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Theory of Intelligent Design, the best explanation of Origins » Theory of evolution » It's not known , and mainstream science is ignorant in regard of how evolution supposedly works

It's not known , and mainstream science is ignorant in regard of how evolution supposedly works

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Mainstream science is ignorant in regard of how  evolution supposedly works

There is no publication in the scientific literature – in prestigious journals, specialty journals, or books – that describes how molecular evolution of any real, complex, biochemical system either did occur, or even might have occurred. There are assertions that such evolution occurred, but absolutely none is supported by pertinent experiments or calculations… despite comparing sequences and mathematical modelling, molecular evolution has never addressed the question of how complex structures came to be.


The modern synthesis ( of evolution ) provides us with explanatory tools to understand adaptations (natural selection) but falls short when it comes to the question of novelties

No coherent causative model of morphogenesis has ever been presented.;jsessionid=79710AE9A71071921BD4A3CAC34D5C80.journals?aid=7928966&fileId=S147355041000025X

“Although the vast majority of research in evolutionary biology is focused on adaption, a general theory for the population-genetic mechanisms by which complex adaptations are acquired remains to be developed.”
Proceedings of the National Academy of Sciences of the U.S., “Scaling expectations for the time to establishment of complex adaptations”, September 7, 2010, doi:10.1073/pnas.1010836107.

“Students should realize that although virtually all scientists accept the general concept of evolution of species, scientists do have different opinions on how fast and by what mechanisms evolution proceeds.”
The American Association for the Advancement of Science, Educational Benchmarks, (F) Evolution of Life

“Scientists are still uncovering the specifics of how, when, and why evolution produced the life we see on Earth today.”
Smithsonian’s National Museum of Natural History’s website, “Foundational Concepts: Evolution” page

“But they are trying to figure out how evolution happens, and that’s not an easy job.”
University of California Museum of Paleontology and the National Center for Science Education

“Much of the recent experimental work on natural selection has focused on three goals: determining how common it is, identifying the precise genetic changes that give rise to the adaptations produced by natural selection, and assessing just how big a role natural selection plays in a key problem of evolutionary biology—the origin of new species.”
Scientific American Magazine, “The Evolution of Evolution: Testing Natural Selection with Genetics”, December 18, 2008.

microbiologist James Shapiro of the University of Chicago declared in National Review that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." (Shapiro 1996)
 In Nature University of Chicago evolutionary biologist Jerry Coyne stated,
"There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. . . . We may forever be unable to envisage the first proto-pathways." (Coyne 1996)

In a particularly scathing review in Trends in Ecology and Evolution Tom Cavalier-Smith, an evolutionary biologist at the University of British Columbia, nonetheless wrote, "For none of the cases mentioned by Behe is there yet a comprehensive and detailed explanation of the probable steps in the evolution of the observed complexity.

Evolutionary biologist Andrew Pomiankowski agreed in New Scientist, "Pick up any biochemistry textbook, and you will find perhaps two or three references to evolution. Turn to one of these and you will be lucky to find anything better than 'evolution selects the fittest molecules for their biological function.'" (Pomiankowski 1996)

Lack of mechanism in macro evolution

Harvard biologist Ernst Mayr wrote: "It must be admitted, however, that it is a considerable strain on one’s credulity to assume that finely balanced systems such as certain sense organs (the eye of vertebrates, or the bird’s feather) could be improved by random mutations."[9]

 The extraordinary migration patterns of butterflies and birds cannot be explained through naturalistic development, and lack any plausible materialistic explanation[10]
 Evolution does not account for the immense amount of information in the genome. While there are various definitions of information, and many types have been observed to occur naturally, DNA contains information that is processed to lead to a result predetermined by the content of that information. Strictly speaking it is inaccurate to refer to DNA as a "code" or "language," as many scientists are prone to doing. In fact DNA is more like a template, which produces messenger RNA (mRNA,) a new template with more appropriate bases for protein production. The mRNA essentially acts as a scaffold to which the appropriate amino acids attach to form a protein molecule. Rather than being a language containing words which each have a meaning, DNA is more like a jig or framework which allows a specific molecule of mRNA, and subsequently a specific protein sequence, to be assembled on it. In effect the information is the sequence of chemical reactions which that length of DNA will catalyse. Given the huge number of useless protein molecules which could be formed and the complexity of even a simple protein such as haemoglobin, this sequence could not have evolved by natural selection as the odds against the initial organism having a functional protein are too great.
 The development of feathers, which could not have conceivably "grown" from the scales of reptiles or any other known structure.[11][12]
 The beauty of God's creation, such as autumn foliage, cannot adequately be explained through the evolutionary paradigm. See: Argument from beauty

