Darwin, Then and Now

Posts Tagged ‘genetics’

Jerry Coyne, in his new book entitled Why Evolution is True, conveniently circumvents any reference to the butterfly, as does Darwin-Discovering the Tree of Life by Niles Eldridge. The California State sponsored website, “Understanding Evolution,” website completely ignores the notorious nature of butterflies—metamorphosis.

So, why is the evolution industry silent on butterfly metamorphosis? The answer is simple—the same DNA is found in all four life cycles; egg, caterpillar (larva), cocoon (pupa) and butterfly (adult). Metamorphosis, to the theory of evolution, is an enigma.

For over 3,500 years, to the Egyptians, Chinese, and Greeks, the butterfly symbolism was derived from the unique butterfly life cycles. The egg first develops into the caterpillar before transitioning into the cocoon. Amazingly, inside the cocoon, the caterpillar is destroyed before developing into the stunningly colorful butterfly cycle.

According to the theory of evolution, the DNA (genotype) determines the form (phenotype). The fact that the metamorphosis of the butterfly uses the same DNA in all four cycles, contradicts the theory of evolution. 

With the same DNA producing different forms, the message is clear: DNA is not the blueprint controller of life. Genetic evidence from the butterfly undermines the Central Dogma of evolution—“one gene, one protein.”

The butterfly is not an isolated phenomenon. Italian geneticist Giuesppe Sermonti points out that “examples of highly divergent forms possessing one and the same DNA are so conspicuous and so numerous that the marvel is that they have attracted so little attention.”

Even more astounding in the case of the butterfly, Sermonti notes, “what we call metamorphosis is not really a change in form. Once the pupa, or chrysalis, stage is reached, the caterpillar starts emptying itself: its organs dissolve, and its outer covering is shed. Only certain groups of cells, called marginal disks, remain vital. From these cells develop all the structures of adult.”

The larva of the butterfly not only changes form, but actually dissolves before rebuilding into the structure of a butterfly—a new life-form. From the same DNA arises a completely different organism. According to Sermonti, the same DNA, then, can play different roles: “DNA may lend itself to such diverse forms, but it is not the DNA that imposes the blueprint.”

The presence of the same DNA in different life-forms has been given the term “genomic equivalence”. This means that control of the cell is beyond the DNA, or “epigenetic.”

Brian Goodman, Canadian developmental biologist and key founder of theoretical biology, focuses on the methods of mathematics and physics to understand processes in biology concludes –

While genes are responsible for determining which molecules an organism can produce, the molecular composition of organisms does not, in general, determine their form.

H. Frederik Nijhout of the Department of Biology at Duke University, a critic of Crick’s central dogma, came to the conclusion that “the only strictly correct view of the function of genes [DNA] is that they supply cells, and ultimately organisms, with chemical materials.”

The butterfly nightmare phenomena in evolution adherents are real, the result of the holding on to the belief: DNA mutation + natural selection = evolution—a theory not supported by evidence in nature.

State funded evolutionary education along with the high priests of evolution, Jerry Coyne, and Niles Eldridge, should now deliver a therapeutic service to humanity by addressing blatant contradictions between the theory of evolution and natural history.

No wonder French geneticist, discoverer of the Down syndrome, Jérôme Lejeune, cut to the chase – “There is no theory of evolution.”

This year, 2010, has not been a good year for the “out of Africa” evolutionary theory of human origins. The following is why.

In October 2009, Time Magazine recognized Ardipithecus ramidus, now known as “Ardi,” the number one of “Top 10 Scientific Discoveries” of 2009. The journal Science declared Ardi the “breakthrough of the year.”

Ardi, an nearly complete fossilized female skeleton, was discovered by Timothy Douglas White, an American Paleoanthropologist and Professor of Integrative Biology at the University of California, Berkeley in the arid badlands near the Awash River in Ethiopia in 1994.

Examination and description of Ardi took nearly 15 years before releasing publication. Although it is not known whether Ardi’s offspring actually developed into Homo sapiens, the discovery was expected to be of great significance since Ardi is the oldest known hominid fossil. Ardi had been theorized to be an ancestor to Australopithecus afarensis, more commonly known as Lucy.

John Noble Wilford, science writer for the New York Times reported that David Pilbeam, a professor of human evolution at Harvard University said that the Ardi skeleton represents “a genus plausibly ancestral to Australopithecus [Lucy]” and began ‘to fill in the temporal and structural ‘space’ between the apelike common ancestor and Australopithecus.”

