Satellite DNA is Essential and Species-Specific in Drosophila melanogaster

Seems Incompatible

This week’s “we thought it was junk but it turned out to be crucial” study comes with the added bonus that the so-called “junk” is also species-specific / taxonomically restricted. The general topic is tandemly repeated satellite DNA in the much studied fruit fly, Drosophila melanogaster. These satellite DNA regions comprise 15-20% of D. melanogaster’s genome, and one of the regions, AAGAG(n), is transcribed across many of D. melanogaster’s cell types.

While evolutionists have hoped and argued that transcription (not to mention mere presence) does not imply function (after all biology is one big hack-job, so RNA polymerase doesn’t always know what it is doing), D. melanogaster is once again not cooperating. Not only is the satellite DNA ubiquitous and widely transcribed, the AAGAG RNA was found to be important for male fertility. Kind of important.

But it gets worse. Much worse.

Not only is D. melanogaster’s satellite DNA ubiquitous, widely transcribed across many cell types, and of crucial importance, it is species-specific. The levels of AAGAG satellite DNA is orders of magnitude lower in D. simulans and D. sechellia, and nearly absent in other species within the Drosophila genus.

This makes no sense on evolution. Now we must say that not only does a massive quantity of AAGAG satellite DNA abruptly appear in a particular fly species, but it immediately takes on an absolutely crucial role. A role which, of course, was somehow already fulfilled in the putative evolutionary ancestor.

In other words, the function in question (male fertility) was rumbling along just fine, and then with a new species, and not in many of its sister species, the crucial function was somehow rewired and reassigned to a relatively new, massive, DNA satellite sequence.

This is absurd.

Even the paper admits that, “Finally, it is worth noting that the expression of simple satellites for essential functions seems incompatible with the fast evolution of satellite DNAs, reflected in dramatic changes in both sequence types and copy numbers across species.”

Ya think?

The next step will be for evolutionists to convert this spectacular failure into compelling evidence that evolution can produce DNA that is both (i) species-specific, and (ii) functionally essential.

And why is that true?

Because, after all, the satellite DNA evolved, of course. And since it is species-specific and essential, we now have evidence evolution can produce such an unexpected outcome.

That’s just good, solid, scientific research.

Religion drives science, and it matters.

New Paper Admits Failure of Evolution

Pop Quiz: Who Said It?

There are many fundamental problems with evolutionary theory. Origin of life studies have dramatically failed. Incredibly complex biological designs, both morphological and molecular, arose abruptly with far too little time to have evolved. The concept of punctuated equilibrium is descriptive, not explanatory. For example, the Cambrian Explosion is not explained by evolution and, in general, evolutionary mechanisms are inadequate to explain the emergence of new traits, body plans and new physiologies. Even a single gene is beyond the reach of evolutionary mechanisms. In fact, the complexity and sophistication of life cannot originate from non-biological matter under any scenario, over any expanse of space and time, however vast. On the other hand, the arch enemy of evolutionary theory, Lamarckian inheritance, in its variety of forms, is well established by the science.

Another Darwin’s God post?

No, these scientific observations are laid out in a new peer-reviewed, scientific paper.

Origin of Life

Regarding origin of life studies, which try to explain how living cells could somehow have arisen in an ancient, inorganic, Earth, the paper explains that this idea should have long since been rejected, but instead it has fueled “sophisticated conjectures with little or no evidential support.”

the dominant biological paradigm - abiogenesis in a primordial soup. The latter idea was developed at a time when the earliest living cells were considered to be exceedingly simple structures that could subsequently evolve in a Darwinian way. These ideas should of course have been critically examined and rejected after the discovery of the exceedingly complex molecular structures involved in proteins and in DNA. But this did not happen. Modern ideas of abiogenesis in hydrothermal vents or elsewhere on the primitive Earth have developed into sophisticated conjectures with little or no evidential support.

In fact, abiogenesis has “no empirical support.”

independent abiogenesis on the cosmologically diminutive scale of oceans, lakes or hydrothermal vents remains a hypothesis with no empirical support

One problem, of many, is that the early Earth would not have supported such monumental evolution to occur:

The conditions that would most likely to have prevailed near the impact-riddled Earth's surface 4.1–4.23 billion years ago were too hot even for simple organic molecules to survive let alone evolve into living complexity

In fact, the whole idea strains credibility “beyond the limit.”