 (Flickr picture, see: license agreement)
 Humans exhibit behaviors such as performing science, creating art and music, dancing, and a number of other intellectual and artistic behaviors which could not have been produced by random mutations. There is no known evolutionary reason why these should be favored.
 Trematode parasites, like many other kinds, lack a plausible evolutionary phylogeny, though they can easily be explained by a teleological design.[13]
 Evolution cannot explain the many complex sex-determining systems. For example, in most mammals, females have two identical sex chromosomes (XX in this case) whereas males two different ones (XY.) However in birds, reptiles, many insects, and other organisms, the situation is reversed to where the male has two identical sex chromosomes and the female has two different ones; for example male birds have a ZZ chromosome pair and females ZW. No evolutionist has proposed a mechanism by which mammals could have a different sex chromosome system from the reptile ancestors they allegedly share with birds.
 Evolution requires that random mutations cause one kind to change into another, but this has never been observed.
 The existence of two symmetrical kidneys, which are unnecessary in most people, lacks a plausible evolutionary explanation based on functionality alone. Because evolution falsehoods mislead most people into thinking they need their second kidney, "the average waiting time for the organs from a deceased donor in the United States is five years" and "3,916 patients waiting for a kidney in 2006 died before one became available."[14]
 Thousands of years of intense selective breeding should have produced a new wolf species from domesticated dogs, yet dogs and wolves remain the same species.

A world-famous chemist tells the truth: there’s no scientist alive today who understands macroevolution

… I will tell you as a scientist and a synthetic chemist: if anybody should be able to understand evolution, it is me, because I make molecules for a living, and I don’t just buy a kit, and mix this and mix this, and get that. I mean, ab initio, I make molecules. I understand how hard it is to make molecules. I understand that if I take Nature’s tool kit, it could be much easier, because all the tools are already there, and I just mix it in the proportions, and I do it under these conditions, but ab initio is very, very hard.

I don’t understand evolution, and I will confess that to you. Is that OK, for me to say, “I don’t understand this”? Is that all right? I know that there’s a lot of people out there that don’t understand anything about organic synthesis, but they understand evolution. I understand a lot about making molecules; I don’t understand evolution. And you would just say that, wow, I must be really unusual.

Let me tell you what goes on in the back rooms of science – with National Academy members, with Nobel Prize winners. I have sat with them, and when I get them alone, not in public – because it’s a scary thing, if you say what I just said – I say, “Do you understand all of this, where all of this came from, and how this happens?” Every time that I have sat with people who are synthetic chemists, who understand this, they go “Uh-uh. Nope.” These people are just so far off, on how to believe this stuff came together. I’ve sat with National Academy members, with Nobel Prize winners. Sometimes I will say, “Do you understand this?”And if they’re afraid to say “Yes,” they say nothing. They just stare at me, because they can’t sincerely do it.

I was once brought in by the Dean of the Department, many years ago, and he was a chemist. He was kind of concerned about some things. I said, “Let me ask you something. You’re a chemist. Do you understand this? How do you get DNA without a cell membrane? And how do you get a cell membrane without a DNA? And how does all this come together from this piece of jelly?” We have no idea, we have no idea. I said, “Isn’t it interesting that you, the Dean of science, and I, the chemistry professor, can talk about this quietly in your office, but we can’t go out there and talk about this?”

If you understand evolution, I am fine with that. I’m not going to try to change you – not at all. In fact, I wish I had the understanding that you have.

But about seven or eight years ago I posted on my Web site that I don’t understand. And I said, “I will buy lunch for anyone that will sit with me and explain to me evolution, and I won’t argue with you until I don’t understand something – I will ask you to clarify. But you can’t wave by and say, “This enzyme does that.” You’ve got to get down in the details of where molecules are built, for me. Nobody has come forward.

The Atheist Society contacted me. They said that they will buy the lunch, and they challenged the Atheist Society, “Go down to Houston and have lunch with this guy, and talk to him.” Nobody has come! Now remember, because I’m just going to ask, when I stop understanding what you’re talking about, I will ask. So I sincerely want to know. I would like to believe it. But I just can’t.

Now, I understand microevolution, I really do. We do this all the time in the lab. I understand this. But when you have speciation changes, when you have organs changing, when you have to have concerted lines of evolution, all happening in the same place and time – not just one line – concerted lines, all at the same place, all in the same environment … this is very hard to fathom.

I was in Israel not too long ago, talking with a bio-engineer, and [he was] describing to me the ear, and he was studying the different changes in the modulus of the ear, and I said, “How does this come about?” And he says, “Oh, Jim, you know, we all believe in evolution, but we have no idea how it happened.” Now there’s a good Jewish professor for you. I mean, that’s what it is. So that’s where I am. Have I answered the question? (52:00 to 56:44)

The foundation of Darwinism is NOT that variations and adaptations can modify EXISTING features, such as larger and/or different shaped leaves, flowers, beaks, feathers, teeth, jaws, etc. Darwinism goes further by claiming that unguided evolutionary forces cause NEW features and organs to miraculously appear, such as the origin of the previous examples.

