could also result in the same phenotypic effect?

I'm a bit confused, when Wells says that "the mutations do not affect the protein produced by the gene, but only where the protein is produced". Which protein(s) is he talking about here? So the hox mutant is not really a mutant of the Hox protein? I am fairly sure that what he is referring to is mutations within the non-coding region of the gene (since only about 1.5% of the gene actually codes for protein). "This is all kind of a big mystery", is the feeling that I get from what is written in this chapter. Actually, I gather from reading articles in the scientific literature about this, that the important thing is not only WHERE the protein is expressed, but WHEN it is expressed. I will discuss more on the hox mutations below. Additional information about Lewis' experiments with the four-winged fruit flies can be found on the Nobel symposium web site: http://www.nobel.se/medicine/laureates/1995/illpres/lewis.html

Four Winged Fruit Flies and Evolution

I think that the four-winged fly is a striking example of how a fairly simple change in the DNA sequence of a single gene can affect the structure of an entire organism. In case "A", you have two wings, and then you have a mutation in a certain hox gene, (known as ultrabithorax, or ubx), and all of the sudden you have case "B", which has four wings. This is an impressive demonstration of the statement that a change in DNA (e.g., a "mutation") can have a large effect on the organism's architecture.

Apparently Wells hasn't done his homework on this mutation. It looks as though he doesn't understand the significance of the hox genes (or the homeodomain genes in general). This fact could certainly be used to build a more credible case, had he grasped it. There are several good entry points into the literature for those interested in learning more about the hox genes. For example, see "Insect evolution: Redesigning the fruitfly", (Current Biology, 9:R86-R89, 1999), for a good overview of the subject. Also see the article by Manzanares et al., ("Conservation and elaboration of Hox gene regulation during evolution of the vertebrate head", Nature, 408:854-857) mentioned above, and also in the "further reading" list. I will discuss more on this in the section dealing with what Wells "forgot" to mention. But let's try and put this in perspective here. I've just done a search on PubMed, a good database of references, with more than 11 million articles. Here is the result of two different searches:

"Four winged fruit fly" - 5 articles

"homeobox evolution" - 572 articles

Based on these results, does it sound like the four-winged fly is really THE "Icon" of evolution here? With more than ONE HUNDRED times as many articles about homeobox and evolution, I'd say perhaps there's more to the story about evolution than merely the four-winged fly. I narrowed the search a bit to look for articles about evolution which included the hox genes of Drosophila:

"Drosophila hox evolution" - 83 articles

But don't take my word for it - please go to PubMed and have a look for yourself:

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?CMD=&DB=PubMed

Evolution in Reverse?

Yes, it is true that the Ultrabithorax gene is large and complex, but nonetheless, it is mutations in THIS SINGLE GENE which can confer many different and striking phenotypes in Drosophila. Wells claims that because the gene regulates a hierarchy, then the WHOLE hierarchy must evolve, not just this gene. Is there any way to test this? Yes, there is. For example, the gene which is responsible for the formation of the eye in Drosophila (named "eyeless") has a counterpart in mice, based on sequence similarity. It turns out that one can take the mouse gene and use it to switch on the eye gene in flies, and also one can take the fly gene and use it to switch on the eye genes in mice. In my opinion, this clearly demonstrates that it is changes in the master regulators which can result in morphological control, and that the cascades which they regulate can change as well, but it is not necessary that the whole system evolved together. I agree that the system is complicated, but that is not the same as saying that it is impossible for it to change slowly over time.

"What the four-winged fruit fly shows us is that mutations can shut down a complex network of interactions." I think Wells is missing the point here. The four-winged fly shows us that there exists a handful of "master regulator" genes, which play an important role in developmental biology (and also in evolution - more on this below). I agree with Wells that the four-winged fly is a "back mutation" - that is, a reversion to a more primitive state. This is kind of like the existence of horses with extra (but useless) toes. But the important point here is NOT that evolutionists are trying to say that this is an example of how evolution can have a gain of function (e.g., going from two wings to four). One of the points is that evolution is not always "progressive". Another (important) point is that these genes can control morphology, and evolution of these genes coincides with evolution of morphology.

Four Winged Fruit Flies - What Jonathan Wells "forgot" to mention.

Wells concludes this section with a question: "Why, then has it become popular to feature the four-winged fruit fly in textbooks and public presentations as defending Darwin's theory?"