In the excitement, the Discovery Channel produced a series of articles and videos arguing how Ardi, not the chimpanzee, were the common ancestors to humans. The American Association for the Advancement of Science, publisher of the journal Science, developed an educational series in five separate publications on Ardi.

Since Ardi was discovered in east Africa, the finding gained further support for the popular “out of Africa” model first proposed by Charles Darwin. In The Descent of Man, Darwin hypothesized - 

In each great region of the world the living mammals are closely related to the extinct species of the same region. It is, therefore, probable that Africa was formerly inhabited by extinct apes closely allied to the gorilla and chimpanzee; and as these two species are now man’s nearest allies, it is somewhat more probable that our early progenitors lived on the African continent than elsewhere

Almost fifty years after the publication of The Descent of Man, Darwin’s speculations seemed to be supported following the discovery of numerous hominid fossils in several areas of Africa. The “out of Africa” model continued to be the most widely recognized theory since the publication of the Descent of Man—until May 2010.

Svante Pääbo of the Department of Evolutionary Genetics at the Max-Planck Institute for Evolutionary Anthropology in Germany published in the journal Science in May 7, 2010, an article on the sequencing of the genome of the Neanderthal man entitled “A Draft Sequence of the Neanderthal Genome”.

According to Gregory Hannon of Cold Spring Harbor Laboratory in Laurel Hollow, N.Y., Svante Pääbo’s “publication of the full Neanderthal genome is a watershed event, a major historical achievement.” Pääbo noted, “In some of us they live on, a little bit” with on major caveat – not in African descendants.

Mark Henderson, science writer for The Sunday Times, London, explains – “Human genomes from France, China, and Papua New Guinea showed Neanderthal signatures, but not those from West and Southern Africa.” The absence of Neanderthal genetic evidence in Africans has devastated Darwin’s treasured “out of Africa” theory pushing the relevance of Ardi as an ancestor to humans into extinction.

Genetics is not Ardi’s only problem with the “out of Africa” theory—so is the paleontological analysis. Time Magazine, and the journals Nature and Science, after more thoroughly examining the available data, has started slow process of recanting on the role of Ardi as an early ancestor to man.

In the Time article entitled “Ardi: The Human Ancestor Who Wasn’t” now highlight that “Two new articles being published in Science question some of the major conclusions of Ardi’s researchers, including whether this small, strange-looking creature is even a human ancestor at all.”  

The British science journal Nature reports: “Ardi may be more of an ape than human.” In the article, Esteban Sarmiento, a primatologist at the Human Evolution Foundation argues in the article Comment on the Paleobiology and Classification of Ardipithecus ramidus, that the Ardi could not be an evolutionary ancestor to humans:

[White] showed no evidence that Ardi is on the human lineage…. Those characteristics that he posited as relating exclusively to humans also exist in ape and ape fossils that we consider not to be in the human lineage.

With Ardi as the celebutante, the evolution industry, in desperation to connect the dots for a human evolution theory, has once again fallen into another humiliating about-face based on the inescapable scientific evidence.

As the “out of Africa” model undergoes extinction, scientists are beginning to investigate the “multiregional origin of humans” theory in which man is simply “a single, continuous human species”—a theory approaching the recorded biblical account for the origin of man.

The fruit fly is celebrating 100 years of research. Charles W. Woodworth at the University of California, Berkley, at the turn of the twentieth century, was the first to use the fruit fly as model in the study of genetics. Today, Drosophila melanogaster, the common fruit fly, has become one of the most studied organisms in biological research, particularly in the field of genetics.

In 1910 following Woodworth’s footsteps, at Columbia University from the top floor of Schermerhorn Hall, now known as the Fly Room, Thomas Hunt Morgan confirmed and extended Gregor Mendel’s basic principles of genetics. A year later, Morgan published his findings in Science, establishing the foundation for the emerging neo-Darwinism movement.

Morgan, in the book entitled The Mechanism of Mendelian Inheritance (1915) demonstrated how mutations using radiation on two-winged fruit flies resulted in four-winged fruit flies. The four-winged fruit fly was widely heralded as the earliest evidence that the first evolutionary step to produce a new species was a mutation.