Aside from the complete lack of empirical evidence for this claim, whether now or in the past, evolutionists can’t even articulate the likely steps that might cause this phenomenon to occur.

Refer to National Center of Science Education’s website where they openly admit that they don’t know how evolution works. Refer to #3:

“Some of the questions that evolutionary biologists are trying to answer include:
1.Does evolution tend to proceed slowly and steadily or in quick jumps?
2.Why are some clades very diverse and some unusually sparse?
3.How does evolution produce new and complex features?
4.Are there trends in evolution, and if so, what processes generate them?”
“Understanding Evolution” by the University of California Museum of Paleontology and the National Center for Science Education, “The Big Issues” page.
(See more admissions to not knowing how evolution works at the end of this page.)

When challenged to give hypothetical genetic scenarios of how novel features appear, evolutionists retreat in silence as seen on our forum:
When likely scenarios are actually proposed, they routinely:

Suggest that a particular ‘need’ produces change, and/or;
Cite a mechanism that has not been scientifically proven to cause the genetic change that is claimed, and/or;
Builds on component structures that appear out of nowhere, and/or;
Omits specific mention of a likely genetic mechanism.

Note that none of them even touch on the neurotransmitters that process the information in the brain:
“The brain can do nothing and perceive nothing unless thousands of its neurons (nerve cells) communicate in a coordinated fashion with thousands of other neurons.”

Example #1

“The simple light-sensitive spot on the skin of some ancestral creature gave it some tiny survival advantage, perhaps allowing it to evade a predator. Random changes then created a depression in the light-sensitive patch, a deepening pit that made “vision” a little sharper. At the same time, the pit’s opening gradually narrowed, so light entered through a small aperture, like a pinhole camera.
Every change had to confer a survival advantage, no matter how slight. Eventually, the light-sensitive spot evolved into a retina, the layer of cells and pigment at the back of the human eye. Over time a lens formed at the front of the eye. It could have arisen as a double-layered transparent tissue containing increasing amounts of liquid that gave it the convex curvature of the human eye.”
Evolution Library, “Evolution of the Eye”, PBS Online.

Critique of terms used:

a. “Random changes then created a depression in the light-sensitive patch, a deepening pit that made “vision” a little sharper.”
No mention of a likely genetic process.

b. “simple light-sensitive spot”
No explanation for the initial evolution of each complex component that makes-up the spot or the response triggers that activate the flagella. Read how complex “spots” are:
“These eyes constitute the simplest and most common visual system found in nature. The eyes contain optics, photoreceptors and the elementary components of a signal-transduction chain. Rhodopsin serves as the photoreceptor, as it does in animal vision. Upon light stimulation, its all-trans-retinal chromophore isomerizes into 13-cis and activates a photoreceptor channel which leads to a rapid Ca2+ influx into the eyespot region. At low light levels, the depolarization activates small flagellar current which induce in both flagella small but slightly different beating changes resulting in distinct directional changes. In continuous light, Ca2+ fluxes serve as the molecular basis for phototaxis. In response to flashes of higher energy the larger photoreceptor currents trigger a massive Ca2+ influx into the flagella which causes the well-known phobic response.”

c. “ … evolved into a retina,”
No explanation for the evolution of the components of a fully formed retina, the optic nerve, or the independent specific mental and neural capacity required for interpreting the information. The following describes the components of a retina:
“The retina is a highly specialized tissue lining the innermost portion of the eye. It contains millions of specialized photoreceptor cells called rods and cones that convert light rays into electrical signals that are transmitted to the brain through the optic nerve. Rods provide the ability to see in dim light while cones allow for sharp and color vision. The macula, located in the center of the retina, is where most of the cone cells are located. It is very small (500µ or about the size of a ballpoint). The fovea, a small depression in the center of the macula, has the highest concentration of cone cells. In front of the retina is a chamber called the vitreous body, which contains a clear, gelatinous fluid called vitreous humor.”