The requirement now, on the basis of orthodox abiogenic thinking, is that an essentially instantaneous transformation of non-living organic matter to bacterial life occurs, an assumption we consider strains credibility of Earth-bound abiogenesis beyond the limit.

All laboratory experiments have ended in “dismal failure.” The information hurdle is of “superastronomical proportions” and simply could not have been overcome without a miracle.

The transformation of an ensemble of appropriately chosen biological monomers (e.g. amino acids, nucleotides) into a primitive living cell capable of further evolution appears to require overcoming an information hurdle of superastronomical proportions, an event that could not have happened within the time frame of the Earth except, we believe, as a miracle. All laboratory experiments attempting to simulate such an event have so far led to dismal failure.

Diversity of Life

But the origin of life is just the beginning of evolution’s problems. For science now suggests evolution is incapable of creating the diversity of life and all of its designs:

Before the extensive sequencing of DNA became available it would have been reasonable to speculate that random copying errors in a gene sequence could, over time, lead to the emergence of new traits, body plans and new physiologies that could explain the whole of evolution. However the data we have reviewed here challenge this point of view. It suggests that the Cambrian Explosion of multicellular life that occurred 0.54 billion years ago led to a sudden emergence of essentially all the genes that subsequently came to be rearranged into an exceedingly wide range of multi-celled life forms - Tardigrades, the Squid, Octopus, fruit flies, humans – to name but a few.

As one of the authors writes, “the complexity and sophistication of life cannot originate (from non-biological) matter under any scenario, over any expanse of space and time, however vast.” As an example, consider the octopus.

Octopus

First, the octopus is an example of novel, complex features, rapidly appearing and a vast array of genes without an apparent ancestry:

Its large brain and sophisticated nervous system, camera-like eyes, flexible bodies, instantaneous camouflage via the ability to switch colour and shape are just a few of the striking features that appear suddenly on the evolutionary scene. The transformative genes leading from the consensus ancestral Nautilus (e.g., Nautilus pompilius) to the common Cuttlefish (Sepia officinalis) to Squid (Loligo vulgaris) to the common Octopus (Octopus vulgaris) are not easily to be found in any pre-existing life form.

But it gets worse. As Darwin’s God has explained, The Cephalopods demonstrate a highly unique level of adenosine to inosine mRNA editing. It is yet another striking example of lineage-specific design that utterly contradicts macroevolution:

These data demonstrate extensive evolutionary conserved adenosine to inosine (A-to-I) mRNA editing sites in almost every single protein-coding gene in the behaviorally complex coleoid Cephalopods (Octopus in particular), but not in nautilus. This enormous qualitative difference in Cephalopod protein recoding A-to-I mRNA editing compared to nautilus and other invertebrate and vertebrate animals is striking. Thus in transcriptome-wide screens only 1–3% of Drosophila and human protein coding mRNAs harbour an A-to-I recoding site; and there only about 25 human mRNA messages which contain a conserved A-to-I recoding site across mammals. In Drosophila lineages there are about 65 conserved A-sites in protein coding genes and only a few identified in C. elegans which support the hypothesis that A-to-I RNA editing recoding is mostly either neutral, detrimental, or rarely adaptive. Yet in Squid and particularly Octopus it is the norm, with almost every protein coding gene having an evolutionary conserved A-to-I mRNA editing site isoform, resulting in a nonsynonymous amino acid change. This is a virtual qualitative jump in molecular genetic strategy in a supposed smooth and incremental evolutionary lineage - a type of sudden “great leap forward”. Unless all the new genes expressed in the squid/octopus lineages arose from simple mutations of existing genes in either the squid or in other organisms sharing the same habitat, there is surely no way by which this large qualitative transition in A-to-I mRNA editing can be explained by conventional neo-Darwinian processes, even if horizontal gene transfer is allowed. 

Lamarck

In the twentieth century Lamarckian Inheritance was an anathema for evolutionists. Careers were ruined and every evolutionist knew the inheritance of acquired characteristics sat right along the flat earth and geocentrism in the history of ideas. The damning of Lamarck, however, was driven by dogma rather than data, and today the evidence has finally overcome evolutionary theory.