The question, however, centered on whether the mutated four-winged fruit fly was a new species or an unsustainable aberrational freek. By 1963 after decades of research, the question could be answered definitively. Ernst Mayr, Charles Darwin’s twentieth century Bulldog, viewed the mutated four-winged fruit flies as “such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination.” Mutation is not the gateway to evolution.

While mutations on the two-winged fruit fly served as a window to study theroretical evolutionary genetics for decades, mutations are now known not supply the raw materials for evolution. Italian geneticist Giueseppe Sermonti explains –

One spur to research on mutations was the hope that an accumulation of these might lead to a new species. But this never happened.

The fruit fly as a model for evolution via mutations gets even worse—there are no “slight, successive” genetic changes even between over 1,400 closely related Drosophila species.

The number of nucleotide base pairs Drosophila species ranges from 127 to 800 million. The probability of constructing a Tree of Life with “slight, successive” changes in nucleotide base pairs from species to species approaches the realm of impossible.

Each species of Drosophila appears to remain distinct and unique. The following table is the number of estimated genome sizes as measured by the number of nucleotide base pairs in several different Drosophila genomes.

Pierre-Paul Grassé, past-president of the French Academie des Sciences in the book entitked  Evolution of Living Organisms concludes – “The fruit fly [Drosophila melanogaster],the favorite pet insect of the geneticists, whose geographical, biotopical, urban, and rural genotypes are now known inside out, seems not to have changed since the remotest times”—evolution never happened. 

No wonder genetic researchers at Bioinformatics Research Center, North Carolina State University now bring into question whether genes even play a role in evolution between related Drosophila species. Wen-Ping Hsieh and collegues published in Genetics -

An emerging issue in evolutionary genetics is whether it is possible to use gene expression profiling to identify genes that are associated with morphological, physiological, or behavioral divergence between species and whether these genes have undergone positive selection. (1)

Genetic researchers from the Department of Ecology and Evolutionary Biology, University of Arizona, similarly discovered that “no strong evidence” in gene selection exists between Drosophila species and the respective proteins produced, “divergent expression”. Between Drosophila species, changes in genes do not correllate with changes in proteins. Jeffrey M. Good and collegues in an article published in Molecular Biology and Evolution, 2006, conclude -

Overall, we found no strong evidence for an increase in the incidence of positive selection on protein-coding regions in genes with divergent expression in Drosophila (2)

Genomic research looking for the “slight, successive” genetic changes required by neo-Darwinism is no friend of evolution. The survivors of 100 years of lab torture continue just as fruit flies.

The genome of D. melanogaster was sequenced in 2000. Most surprisingly, nearly 75% of known human disease genes are now known to have a recognizable match in the genetic code of fruit flies, and 50% of fly protein sequences have mammalian homologs. Mutations are either neutral or lead to disease—not evolution.

Today, over 100 years later, Drosophila serves as a genetic model for several human diseases including the neurodegenerative disorders Parkinson’s, Huntington’s, spinocerebellar ataxia and Alzheimer’s disease.

Reflecting on the limits of genetics in establishing the validity of evolution, Italian geneticist Giuseppe Sermonti weighs in –

Science has taken on the great wager … and lost.

1.  Wen-Ping Hsieh, Tzu-Ming Chu, Russell D. Wolfinger, and Greg Gibson. Mixed-Model Reanalysis of Primate Data Suggests Tissue and Species Biases in Oligonucleotide-Based Gene Expression Profiles. Genetics. 2003. 165: 747-757

2.  Jeffrey M. Good, Celine A. Hayden, and Travis J. Wheeler. Adaptive Protein Evolution and Regulatory Divergence in Drosophila. Molecular Biology and Evolution. 2006, 23(6):1101-1103

Genetic evidence now points to one ugly fact for the theory or evolution; Autism and Alzheimer’s disease are the result of genetic mutations.

ScienceDaily on May 3 reported that investigators at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, that new research has uncovered two additional genes involved with autism.

An estimated one in 110 U.S. children has autism, which negatively affects behavior, social skills, and communication.

The risk for the disorder can be now be considered an inherited genetic disease, based on a study performed by professors Daniel Notterman at Penn State, and Ning Lei at Princeton University.