Example #2

“This ancient animal probably had very simple eye spots with no image-forming ability, but still needed some diversity in eye function. It needed to be able to sense both slow, long-duration events such as the changing of day into night, and more rapid events, such as the shadow of a predator moving overhead. These two forms arose by a simple gene duplication event and concomitant specialization of association with specific G proteins, which has also been found to require relatively few amino acid changes. This simple molecular divergence has since proceeded by way of the progress of hundreds of millions of years and amplification of a cascade of small changes into the multitude of diverse forms we see now. There is a fundamental unity that arose early, but has been obscured by the accumulation of evolutionary change. Even the eyes of a scorpion carry an echo of our kinship, not in their superficial appearance, but deep down in the genes from which they are built.”
PZ Myers, “Eyeing the Evolutionary Past”, March 6, 2008, Seed Online.


a. “ … but still needed some diversity in eye function. It needed to be able to sense …”
An organism senses a need? This suggests that a particular need produces change:
“Contrary to a widespread public impression, biological evolution is not random, even though the biological changes that provide the raw material for evolution are not directed toward predetermined, specific goals.”
“Science, Evolution, and Creationism,” 2008, National Academy of Sciences (NAS), The National Academies Press, 3rd edition, page 50.

b. “ … very simple eye spots,”
Refer to above “Example #1.”

c. “ … simple gene duplication event”
There is NO scientific proof that gene duplication can create genes with more complex functions. Research papers reflect this admission by using words “most likely”:
“Duplicate gene evolution has most likely played a substantial role in both the rapid changes in organismal complexity apparent in deep evolutionary splits and the diversification of more closely related species. The rapid growth in the number of available genome sequences presents diverse opportunities to address important outstanding questions in duplicate gene evolution.”
An erroneous example cited is the claim that, over 100 million years ago, two genes of the yeast S. cerevisiae supposedly evolved from one gene of another specie of yeast (K. lactis).
Refer to:
What is the evidence for their claim? Nothing but the presupposition that Darwinism is true so the very existence of two genes that total the same functions of the one gene proves that they must have evolved from each other:
”The primary evidence that duplication has played a vital role in the evolution of new gene functions is the widespread existence of gene families.”
Also, what Darwinists fail to present is a feasible step-by-step scenario how each gene could:
- split their functions in a precise manner so that neither function would be disabled until ‘random chance’ completed the event;
- become fixed in the population during each new step:
“A duplicated gene newly arisen in a single genome must overcome substantial hurdles before it can be observed in evolutionary comparisons. First, it must become fixed in the population, and second, it must be preserved over time. Population genetics tells us that for new alleles, fixation is a rare event, even for new mutations that confer an immediate selective advantage. Nevertheless, it has been estimated that one in a hundred genes is duplicated and fixed every million years (Lynch and Conery 2000), although it should be clear from the duplication mechanisms described above that it is highly unlikely that duplication rates are constant over time.”

For more information on gene duplication, go to:

d. “concomitant specialization”
This apparently means that two genes have similar yet specialized functions. Evolutionists devise all sorts of redundant and scientific sounding terms when they want to make something sound complicated. This term adds nothing to describe what caused the genetic process to occur.

e. “of association with specific G proteins”
Because of the split in function between the two genes, the molecular switch (G protein) must also be modified to coincide with the specific regulation needed to precisely regulate the new gene. There is NO explanation of how that might occur:
• “Moreover, in order for the organism to respond to an every-changing environment, intercellular signals must be transduced, amplified, and ultimately converted to the appropriate physiological response.”
See movie on G-proteins:

Example #3

The following two links are video presentations that attempt to explain the evolution of an eye. They both use the same progressive steps but forget to mention how the components appeared and/or any mention of what genetic change was used to create new features to appear.

Video narration by Richard Dawkins on YouTube:
‘Scientific’ highlights from the video:
“Skin cells like these often have a little light sensitive pigment to start with, so something interesting could happen …”
“Let’s drop ourselves lightly into a shallow pit and things begin to get better …
“I brought in a simple in-home camera … now I can resolve images must more accurately.”
“Let’s go on and now just imagine some of those cells happen to secrete a little mucus. It collects into a blob … and lodges in the pinhole. Real progress, I’ve got a crude lens, now the incoming light can be focused.”

Video narration by NCSE’s executive director, Eugenie Scott on YouTube:
Ms. Scott uses the same steps but uses ‘next’ repeatedly while pulling in component parts out of thin air. Her most scientific moment comes when she states, “If it can grow, it can evolve …”

Upon discovering that none of the known genetic mechanisms can account for how evolution supposedly occurs, evolutionists are now devising even more absurd fables. This new mechanism is called “preadaptation”:

“The process by which parts accumulate until they’re ready to snap together is called preadaptation. It’s a form of “neutral evolution,” in which the buildup of the parts provides no immediate advantage or disadvantage. Neutral evolution falls outside the descriptions of Charles Darwin. But once the pieces gather, mutation and natural selection can take care of the rest, ultimately resulting in the now-complex form of TIM23 …
“You look at cellular machines and say, why on earth would biology do anything like this? It’s too bizarre,” he said. “But when you think about it in a neutral evolutionary fashion, in which these machineries emerge before there’s a need for them, then it makes sense.””
Brandon Keim, “More ‘Evidence’ of Intelligent Design Shot Down by Science,” August 27, 2009, Wired Science based on “The reducible complexity of a mitochondrial molecular machine,” Yale University, Proceedings of the National Academy of Sciences, Vol. 106 No. 33, August 25, 2009.
So, complex parts with absolutely NO purpose miraculously assemble themselves, and then “snap” together to form a complex cellular machine? They’re kidding, right?