Here is where I think he totally misses the point - the four winged fruit fly is a symbol of the power of developmental genetics to change the morphology of an organism. Perhaps I should go into more detail here. I apologise if this might seem boring to some, but there is a wonderful story here about evolution that Wells conveniently forgets to mention in his zeal to attack the Windmill Icon of the four-winged fly.

The four-winged fruit fly results from a mutation in the ubx gene, as is stated in this chapter. But what is known about this gene? If this is the reader's first experience into Drosophila genetics, they could well think that not much is known about this gene (or indeed, whether it is even true that genes play an important role in genetics). Are there any good resources available which contain information about the hox genes in Drosophila? A good place to start is The WWW Virtual Library: Drosophila (http://ceolas.org/fly/). There are a number of good links found here, including one to "FLYBASE - A Database of the Drosophila Genome", which is a wonderful hypertext encyclopedia, dedicated to Drosophila. (http://flybase.bio.indiana.edu:82/)

There are a few facts which I think are of particular interest to this review. Note that there are 310 different recorded mutant alleles, and quite a few references on this gene.) I accessed this page on the 27th of December, 2000, but many of the links are automatically updated with time. For those really interested in knowing more about Drosophila genetics of the Ubx gene, I would strongly recommend having a look at the web page for many links as well as updated reports. http://flybase.bio.indiana.edu:82/.bin/fbidq.html?FBgn0003944&content=short-report

Beyond the Gene.

As I mentioned before, this section is downright bizarre. Wells talks about "epigenetic factors" and seems to think that the "central dogma" of molecular biology is suspect, and that there's some sort of conspiracy amongst the evolutionists to try and cover up the evidence that DNA does not really code for proteins, and that genetics is not what is REALLY determining cellular differentiation.

"DNA sequences do not uniquely determine the sequence of amino acids in proteins, much less the larger features of cells or embryos."

- anonymous German researcher,
quoted by Wells on pages 192-193 of Ch. 9

I was thinking the other day about what Wells had said in this chapter when discussing the new "Drosophila DNA chip" with a visiting scientist from Affymetrix, a California-based company who manufactures DNA chip microarrays. These chips can be used to quantitate the expression of all of the genes in Drosophila melanogaster, in a single experiment, all at once. It is truly remarkable what modern technology can do. Maybe I should have told the person from the company selling the chips that a thousand dollars is an awful lot of money to pay for something which won't give us any useful information, since we're not really sure if the idea that DNA codes for mRNA which makes protein is really true, according to Wells. Perhaps I should write a letter to Science magazine, telling them that the special issue about sequencing the Drosophila genome which came out last spring (March, 2000) was all bogus, and just a bunch of bull, according to Wells. And I guess the hundreds of thousands of papers published about gene expression in Drosophila melanogaster are all simply fabrications, right? I mean, after all, what are the chances that they could all be right, when we have reason to believe this is not true, based on a murky implication by Jonathan Wells?

But the idea that DNA has nothing to do with development in Drosophila melanogaster is not the main point of this chapter. The main point of course has to do with the hoax of the four-winged fruit fly. Yes, it really exists, Wells tells us, but only in certain cases where you have THREE cleverly designed mutations, and this could never happen in nature. Anyway, the muscles in this particular mutant aren't developed properly, so therefore anyone who uses the Ubx gene as an example of evolution is misleading the public. So what does the evidence say? Is there REALLY some kind of "Darwinian conspiracy" to dupe the public into believing that four-winged flies tell us something about evolution (and that DNA contains the genetic material), in order to lure them into believing in materialism? I will leave it to the reader to decide.

Summary

Preamble:

1. Nearly all mutations are bad, and neutral mutations are rare.
   Neutral mutations are VERY common, and often result from gene duplications and horizontal gene transfer.
   
   No one has ever documented a "good mutation" in Drosophila.
   There are several documented "good mutations" in Drosophila - see the references below.
   
   
2. Biochemical mutations in bacteria aren't really MUTATIONS after all.
   Mutations in bacteria are the result of changes in the DNA sequence of bacterial proteins - this is indeed an example of evolution.

   Main "Icon": Four winged fruit flies

3. The Four-winged fruit fly could never happen in the wild.
   I think it's a bit dangerous to say NEVER, but whether four-winged flies can or can't happen spontaneously is not that important to the discussion here.
   