Lei and colleagues analyzed data from the Autism Genetic Resource Exchange (AGRE) on 943 families, most of whom had more than one child diagnosed with autism and had undergone genetic testing. Investigators compared the prevalence of 25 gene mutations in the AGRE families with a control group of 6,317 individuals without developmental or neuropsychiatric illness.

Mutations in four genes within the AGRE families were identified. Two of the genes previously were shown to be associated with autism and often are involved in forming or maintaining neural synapses — the point of connection between individual neurons.

One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain — a region previously associated with autism.

“While mutations in the NCAM2 gene were found in a small percentage of the children that we studied, it is fascinating that this finding continues a consistent story — that many of the genes associated with autism are involved with formation or function of the neural synapse,” Dr. Lei said. “Studies such as this provide evidence that autism is a genetically based disease that affects neural connectivity.”

According to Jerry Coyne in his widely acclaimed book entitled Why Evolution is True, evolution originates from mutations. Coyne explains,

The first is the idea of evolution itself. This simply means that a species undergoes genetic change over time. That is, over many generations a species can evolve into something quite different, and those differences are based on changes in DNA, which originate as mutations.

With Autism, however, the genetic change is certainly not beneficial. The same is true for the newly discovered genetic mutation associated with Alzheimer’s disease.

 In the June 10 online issue of the journal Cell, researchers from New York Universty’s Center of Excellence on Brain Aging and the Silberstein Alzheimer’s Institute, reported their findings that a mutation of a gene associated with early onset Alzheimer’s blocks a key recycling process necessary for brain cell survival.

The gene, presenilin 1 (PS1), performs a crucial house-cleaning service by helping brain cells digest unwanted, damaged and potentially toxic proteins. Once mutated, however, the gene fails to recycle and eliminate the potential toxins from causing cellular damage to brain cells resulting in Alzheimer’s disease.

“We believe we have identified the principal mechanism by which mutations of PS1 cause the most common genetic form of Alzheimer’s disease,” said study co-author Ralph A. Nixon, professor in the departments of psychiatry and cell biology as well as director at New York University.

Scientific evidence from Autism to Alzheimer’s disease, rather than supporting evolution as campaigned evolution militants like Jerry Coyne and Richard Dawkins, contradicts the theory of evolution.

Evolution is a theory in crisis. No small wonder, even ardent atheists Fodor and Piattelli-Palmarini were compelled to write “Why Evolution is Not True” (2010).  

In a letter to Sir Joseph Dalton Hooker, his closet friend in 1857, Charles Darwin confided,

I cannot swallow Man [being that] distinct from a Chimpanzee.

Charles Darwin writes in his Autobiography,

My Descent of Man was published in Feb. 1871. As soon as I had become, in the year 1837 or 1838, convinced that species were mutable products, I could not avoid the belief that man must come under the same law

The chimp, since the nineteenth century, has been the poster-child missing link to humans. In twenty-first century terms, the mammalian Y chromosomes were expected to be similar, as speculated by Darwin. However, new evidence demonstrates Darwin’s speculation to be wrong—the chimp Y chromosome differs radically from humans.

The British journal Nature published a paper in January 2010 titled, “Chimpanzee and Human Y Chromosomes are Remarkably Divergent in Structure and Gene Content,” found that Y chromosomes in the chimp and humans “differ radically in sequence structure and gene content”. In fact,

More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome

Jennifer F. Hughes led the research team at the Whitehead Institute for Biomedical Research, one of the world’s leading centers for genomic research, is located in Cambridge, Massachusetts. The research team concluded –

By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content

“By conducting the first comprehensive interspecies comparison of Y chromosomes,” ScienceDaily noted, “Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys… The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content.”

The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections had typically confound standard sequencing techniques. The chimp Y chromosome is only the second Y chromosome to be comprehensively sequenced.

 Wes Warren, Assistant Director of the Washington University Genome Center, noted

These findings demonstrate that our knowledge of the Y chromosome is still advancing.

Earlier comparative studies between the chimp and human genome had centered on DNA regions that only result in the production of proteins. In addition, not only is the chimp DNA 12% larger than human DNA, the Chimp has 23 chromosomes while humans have only 22 (excluding sex chromosomes in both species).

While the researchers advance the concept that “divergence” from the Chimp occurred 6 million years ago, the more logical explanation is that the chimp is simply a distinct species.

The research was funded by the National Institutes of Health (NIH) and the Howard Hughes Medical Institute (HHMI)