An example that evolutionists use to claim that evolution can make a new feature appear is the appearance of a cecal in a lizard:

Here are the problems with that claim:

1% of ALL scaled reptiles posses cecal valves, so latent DNA is the most likely answer to how they appeared. Example: Organisms restore latent DNA for features several generations AFTER the feature has disappeared:
“Here we show that Arabidopsis plants homozygous for recessive mutant alleles of the organ fusion gene HOTHEAD5 (HTH) can inherit allele-specific DNA sequence information hat was not present in the chromosomal genome of their parents but was present in previous generations. This previously undescribed process is shown to occur at all DNA sequence polymorphisms examined and therefore seems to be a general mechanism for extra-genomic inheritance of DNA sequence information. We postulate that these genetic restoration events are the result of a template-directed process that makes use of an ancestral RNA-sequence cache.”
“Here, we show that a rice triploid and diploid hybridization resulted in stable diploid progenies, both in genotypes and phenotypes, through gene homozygosity. Furthermore, their gene homozygosity can be inherited through 8 generations, and they can convert DNA sequences of other rice varieties into their own. Molecular-marker examination confirmed that this type of genome-wide gene conversion occurred at a very high frequency. Possible mechanisms, including RNA-templated repair of double-strand DNA, are discussed.”
If cecal valves miraculously appeared without latent DNA, evolutionists need to explain in detail how random genetic changes could possible create an exact genetic duplicate of the cecal valve that previously ‘evolved’ by random genetic changes.
Evolutionists refer to this as ‘convergent evolution,’ which is an absolutely ridiculous premise supported ONLY by the presupposition that evolution is true … so it must have occurred!
Since the valves supposedly evolved in just 35 years, it should NOT be difficult to find the beginnings of a valve, which might display an actual evolution-in-process event.


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It's a struggle out there. You have to be fit to survive. When the pressure is on, nature favors the ones who can take the heat.

It's a theme that has been drummed into our heads since school. It's a cultural meme. Social Darwinists used it to justify atrocities -- see the new documentary The Biology of the Second Reich. Today's kinder, gentler Darwinists downplay the violence in the struggle for existence, yet the fact as they see it is inescapable: environmental circumstances select random genetic mutations that confer fitness, i.e., survival, by allowing organisms to adapt.

That in a nutshell explains the development of complex life forms. We're assured there are gobs of evidence for it, too.

Looking into a recent paper in PNAS about evolutionary fitness tradeoffs, you have to feel sorry for a team of five evolutionists from UC Irvine who did their level best to produce clear evidence for the favored story. They began with a startling revelation:

Despite the centrality of adaptation to evolution, surprisingly little is known about the diversity of mutations that contribute to adaptation or about their phenotypic and fitness effects (1). There are, in fact, only a few well-known examples linking genotype, phenotype, and adaptation in nature (2-4). (Emphasis added.)

Those references are worth a glance. Reference (1) is to H. Allen Orr (2005), "The genetic theory of adaptation: a brief history,"where he states, "Here I survey the history of adaptation theory, focusing on the rise and fall of various views over the past century and the reasons for the slow development of a mature theory of adaptation."

References (2-4) surely must represent what, in the authors' opinions, constitute the best "well-known examples linking genotype, phenotype, and adaptation in nature." What are they? #2 is about stickleback fish that gained or lost body armor, but the authors admit, like these ones do, that "the genetic and molecular basis of morphological evolution is poorly understood." #3 is about mice with varying coat colors due to a single mutation that allows light-colored mice to survive better on light backgrounds and dark-colored mice to survive better on dark backgrounds (a kind of "peppered mice" story). #4 is about a gene in butterflies that affects wing pattern mimicry. So these are their best examples linking genes to adaptation. What became of Darwin's finches and peppered moths?

Moving right along, the UC Irvine team next offers an excuse for this lack of evidence:

In nature, this connection is often complicated by factors such as varying selection pressures or underlying genetic heterogeneities. Although the task is difficult, the general inability to connect phenotype to genotype in the context of environmental adaptation has been a major failing in the field of evolution.