Indeed there is much contemporary discussion, observations and critical analysis consistent with this position led by Corrado Spadafora, Yongsheng Liu, Denis Noble, John Mattick and others, that developments such as Lamarckian Inheritance processes (both direct DNA modifications and indirect, viz. epigenetic, transmissions) in evolutionary biology and adjacent fields now necessitate a complete revision of the standard neo-Darwinian theory of evolution or “New Synthesis " that emerged from the 1930s and 1940s.

Indeed, we now know of a “plethora of adaptive Lamarckian-like inheritance mechanisms.”

There is, of course, nothing new in this paper. We have discussed these, and many, many other refutations of evolutionary theory. Yet the paper is significant because it appears in a peer-reviewed journal. Science is, if anything, conservative. It doesn’t exactly “follow the data,” at least until it becomes OK to do so. There are careers and reputations at stake.

And of course, there is religion.

Religion drives science, and it matters.

Centrobin Found to be Important in Sperm Development

Numerous, Successive, Slight Modifications

Proteins are a problem for theories of spontaneous origins for many reasons. They consist of dozens, or often hundreds, or even thousands of amino acids in a linear sequence, and while many different sequences will do the job, that number is tiny compared to the total number of sequences that are possible. It is a proverbial needle-in-the-haystack problem, far beyond the reach of blind searches. To make matters worse, many proteins are overlapping, with portions of their genes occupying the same region of DNA. The same set of mutations would have to result in not one, but two proteins, making the search problem that much more tricky. Furthermore, many proteins perform multiple functions. Random mutations somehow would have to find those very special proteins that can perform double duty in the cell. And finally, many proteins perform crucial roles within a complex environment. Without these proteins the cell sustains a significant fitness degradation. One protein that fits this description is centrobin, and now a new study shows it to be even more important than previously understood.

Centrobin is a massive protein of almost a thousand amino acids. Its importance in the division of animal cells has been known for more than ten years. An important player in animal cell division is the centrosome organelle which organizes the many microtubules—long tubes which are part of the cell’s cytoskeleton. Centrobin is one of the many proteins that helps the centrosome do its job. Centrobin depletion causes “strong disorganization of the microtubule network,” and impaired cell division.

Now, a new study shows just how important centrobin is in the development of the sperm tail. Without centrobin, the tail, or flagellum, development is “severely compromised.” And once the sperm is formed, centrobin is important for its structural integrity. As the paper concludes:

Our results underpin the multifunctional nature of [centrobin] that plays different roles in different cell types in Drosophila, and they identify [centrobin] as an essential component for C-tubule assembly and flagellum development in Drosophila spermatogenesis.

Clearly centrobin is an important protein. Without it such fundamental functions as cell division and organism reproduction are severely impaired.

And yet how did centrobin evolve?

Not only is centrobin a massive protein, but there are no obvious candidate intermediate structures. It is not as though we have that “long series of gradations in complexity” that Darwin called for:

Although the belief that an organ so perfect as the eye could have been formed by natural selection, is enough to stagger any one; yet in the case of any organ, if we know of a long series of gradations in complexity, each good for its possessor, then, under changing conditions of life, there is no logical impossibility in the acquirement of any conceivable degree of perfection through natural selection.

Unfortunately, in the case of centrobin, we do not know of such a series. In fact, centrobin would seem to be a perfectly good example of precisely how Darwin said his theory could be falsified:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case.  

Darwin could “find out no such case,” but he didn’t know about centrobin. Darwin required “a long series of gradations,” formed by “numerous, successive, slight modifications.”

With centrobin we are nowhere close to fulfilling these requirements. In other words, today’s science falsifies evolution. This, according to Darwin’s own words.

Religion drives science, and it matters.

Rewrite the Textbooks (Again), Origin of Mitochondria Blown Up

There You Go Again

Why are evolutionists always wrong? And why are they always so sure of themselves? With the inexorable march of science, the predictions of evolution, which evolutionists were certain of, just keep on turning out false. This week’s failure is the much celebrated notion that the eukaryote’s power plant—the mitochondria—shares a common ancestor with the alphaproteobacteria. A long time ago, as the story goes, that bacterial common ancestor merged with an early eukaryote cell. And these two entities, as luck would have it, just happened to need each other. Evolution had just happened to create that early bacterium, and that early eukaryote, in such a way that they needed, and greatly benefited from, each other. And, as luck would have it again, these two entities worked together. The bacterium would just happen to produce the chemical energy needed by the eukaryote, and the eukaryote would just happen to provide needed supplies. It paved the way for multicellular life with all of its fantastic designs. There was only one problem: the story turned out to be false.