   
4. Four-winged fruit flies are reflections of an earlier ground state.
   I agree with Wells here. YES, they are reflections of an earlier ground state - this is an example that evolution is not always "progressive" (that is, going from two wings to four wings).
   
   
5. "Four-winged fruit flies are no better than a two-headed calf" in terms of providing evidence for evolution.
   The four-winged flies are a very clear example of how genes can control development, and point to a set of genes which play a very important role in determing the morphology of an organism.
   
   

   Bizarre conclusion:

6. Mutations aren't REALLY the raw material of evolution
   I think the evidence is clear that variations (that is, MUTATIONS in DNA sequences) do exist in abundance in nature, and that these variations are continually being selected upon in evolution.
   
   
7. The idea that DNA makes mRNA makes proteins and that genetics plays an important role in development are part of a "Darwinist conspiracy" to try and cook up false evidence for evolution.
   There are entire journals devoted to the subject of "Genes and Development", with new research articles being published in this exciting area continuously. No we don't know ALL the answers, but that doesn't mean that we know nothing at all about the relationship between genes and development of embryos.
   
   

1. Master Control Genes in Development and Evolution: The Homeobox Story (Terry Lectures), by Walter J. Gehring, (Yale University Press, 1998).     Amazon.com     Barnes&Noble
   
   
   

   Some good introductory text books:

2. Molecular Cell Biology, 4th edition, by H. Lodish et al.; (W.H.Freeman &s; Co., New York, USA, 2000). An entire chapter (Chapter 14 - Gene Control and Development, pages 537-577) is devoted to the subject of the roles genes play in development, (contrary to Wells' claim that genes don't play a major role in development), and includes a section on the four-winged fly and the Ubx gene.

3. GENETICS - Principles and Analysis, 4th Edition, by Daniel L. Hartl and Elizabeth Jones (Jones and Bartlett Publishers, Sudbury, Massachusetts, 1997). See Chapter 12 (The Genetic Control and Development), pages 537-553, for a very good discussion of the subject, including a quite nice section on development in Drosophila.

4. Lehninger Principles of Biochemistry, revised and updated by David L. Nelson, and Michael M. Cox, 3rd edition; (Worth Publishers, New York, USA, 2000). For a good discussion of the role of genes in development, see the sections at the end of Chapter 28 ("Regulation of Gene Expression"), on pages 1109 to 1115.
   
   
   

   Other books mentioned in the review:

   
   

5. Materials for the Study of Variation, by William Bates, (McMillan, New York, 1894).

6. CHANCE and NECESSITY - An Essay on the Natural Philosophy of Modern Biology, by Jacques Monod (translated from the French by Austryn Wainhouse; Vintage Books, A Division of Random House, New York, 1971).     Amazon.com     Barnes&Noble

7. The Logic of Life- A History of Heredity, by François Jacob, (Vintage Books, New York, 1976).     Amazon.com     Barnes&Noble

8. Information and the Origin of Life, by Bernd-Olaf Kuppers (The MIT Press, Cambridge, Massachusetts, 1990; translated by Manu Scripta, Aarhus, Denmark - originally published under the title Der Ursprung biologischer Information: Zur Naturphilosophie der Lebensentstehung, in 1986 by R. Piper BmbH & Co.)     Amazon.dk (original book, in German)     Amazon.com (U.S., in English)     Barnes&Noble

9. The Ontogeny of Information : Developmental Systems and Evolution, by Susan Oyama, Richard C. Lewontin (Duke University Press, Durham, North Carolina, 2000)     Amazon.com     Barnes&Noble

10. The Touchstone of Life : Molecular Information, Cell Communication, and the Foundations of Life, by Werner R. Loewenstein (Oxford University Press, New York, 1999)     Amazon.com     Barnes&Noble

11. FOSSILS - The Evolution and Extinction of Species, by Niles Eldredge, (Princeton University Press, New Jersey, 1997). This is a very nice coffee-table book, with lots of colour photos of fossils, including the background for this html page. Of course, Niles Eldredge also writes excellent text to go with the wonderful pictures. I would highly recommend having a look at this book, for the aesthetic beauty as well as for the science.      Amazon.com     Amazon.com.UK (England)     Barnes&Noble

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