So they are here to fix that epic fail. After listing four complicating factors in their study, they say this in the last sentence of the paper:

Given the breadth of these complexities in a well-controlled experimental system, it is no wonder that the mapping of genotype, phenotype, and fitness continues to be a daunting task in natural populations.

In a moment we will see what they did and what went wrong, but first pause to be astonished. This is the theory that is so well-established by mountains of evidence, we are constantly told, that any criticism of it must be stifled as ignorant, and only this theory must be allowed to be considered scientific. They have just told us otherwise. "Surprisingly little is known" about it, and the best examples they could produce are all instances of trivial variations among existing species. If they had better examples, they surely would have brandished them proudly instead of giving excuses about how hard it is to find genetic evidence for adaptation.

The Experimental Test

Their experiment should have been ideal for testing the genetics of adaptation: 2,000 generations of E. coli bacteria subjected to heat. "In total, we performed >800 fitness competitions, making this one of the largest studies of its kind." The games are on! Evolve or perish! Long live the fittest!

Their "large-scale experiment" started with an "ancestral strain" of E. coli bacteria that they replicated 115 times and subjected to high temperatures (42.2 °C, or 108 °F) for 2,000 generations. "At the end of the experiment, fitness was measured at 42.2 °C for a single clone from each of 114 lineages; on average, fitness increased ∼40% during the yearlong experiment" (meaning, there were still some that hadn't died of heat exhaustion).

The hunt was on for genetic mutations that conferred ability to take the heat. "We sequenced the genome of these 114 clones, identifying 1,258 mutations relative to the ancestral genome," they say. To decide which mutations most likely had something to do with fitness, they identified two "adaptive pathways," both affecting RNA polymerase (RNAP). Clones could survive with one or the other mutation, but not the two together: "mutations in the two pathways were strongly negatively associated." (This is called negative epistasis; more on that later).

Their challenge of linking genetic mutations to fitness, though, was only beginning.

Our thermal stress experiment has identified many putatively beneficial mutations that lead to higher fitness under thermal stress. However, we still do not know the phenotypic consequences of these mutations or their relationship with fitness. Do the apparently distinct adaptive pathways converge on similar phenotypes? Or might the two pathways ... lead to alternative phenotypic solutions to a common selective pressure?

Here we begin to address these questions by measuring a complex phenotype: the magnitude of fitness tradeoffs across a thermal gradient. Evolutionary tradeoffs, which are defined as reduced fitness in a nonselected environment, are of great interest in their own right; they are widely observed and frequently assumed to govern and constrain trait evolution.

The operative word there is "assumed." For example, all these mutations may have been neutral, with no phenotypic consequences. Or, mutations for better survival in heat might have had negative consequences for surviving cold (an evolutionary trade-off), with no overall gain in fitness. "Whatever the cause, tradeoffs have rarely been linked to specific genetic variants" -- another embarrassing revelation.

Paltry Results

In this ideal setup (one of the largest of its kind, remember), they were not even looking for a glamorous innovation, like a wing or an eye. Just connecting a particular mutation to a functional phenotype would have been rated a great success, even if all it meant was shifting the germ's optimum temperature range by a few degrees. Trade-offs notwithstanding, so what if the fittest germ in the hot tub would shiver in the cold bath? They would at least be able to connect "genotype, phenotype and adaptation" together -- the kind of evidence neo-Darwinians need and want.

They found that half the clones shifted their thermal range upward by a few degrees (losing ability to survive cold -- the trade-off), and others survived the heat without losing ability to survive cold. Then they found two independent mutations in the RNAP gene that appear relevant to those shifts, as long as they don't occur together. Success? Not so fast.

For one thing, they don't know why those mutations had that effect. They suggested that they might slow RNAP down when its tendency under heat stress is to speed up, thus improving its likelihood to finish a protein synthesis, but this was not clear. Also, to their surprise, the ancestral strain could sometimes bounce back from doom through the "Lazarus effect" (resurrection from the dead) -- but they don't know how that effect works.

Surprisingly, however, wa [absolute fitness] of the ancestor was negative (wa = −0.290) but not significantly <0.00 at 45.0 °C (Table S2 and Fig. S1). This unexpected behavior was caused by the occasional sudden recovery of populations whose densities had initially declined markedly, a phenomenon known as the "Lazarus effect".

So how is Lazarus coming out of the grave? They don't know. Maybe there is some "preadaptation" to heat in these bacteria:

At the upper end of the thermal niche, most (>95%) of the clones persist at 45 °C, signaling an expansion of their niche at least 2 °C beyond that of the ancestor (Fig. 1B). This observation contrasts with a previous study in which only one of six 42 °C-adapted lines expanded their upper thermal limit but suggests a degree of "preadaptation" to temperatures beyond the clones' immediate experience. Above 45 °C the analyses become complicated by the Lazarus effect, in which declining populations suddenly recover, presumably due to major effect mutations. Indeed, the ancestral clone, which is habituated to laboratory conditions of 37 °C, does not persist at 43 °C but often recovers at 45 °C (Fig. S2). We do not yet know the molecular processes underlying the Lazarus effect, but two seem possible: either the fitness effects of mutations change as a function of the intensity of stress or the mutation rate increases under high stress (33, 34). We do not yet know which of these two mechanisms predominates.