The story that mitochondria evolved from the alphaproteobacteria lineage has been told with great conviction. Consider the Michael Gray 2012 paper which boldly begins with the unambiguous truth claim that “Viewed through the lens of the genome it contains, the mitochondrion is of unquestioned bacterial ancestry, originating from within the bacterial phylum α-Proteobacteria (Alphaproteobacteria).”

There was no question about it. Gray was following classic evolutionary thinking: similarities mandate common origin. That is the common descent model. Evolutionists say that once one looks at biology through the lens of common descent everything falls into place.

Except that it doesn’t.

Over and over evolutionists have to rewrite their theory. Similarities once thought to have arisen from a common ancestor turn out to contradict the common descent model. Evolutionists are left having to say the similarities must have arisen independently.

And big differences, once thought to show up only in distant species, keep on showing up in allied species.

Biology, it turns out, is full of one-offs, special cases, and anomalies. The evolutionary tree model doesn’t work.

Now, a new paper out this week has shown that the mitochondria and alphaproteobacteria don’t line up the way originally thought. That “unquestioned bacterial ancestry” turns out to be, err, wrong.

The paper finds that mitochondria did not evolve from the currently hypothesized alphaproteobacterial ancestor, or from “any other currently recognized alphaproteobacterial lineage.”

The paper does, however, make a rather startling claim. The authors write:

our analyses indicate that mitochondria evolved from a proteobacterial lineage that branched off before the divergence of all sampled alphaproteobacteria.

Mitochondria evolved from a proteobacterial lineage, predating the alphaproteobacteria?

That is a startling claim because, well, simply put there is no evidence for it. The lack of evidence is exceeded only by the evolutionist’s confidence. Note the wording: “indicate.”

The evolutionist’s analyses indicate this new truth.

How can the evolutionists be so sure of themselves in the absence of literally any evidence?

The answer is, because they are evolutionists. They are completely certain that evolution is true. And since evolution must be true, the mitochondria had to have evolved from somewhere. And the same is true for the alphaproteobacteria. They must have evolved from somewhere.

And in both cases, that somewhere must be the earlier proteobacterial lineage. There are no other good evolutionary candidates.

Fortunately this new claim cannot be tested (and therefore cannot be falsified), because the “proteobacterial lineage” is nothing more than an evolutionary construct. Evolutionists can search for possible extant species for hints of a common ancestor with the mitochondria, but failure to find anything can always be ascribed to extinction of the common ancestor.

This is where evolutionary theory often ends up: failures ultimately lead to unfalsifiable truth claims. Because heaven forbid we should question the theory itself.

Religion drives science, and it matters.

The Dinosaur “Explosion”

As Though They Were Planted There

In the famed Cambrian Explosion most of today’s animal phyla appeared abruptly in the geological strata. How could a process driven by blind, random mutations produce such a plethora of new species? Evolutionist Steve Jones has speculated that the Cambrian Explosion was caused by some crucial change in DNA. “Might a great burst of genetic creativity have driven a Cambrian Genesis and given birth to the modern world?” [1] What explanations such as this do not address is the problem of how evolution overcame such astronomical entropic barriers. Rolling a dice, no matter how creatively, is not going to design a spaceship.

The Cambrian Explosion is not the only example of the abrupt appearance of new forms in the fossil record, and the other examples are no less easy for evolution to explain. Nor has the old saw, that it’s the fossil record’s fault, fared well. There was once a time when evolutionists could appeal to gaps in the fossil record to explain why the species appear to arise abruptly, but no more. There has just been too much paleontology work, such as a new international study on dinosaurs published this week, confirming exactly what the strata have been showing all along: new forms really did arise abruptly.

The new study narrows the dating of the rise of dinosaurs in the fossil record. It confirms that many dinosaur species appeared in an “explosion” or what “we term the ‘dinosaur diversification event (DDE)’.” It was an “explosive increase in dinosaurian abundance in terrestrial ecosystems.” As the press release explains,

First there were no dinosaur tracks, and then there were many. This marks the moment of their explosion, and the rock successions in the Dolomites are well dated. Comparison with rock successions in Argentina and Brazil, here the first extensive skeletons of dinosaurs occur, show the explosion happened at the same time there as well.

