Dawkins answers Behe in three ways. First, after the sneers, he quotes Judge John E. Jones’s decision in the Dover case, labeling the Dover citizens’ efforts to discuss intelligent design and to freely criticize Darwin’s theory in schools “breathtaking inanity”. Then he extols biologist Ken Miller’s speculations as to how the bacterial flagellar motor ‘could have’ evolved as offering decisive refutation of Behe’s concept of irreducible complexity. Neither of Dawkins’ answers involves a scientific refutation of Behe.

Finally, Dawkins offers science, and I assume it’s his best shot. He points out that dog breeding provides evidence that mutation rates don’t limit evolutionary change. He cites Jack Russell terriers! We’ll leave aside Dawkins’ highly questionable assumption that the variation with which dog breeders work is primarily the result of new mutations, rather than established variation in the population. In his dog breeding analogy, Dawkins uses a bit of ‘pseudo-Darwinism’, a rhetorical tic in which Darwinists try to defend Darwin’s theory of random variation and natural selection by invoking either non-random variation (bioengineering) or artificial selection (breeding). Dawkins’ invocation of pseudo-Darwinism means one thing: he doesn’t have actual convincing examples of the generation of significant new specified biological complexity by real Darwinism- random mutation and natural selection. Which is Behe’s point.

Dawkins was unable to offer a convincing example of natural selection, so he used artificial selection. I’ll use an example of the real thing:

Imagine that I am a microbiologist, and I culture bacteria in a medium containing an antibiotic, and put the culture of bacteria in an incubator while I go on vacation. I return a week later. When I open the incubator, I find two changes in the culture. The bacteria have developed resistance to the antibiotic, and there are cockroaches crawling in the petri dish. I conclude two things:

1) Random mutation and natural selection are likely responsible for the bacterial resistance to the antibiotic.
2) Random mutation and natural selection are not responsible for the cockroaches. They didn’t evolve from the bacteria in a week. They came from somewhere else (they crawled into the incubator from the outside).

Yet, according to Darwin’s theory, cockroaches really did evolve from ‘bacteria-like’ ancestors over billions of years. So, what’s the threshold of time after which I could plausibly infer that random mutation and natural selection was an adequate explanation for the cockroaches, starting with bacteria? How long would I have to leave the bacteria in the incubator before it would be plausible to infer that the cockroaches evolved from the bacteria? A million years? A billion years? Perhaps a trillion years?

So I ask Dr. Dawkins:

1) How long could I leave the bacteria in the incubator before I could reasonably infer that the cockroaches evolved from the bacteria by random mutation and natural selection? Please provide me with the experimental evidence (data and journal references) that you use to arrive at your answer.
2) If you can’t tell me, then why isn’t Dr. Behe’s question- what are the limits to what Darwinism can accomplish- a fair question?

The New Gene Expression Theory

Genes are activated or deactivated throughout life and not every gene is expressed in every cell. Activated genes are expressed by being transcribed and translated. All genes are surrounded by DNA sequences that control their expression. Proteins called transcription factors bind to these sequences and can switch the genes on or off. Gene expression is therefore controlled by the availability and activity of different transcription factors. As transcription factors are proteins themselves, they must also be produced by genes, and these genes must be regulated by other transcription factors. Will the scientists ever explain, in godless way, how the first genes could assemble without pre-existing genetic material and how the further evolutes developed without highly specified, pre-existing information? Till now all the answers are speculatively theoretical without any laboratory experimental proof.

Science Daily — An international research consortium just published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood.

"This impressive effort has uncovered many exciting surprises and blazed the way for future efforts to explore the functional landscape of the entire human genome," said NHGRI Director Francis S. Collins, M.D., Ph.D. "Because of the hard work and keen insights of the ENCODE consortium, the scientific community will need to rethink some long-held views about what genes are and what they do, as well as how the genome's functional elements have evolved. This could have significant implications for efforts to identify the DNA sequences involved in many human diseases."

The completion of the Human Genome Project in April 2003 was a major achievement, but the sequencing of the genome marked just the first step toward the goal of using such information to diagnose, treat and prevent disease. Having the human genome sequence is similar to having all the pages of an instruction manual needed to make the human body. Researchers still must learn how to read the manual's language so they can identify every part and understand how the parts work together to contribute to health and disease.

In recent years, researchers have made major strides in using DNA sequence data to identify genes, which are traditionally defined as the parts of the genome that code for proteins. The protein-coding component of these genes makes up just a small fraction of the human genome -- 1.5 percent to 2 percent. Evidence exists that other parts of the genome also have important functions.

However, until now, most studies have concentrated on functional elements associated with specific genes and have not provided insights about functional elements throughout the genome. The ENCODE project represents the first systematic effort to determine where all types of functional elements are located and how they are organized.

In the pilot phase, ENCODE researchers devised and tested high-throughput approaches for identifying functional elements in the genome. Those elements included genes that code for proteins; genes that do not code for proteins; regulatory elements that control the transcription of genes; and elements that maintain the structure of chromosomes and mediate the dynamics of their replication.

The collaborative study focused on 44 targets, which together cover about 1 percent of the human genome sequence, or about 30 million DNA base pairs. The targets were strategically selected to provide a representative cross section of the entire human genome. All told, the ENCODE consortium generated more than 200 datasets and analyzed more than 600 million data points.

"Our results reveal important principles about the organization of functional elements in the human genome, providing new perspectives on everything from DNA transcription to mammalian evolution. In particular, we gained significant insight into DNA sequences that do not encode proteins, which we knew very little about before," said Ewan Birney, Ph.D., head of genome annotation at the European Molecular Biology Laboratory's European Bioinformatics Institute (EBI) in Hinxton, England, who led ENCODE's massive data integration and analysis effort.