Complicating matters even more are things like "negative epistasis" (mutations that counteract each other) and "antagonistic pleiotropy" (unintended consequences of a "beneficial" mutation on other parts of the genome).

In short, it was hard to find anything beyond a "suggestion" or a "scenario" that these bacteria improved their fitness in any way by genetic mutations, other than the gross observation that some of the clones managed to survive at 45 °C. But even the ancestor could do that sometimes through the "Lazarus effect." The authors also ignored the possibility that E. coli have ways to generate their own mutations under stress. That would be supportive of intelligent design, as would the notion that bacteria contain "a degree of preadaptation" to temperatures beyond their immediate experience.

Some experiment. What we learn from this paper is that under ideal conditions, with the best methods, scientists have a devil of a time trying to establish neo-Darwinian theory in a scientifically rigorous way. A look at their references shows a debt to Lenski's methods that similarly produced paltry results on one of the longest-running experiments in history trying to demonstrate evolution in a lab.

Is this a theory that deserves to rule the world?

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Admissions of Ignorance in Evolutionary Theory  
August 11, 2008 — For a scientific idea some have proclaimed as a fact no longer in need of proof, and as well-established as gravity, Darwin’s theory of evolution still reveals surprising weaknesses when its defenders speak about the details.  Detecting these weaknesses requires tuning out the media hype, and tuning into scientific papers and pro-evolution journals where evolutionary theory is debated.  Elisabeth Pennisi wrote one such account in Science last week.1  It revealed that the public is getting a very misleading view of evolution – both its operation and the strength of the evidence for it.
    It would seem obvious that evolution needs a genetic basis.  Darwin attempted to explain it in his day, unsuccessfully.  The neo-Darwinian synthesis of the 1930s was supposed to explain it.  Serious questions about how evolution works at the genetic level remain, however, to this day.  This was evident in Pennisi’s use of war metaphors to describe two groups of evolutionists that are “locking horns” over a current issue: whether genes or regulatory elements (in particular, cis regulatory factors) are key to evolutionary change.  The latter, a “fashionable idea,” has been growing in popularity among those in the evo-devo subculture: i.e., evolutionary biologists who focus more on developmental than genetic influences.  When Jerry Coyne and Hopi Hoekstra wrote a pointed critique of the regulatory-element hypothesis in the journal Evolution last year, “Egos were bruised.  Tempers flared.  Journal clubs, coffee breaks at meetings, and blogs are still all abuzz,” she wrote.
    None of the combatants doubt Darwin’s theory in the slightest, of course.  Still, some statements in Pennisi’s account could give a Darwin-doubter cause for gloating.  Consider this paragraph:

[Sean] Carroll [U of Wisconsin] argued that mutations in cis regions were a way to soft-pedal evolutionary change.  Genes involved in establishing body plans and patterns have such a broad reach--affecting a variety of tissues at multiple stages of development--that mutations in their coding regions can be catastrophic.  In contrast, changes in cis elements, several of which typically work in concert to control a particular gene’s activity, are likely to have a much more limited effect.  Each element serves as a docking site for a particular transcription factor, some of which stimulate gene expression and others inhibit it.  This modularity makes possible an infinite number of cis-element combinations that finely tune gene activity in time, space, and degree, and any one sequence change is unlikely to be broadly disruptive.

This sounds like damage control.  Is the standard explanation too risky?  Yet critics of the evo-devo alternative argue that every such “fine-tuning” change must be adaptive to persist through natural selection.  Precious few examples, they say, can be found to illustrate a regulatory change related to a morphological change.  One regulatory change in a mouse, for instance, can make its digits grow slightly longer (see 01/18/2008), but the mutant mouse is hardly ready to take off flying like a bat.
    “Where’s the beef?” challenged Pennisi, giving the floor to Coyne and Hoekstra, who countered that mutations for evolutionary change must occur in genes:

But Hoekstra and Coyne say this enthusiasm doesn’t rest on solid evidence.  In their Evolution article, they picked apart these examples and the rationale behind them.  They pulled quotes from Carroll’s work tocriticize his fervor and berated the evo-devo community for charging full speed ahead with the cis-regulatory hypothesis.  “Evo devo’s enthusiasm for cis-regulatory changes is unfounded and premature,” they wrote.  Changes in gene regulation are important, says Hoekstra, but they are not necessarily caused by mutations in cis elements.  “They do not have one case where it’s really nailed down,” she says.