As lead author Dr Massimo Bernardi at the University of Bristol explains, “it’s amazing how clear cut the change from ‘no dinosaurs’ to ‘all dinosaurs’ was.”

There just isn’t enough time, and it is another example of a failed prediction of the theory of evolution.

1. Steve Jones, Darwin’s Ghost, p. 206, Random House, New York, 2000.

h/t: The genius.

Andreas Wagner: Genetic Regulation Drives Evolutionary Change

A Hall of Mirrors

A new paper from Andreas Wagner and co-workers argues that a key and crucial driver of evolution is changes to the interaction between transcription factor proteins and the short DNA sequences to which they bind. In other words, evolution is driven by varying the regulation of protein expression (and a particular type of regulation—the transcription factor-DNA binding) rather than varying the structural proteins themselves. Nowhere does the paper address or even mention the scientific problems with this speculative idea. For example, if evolution primarily proceeds by random changes to transcription factor-DNA binding, creating all manner of biological designs and species, then from where did those transcription factors and DNA sequences come? The answer—that they evolved for some different, independent, function; itself an evolutionary impossibility—necessitates astronomical levels of serendipity. Evolution could not have had foreknowledge. It could not have known that the emerging transcription factors and DNA sequence would, just luckily, be only a mutation away from some new function. This serendipity problem has been escalating for years as evolutionary theory has repeatedly failed, and evolutionists have applied ever more complex hypotheses to try to explain the empirical evidence. Evolutionists have had to impute to evolution increasingly sophisticated, complex, higher-order, mechanisms. And with each one the theory has become ever more serendipitous. So it is not too surprising that evolutionists steer clear of the serendipity problem. Instead, they cite previous literature as a way of legitimizing evolutionary theory. Here I will show examples of how this works in the new Wagner paper.

The paper starts right off with the bold claim that “Changes in the regulation of gene expression need not be deleterious. They can also be adaptive and drive evolutionary change.” That is quite a statement. To support it the paper cites a classic 1975 paper by Mary-Claire King and A. C. Wilson entitled “Evolution at two levels in humans and chimpanzees.” The 1975 paper admits that the popular idea and expectation that evolution occurs by mutations in protein-coding genes had largely failed. The problem was that, at the genetic level, the two species were too similar:

The intriguing result, documented in this article, is that all the biochemical methods agree in showing that the genetic distance between humans and the chimpanzee is probably too small to account for their substantial organismal differences.

Their solution was to resort to a monumental shift in evolutionary theory: evolution would occur via the tweaking of gene regulation.

We suggest that evolutionary changes in anatomy and way of life are more often based on changes in the mechanisms controlling the expression of genes than on sequence changes in proteins. We therefore propose that regulatory mutations account for the major biological differences between humans and chimpanzees.

In other words, evolution would have to occur not by changing proteins, but by changing protein regulation. What was left unsaid was that highly complex, genetic regulation mechanisms would now have to be in place, a priori, in order for evolution to proceed.

Where did those come from?

Evolution would have to create highly complex, genetic regulation mechanisms so that evolution could occur.

Not only would this ushering in of serendipity to evolutionary theory go unnoticed, it would, incredibly, be cited thereafter as a sort of evidence, in its own right, showing that evolution occurs by changes to protein regulation.

But of course the 1975 King-Wilson paper showed no such thing. The paper presupposed the truth of evolution, and from there reasoned that evolution must have primarily occurred via changes to protein regulation. Not because anyone could see how that could occur, but because the old thinking—changes to proteins themselves—wasn’t working.

This was not, and is not, evidence that changes in the regulation of gene expression can be “adaptive and drive evolutionary change,” as the Wagner paper claimed.

But this is how the genre works. The evolution literature makes unfounded claims that contradict the science, and justifies those claims with references to other evolution papers which do the same thing. It is a web of deceit.

Ultimately it all traces back to the belief that evolution is true.

The Wagner paper next cites a 2007 paper that begins its very first sentence with this unfounded claim:

It has long been understood that morphological evolution occurs through alterations of embryonic development.

I didn’t know that. And again, references are provided. This time to a Stephen Jay Gould book and a textbook, neither of which demonstrate that “morphological evolution occurs through alterations of embryonic development.”