The ENCODE consortium's major findings include the discovery that the majority of DNA in the human genome is transcribed into functional molecules, called RNA, and that these transcripts extensively overlap one another. This broad pattern of transcription challenges the long-standing view that the human genome consists of a relatively small set of discrete genes, along with a vast amount of so-called junk DNA that is not biologically active.

The new data indicate the genome contains very little unused sequences and, in fact, is a complex, interwoven network. In this network, genes are just one of many types of DNA sequences that have a functional impact. "Our perspective of transcription and genes may have to evolve," the researchers state in their Nature paper, noting the network model of the genome "poses some interesting mechanistic questions" that have yet to be answered.

Other surprises in the ENCODE data have major implications for our understanding of the evolution of genomes, particularly mammalian genomes. Until recently, researchers had thought that most of the DNA sequences important for biological function would be in areas of the genome most subject to evolutionary constraint -- that is, most likely to be conserved as species evolve. However, the ENCODE effort found about half of functional elements in the human genome do not appear to have been obviously constrained during evolution, at least when examined by current methods used by computational biologists.

According to ENCODE researchers, this lack of evolutionary constraint may indicate that many species' genomes contain a pool of functional elements, including RNA transcripts, that provide no specific benefits in terms of survival or reproduction. As this pool turns over during evolutionary time, researchers speculate it may serve as a "warehouse for natural selection" by acting as a source of functional elements unique to each species and of elements that perform the similar functions among species despite having sequences that appear dissimilar.

Other highlights of the ENCODE work include:

• Identification of numerous previously unrecognized start sites for DNA transcription.
• Evidence that, contrary to traditional views, regulatory sequences are just as likely to be located downstream of a transcription start site on a DNA strand as upstream.
• Identification of specific signatures of change in histones, which are the proteins that organize DNA, and correlation of these signatures with different genomic functions.
• Deeper understanding of how DNA replication is coordinated by modifications in histones.

"Teamwork was essential to the success of this effort. No single experimental approach can be used to identify all functional elements in the genome. So, it was necessary to conduct multiple, diverse experiments and then analyze them using multiple computational methods," said Elise A. Feingold, Ph.D., program director for ENCODE in NHGRI's Division of Extramural Research, which provided most of the funding for the pilot project.

Note: This story has been adapted from a news release issued by NIH/National Human Genome Research Institute.

 Example of Degeneration

The taxonomic relationship of mycoplasmas to other microbes has been controversial (Razin, 1992). Prior to the 1930's, mycoplasmas were considered to be viruses because they were so small that they passed through filters that blocked passage of ordinary bacteria. Later they were thought to be symbionts growing with the Streptobacillus bacteria, and then they were proposed to be ordinary bacteria that had lost their cell wall (L form bacteria). By the 1960's, both base composition and hybridization analysis of the genomic DNA showed that mycoplasmas were not related to stable L forms of ordinarily walled bacteria. However, current explanations for the evolution of mycoplasmas argue for "degenerative" evolution from walled bacteria; thus the induction of L forms may be a present-day recapitulation of one step in mycoplasma evolution.

QUOTES

Professor Fred Alan Wolf:

I believe that the findings of quantum physics increasingly support Plato [who taught that there is a more perfect, non-material realm of existence]. There is evidence that suggests the existence of a non-material, non-physical universe that has a reality even though it might not as yet be clearly perceptible to our senses and scientific instrumentation. When we consider out-of-body experiences, shamanic journeys and lucid dream states, though they cannot be replicated in the true scientific sense, they also point to the existence of non-material dimensions of reality. (1998:24)

Development of Novel Forms

Notable differences in the developmental pathways of similar organisms have been observed. For example, congeneric species of sea urchins (from genus Heliocidaris) exhibit striking differences in their developmental pathways (Raff 1999:110-121). Thus, it might be argued that such differences show that early developmental programs can in fact be mutated to produce new forms. Nevertheless, there are two problems with this claim. First, there is no direct evidence that existing differences in sea urchin development arose by mutation. Second, the observed differences in the developmental programs of different species of sea urchins do not result in new body plans, but instead in highly conserved structures. Despite differences in developmental patterns, the endpoints are the same. Thus, even if it can be assumed that mutations produced the differences in developmental pathways, it must be acknowledged that such changes did not result in novel form.

Degeneration

During the 19th century--before Darwin's publications--scientists considered the human race to be targeted by a process of degeneration due to abandonment of the "natural" environment. Numerous physical and behavioral signs and symptoms of degeneration were subsequently described by anthropologists and by physicians in the dawn of a scientific psychiatry. The degeneration hypothesis became so influential, particularly in psychiatry, because it served as the first causal explanation for almost all psychiatric disorders, as well as for criminal behavior. Degeneration was also strongly associated with the idea of the inheritance of acquired traits (Lamarckism), which was still accepted in part in the beginning of the 20th century (see overview in Hermle 1986). For example, the concept of germ lesion, or "blastophthoria," was advocated by Emil Kraepelin (1908) as a model of "inheritance" of various psychiatric disorders, including paralysis and alcoholism. The scientific underpinnings, however, were rather vague, and Lamarckism had been discarded, at least outside psychiatry. (Ironically, the degeneration paradigm has recently resurfaced in the concept of "anticipation," the increasingly earlier manifestation of "triplet repeat" disorders in subsequent generations, which has been demonstrated in a variety of autosomal dominant and X-chromosome-linked neurological disorders, but not [yet] in psychiatric disorders [Spitzer and Hermle 1995].)

The Irony

Although evolution theory is very popular, still there is no complete explanation how it works and worked at the biochemical level