Those be fightin’ words, indeed.  Coyne even used psychological warfare, telling Science, “I’m distressed that Sean Carroll is preaching to the general public that we know how evolution works based on such thin evidence.”
    The opposition did not take this sitting down.  “Almost as soon as their article appeared, lines were drawn and rebuttals planned,” Pennisi reported like a war correspondent.  But did they come back with a knock-down case for evolution?  All Sean Carroll could reply was that his view is the best of a bad lot:

“I am not trying to say that regulatory sequence is the most important thing in evolution,” he told Science.  But when it comes to what’s known about the genetic underpinnings of morphological evolution, “it’s a shutout” in favor of cis elements, he asserts.

That one statement could come as a shock to students who have been taught all their lives that evolution by natural selection acting on genetic mutations is well understood.  The article degenerated from here into the battle of the T-shirts and other fluff.  Coyne, for instance, sported a T-shirt that said “I’m no CISsy,” and entitled his talk at a recent conference, “Give me just one cis-regulatory mutation and I’ll shut up.
    Pennisi reported statistics from pro-evo-devo people purporting to show the extent of regulatory elements involved in mutated genes.  “Yet even these data are inconclusive,” another was quoted admitting.  At the end of the article, there was no winner.  Pennisi’s closing theme, with variations, was how little is known.  Everyone was making excuses.  Evo-devo devotees complained that associations between regulatory elements and morphological effects are hard to measure.  “I really want to emphasize,” Carroll bluffed, “that evo-devo [researchers] haven’t come to this way of thinking simply through storytelling” but through data.  Was this a response to ridicule he has heard?  Or was it a backhanded charge that his opponents are the storytellers?  Either way, it’s hard to feel his conclusions are compelling when the relevance of certain regulatory elements, and their interactions, are confusing, and “the numbers may be misleading.”  How much more so when genetic mutations can affect the regulatory elements themselves?  What role do RNA elements play?  What about gene duplications?  Patricia Wittkop (U of Michigan) suggested there may be more noise than signal when she said, “The important question is about finding out whether there are principles that will allow us to predict the most likely paths of change for a specific trait or situation.”  It would seem any scientific claim needs such principles to be deemed scientific.
    If the evolutionists cannot resolve their conflict, they can at least improve their battlefield protocols.  Pennisi ended with this:

With so much unknown, “we don’t want to spend our time bickering,” says [Gregory] Wray [Duke U].  He and others worry that Hoekstra, Coyne, and Carroll have taken too hard a line and backed themselves into opposite corners.  Coyne doesn’t seem to mind the fuss, but Hoekstra is more circumspect about their Evolution paper.  “I stand by the science absolutely,” she says.  “But if I did it over again, I would probably tone down the language.

1.  Elisabeth Pennisi, “Evolutionary Biology: Deciphering the Genetics of Evolution,” Science, 8 August 2008: Vol. 321. no. 5890, pp. 760-763, DOI: 10.1126/science.321.5890.760.

The vast majority of the public, including high school students, never sees the bickering between Darwiniacs over the most fundamental aspects of their theory.  That’s why you need to see it exposed here.
    The lesson in this story is that almost nothing is understood in their tale at a scientific level.  Evolutionists want us to believe that humans have bacteria ancestors.  All the amazing structures in all of life had to emerge from a simple, primordial cell by some undirected biological process at the genetic level.  When it comes to positive evidence for such a fantastic, astonishing claim, the paltry best these true believers could exhibit were inconclusive effects of mutations or regulatory elements on existing complex species: reversible changes to the amount of armor on stickleback fish, bristles or the lack of them on fruit flies (with no idea whether they provide any adaptive advantage), slightly longer digits on mice, and other trivia.  When it comes to negative evidence, look at how both sides falsified each other.  The charges and counter-charges were hilarious.  They go like this:
“You have no evidence.”
“Oh yeah?  Well, we have a lot more than you!”
This is like the Dumb and Dumber T-shirts you see friends wearing at amusement parks.  We’ve taken off the Darwiniacs’ white lab coats and shown you their T-shirts: not just Dumb and Dumber, but Fussy and Fussier, and Deceived and Deceiver.  Should such people be “preaching to the general public” that “they know how evolution works, based on such thin evidence”?  Look under the T-shirt and you see just a skeleton with no scientific fitness.  “Where’s the beef?” indeed.  These Popeyes (05/31/2005) will find no salvation in spinach (01/24/2005).  Their ID nemesis, already fit to the hilt, has already eaten it all.  Skinny lightweights only win in the cartoons.

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