These sorts of high claims by evolutionists are ubiquitous in the literature, but they never turn out to be true. Citations are given, and those in turn provide yet more citations. And so on, in a seemingly infinite hall of mirrors, where monumental assertions are casually made and immediately followed by citations that simply do the same thing.

Religion drives science, and it matters.

Brochosome Proteins Encoded By Orphan Genes

A Pattern Problem

A few years ago Paul Nelson debated Joel Velasco on the topic of design and evolution. Nelson masterfully demonstrated design in nature. For his part Velasco also provided an excellent defense of evolution. But the Epicurean claim that the world arose via random chance is not easy to defend, and Velasco’s task would be challenging. Consider, for example, the orphans which Nelson explained are a good example of taxonomically-restricted designs. Such designs make no sense on evolution, and though Velasco responded with many rebuttals, none were very convincing. Since that debate the orphan problem has become worse, as highlighted by a new study of brochosomes.

Background

The term orphan refers to a DNA open reading frame, or ORF, without any known similar sequence in other species or lineages, and hence ORFan or “orphan.” Since orphans are unique to a particular species or lineage, they contradict common ancestry’s much celebrated nested hierarchy model.

The Nelson-Valasco Debate

Velasco addressed the orphan problem with several arguments. First, Velasco reassured the audience that there isn’t much to be concerned with here because “Every other puzzle we’ve ever encountered in the last 150 years has made us even more certain of a fact that we already knew, that we’re all related.”

Second, Velasco argued that the whole orphan problem is contrived, as it is nothing more than a semantic misunderstanding—a confusion of terms. These are nothing more than open reading frames without significant similarity to any known sequence.

Third, Velasco argued that many of the orphans are so categorized merely because the search for similar sequence is done only in “very distantly related” species.

Furthermore, and fourth, Velasco argued that orphans are really nothing more than a gap in our knowledge. For the more we know about a species, the more the orphan problem goes away. And which species do we know the most about? Ourselves of course. And we have no orphans: “Well what about humans, we know a lot about humans. How many orphan genes are in humans? What do you think? Zero.”

In fact, and fifth, Velasco argued that while new orphans are discovered with each new genome that is decoded, the trend is slowing and is suggestive that in the long run relatives for these orphans will be found: “In fact if you trend the absolute number going up, as opposed to the percentage of orphan genes in organisms, that number is going down.”

So to summarize Velasco’s position, the orphan problem will be solved so don’t worry about, but actually orphans are not a problem at all but rather a semantic misunderstanding, but on the other hand the orphan problem is a consequence of incomplete genomic data, but actually on the other hand the problem is a consequence of insufficient knowledge about the species, and in any case even though the number of known orphans keeps on rising, they will eventually go away because the orphans, as a percentage of the overall genomic data (which has been exploding exponentially) is going down.

This string of evolution arguments reminds us of the classic dog-owner’s defense: He’s not my dog, he didn’t bite you, and besides you hit the dog first anyway. Not surprisingly, each of Velasco’s arguments fails, as I explained here.

In fact, there are many orphans, and while function can be difficult to identify, it has been found for many orphans. As science writer Helen Pilcher explained:

In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.

Up to a third of genomes have been found have been found to be unique, as this review explains:

Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes. 

And this is yet another failed prediction of evolution, as this paper explains:

The frequency of de novo creation of proteins has been debated. Early it was assumed that de novo creation should be extremely rare and that the vast majority of all protein coding genes were created in early history of life. However, the early genomics era lead to the insight that protein coding genes do appear to be lineage-specific. Today, with thousands of completely sequenced genomes, this impression remains.

Why then was Velasco so confident and almost nonchalant in his argumentation? Why was he so assured that, one way or another, the orphan problem was not a problem? And why did he believe there are zero orphans in humans, and so it merely is a matter of studying biology, and the orphans will go away?

Lander Orphan Study

It could be due to a significant 2007 study from Eric Lander’s group which rejected most of the large number (several thousands) of orphans that had been tentatively identified in the human genome. The study confidently concluded that “the vast majority” of the orphans were “spurious”:

The analysis here addresses an important challenge in genomics— determining whether an ORF truly encodes a protein. We show that the vast majority of ORFs without cross-species counterparts [i.e., orphans] are simply random occurrences. The exceptions appear to represent a sufficiently small fraction that the best course is would be [sic] consider such ORFs as noncoding in the absence of direct experimental evidence.

