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. Continue reading more

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.

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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.

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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)

In 1943, published in a paper entitled “Mutations of Bacteria from Virus Sensitivity to Virus Resistance,” microbiologist Salvador Luria, biophysicist Max Delbrück, and bacteriologist and geneticist Alfred Hershey discovered that mutations occur at a constant rate. In 1969, they were awarded the Nobel Prize in Physiology and Medicine “for their discoveries concerning the replication mechanism and genetic structure of virus.”

The Luria-Delbrück Experiment opened the question, are mutations inherent to microbes for the purpose of adaption to rapidly changinging environments and not for evolution? While microbe resistance through mutation is a logical mechanism for evolution, the reality is the bacteria have remained a bacteria and the virus has remained a virus. Preexistent genetic variants determine the range of mutations. Pierre-Paul Grassé, president of the French Academy of Sciences, observed, “bacteria, the study of which has formed a great part of the foundation of genetics and molecular biology … stabilized a billion years ago.”

The question is whether the mutations are the “raw material for evolution” or nature’s means for the microbes to adapt to the environment. In a 2009 review article by entitled “Darwinian evolution in the light of genomics”, published in Nucleic Acid Research, Eugene V Koonin concluded, “There is no consistent tendency of evolution towards increased genomic complexity” through mutation as expected with current evolutionary theories. Mechanisms of evolution remain beyond any known natural law.

Reflecting on the role of mutations, Grassé questioned, “What is the use of their unceasing mutations if they do not change?” Grassé concludes, “the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.” Microbes undergo constant mutations, but do not evolve – mutation stasis.

*Nucleic Acids Res. 2009 March; 37(4): 1011–1034 

Pangenesis was Darwin’s hypothetical mechanism for the origin of variation and inheritance through particles called gemmules. This “provisional hypothesis” on the origin of variation was presented in his 1868 work The Variation of Animals and Plants under Domestication through gemmules acquiring new variations that brings “together a multitude of facts which are at present left disconnected by any efficient cause”.

The etymology of pangenesis comes from the Greek words pan (a prefix meaning “whole”, “encompassing”) and genesis (birth) or genos (origin). Gemmules were thought to learn from experiences.

The origin of new variations was critical for Darwin’s theory since the “slight, successive” changes in evolution requires a constant stream of new variations for the actions of natural selection. Gemmules were imagined particles. These learned gemmules particles sent from every cell (pan) in the body with new variations (genos) accumulated in the germ cells and had a ‘vote’ in the constitution of the offspring (genesis).

This hypothesis provided a possible mechanism for the inheritance of acquired characteristics, as proposed by Jean-Baptiste Lamarck, which Darwin believed to be the origin of new variations in living organisms.

Little did Darwin know that even before the publication of the fourth edition of The Origin of Species in 1866, Gregor Mendel had presented the now-famous paper entitled “Experiments on Plant Hybridization,” laying the foundations of modern genetics.

Although, Mendel’s discovery went unnoticed until the turn of the twentieth century, German biologist August Weismann, at the University of Freiburg, launched the first scientific evidence directly challenging Darwin’s theory. Now known as the “Weisman Barrier,” in 1883, Weismann cut off the tails of mice from 21 generations. Seeing that the 22^nd generation still had tails, Weismann concluded that the evidence contradicted Darwin’s theory of pangenesis despite obvious reasons for change in the mice, “continuity” was observed, not new variations.

Ernst Mayr, Darwin’s twentieth-century bull-dag, stated Weismann as “The second most notable evolutionary theorist of the 19th century.” What is still unresolved now 150 years later is—what is the origin of variation?

Charles Darwin used the term species more than any other term in The Origin of Species— 1,926 times. Defining the term species, however, has been a problem. Darwin wrote, there “is no possible test but individual opinion to determine which of them shall be considered as species”.

Naturalist Henry Alleyne Nicholson explains, “No term is more difficult to define than ‘species,’ and on no point are zoologists more divided than as to what should be understood by this word.”

Geneticist Laura M. Zahn in looking for the genetic distinction between species, published there results in paper entitled “Background Matters” in the October 2009 edition of Evolution and abstracted in Science. Much to their surprise, Zahn and colleagues discovered that no single genetic allele is known to exist that can define the difference between species.

After 150 years, Darwin’s statement continues to be dead on, “It is all-important to remember that naturalists have no golden rule by which to distinguish species.”

Ironically, a book on the origins of an indefinable term, then and now, ascended into a historical phenomenon.