The authors went on to propose that “it is time to undertake a thorough revision of the
human gene catalogs by applying this principle to filter the entries.”

That peer-reviewed paper, in a leading journal, was well received (e.g., Larry Moran called it an “excellent study”) and it certainly appeared to be authoritative. So it is not surprising that Velasco would be confident about orphans. For all appearances, they really were no problem for evolution.

There was just one problem. This was all wrong.

There was no scientific evidence that those human sequences, identified as orphans, were “spurious.” The methods used in the Lander study were full of evolutionary assumptions. The results entirely hinged on evolution. Although the paper did not explicitly state this, without the assumption of evolution no such conclusions could have been made.

This is what philosophers refer to as theory-ladenness. Although the paper authoritatively concluded the vast majority of the orphans in the human genome were spurious, this was not an empirical observation or inference, as it might seem to some readers. Their data (and proposed revisions to human gene catalogs), methods, and conclusions were all laden, at their foundation, with the theory of evolution.

So Velasco’s argument was circular. To defend evolution he claimed there were zero orphans in the human genome, but that “fact” was a consequence of assuming evolution is true in the first place. If the assumption of evolution is dropped, then there is no evidence for that conclusion.

Brochosomes

Since the Nelson-Velasco debate the orphan problem has just gotten worse. Consider, for example, brochosomes which are intricate, symmetric, secretory granules forming super-oily coatings on the integuments of leafhoppers. Brochosomes develop in glandular segments of the leafhopper’s Malpighian tubules.

The main component of brochosomes, as shown in a recent paper, is proteins. And these constituent proteins, as well as brochosome-associated proteins, are mostly encoded by orphan genes.

As the paper explains, most of these proteins “appear to be restricted to the superfamily Membracoidea, adding to the growing list of cases where taxonomically restricted genes, also called orphans, encode important taxon-specific traits.”

And how did all these orphan genes arise so rapidly? The paper hypothesizes that “It is possible that secreta exported from the organism may evolve especially rapidly because they are not strongly constrained by interactions with other traits.”

That evolutionists can so easily reach for just-so stories, such as this, is yet another example of how false predictions have no consequence for evolutionary theory. Ever since Darwin evolutionists have proclaimed how important it is that the species fall into the common descent pattern. This has especially been celebrated at the molecular level.

But of course the species fall into no such pattern, and when obvious examples present themselves, such as the brochosome proteins, evolutionists do not miss a step.

There is no empirical content to this theory. Predictions hailed as great successes and confirmations of the truth of evolution suddenly mean nothing and have no consequence when the falsification becomes unavoidable.

Religion drives science, and it matters.

h/t: El Hombre

This Didn’t Evolve a Few Mutations At a Time

Action Potentials

Are there long, gradual, pathways of functional intermediate structures, separated by only one or perhaps a few mutations, leading to every single species, and every single design and structure in all of biology? As we saw last time, this has been a fundamental claim and expectation of evolutionary theory which is at odds with the science.* If one mutation is rare, a lot of mutations are astronomically rare. For instance, if a particular mutation has a one-in-a-hundred million (one in 10^8) chance of occurring in a new individual, then a hundred such particular mutations have a one in 10^800 chance of occurring. It’s not going to happen. Let’s have a look at an example: nerve cells and their action potential signals.

[* Note: Some evolutionists have attempted to get around this problem with the neutral theory, but that just makes matters worse].

Nerve cells have a long tail which carries an electronic impulse. The tail can be several feet long and its signal might stimulate a muscle to action, control a gland, or report a sensation to the brain.

Like a cable containing thousands of different telephone wires, nerve cells are often bundled together to form a nerve. Early researchers considered that perhaps the electronic impulse traveled along the nerve cell tail like electricity in a wire. But they soon realized that the signal in nerve cells is too weak to travel very far. The nerve cell would need to boost the signal along the way for it to travel along the tail.

After years of research it was discovered that the signal is boosted by membrane proteins. First, there is a membrane protein that simultaneously pumps two potassium ions into the cell and three sodium ions out of the cell. This sets up a chemical gradient across the membrane. There is more potassium inside the cell than outside, and there is more sodium outside than inside. Also, there are more negatively charged ions inside the cell so there is a voltage drop (50-100 millivolt) across the membrane.

In addition to the sodium-potassium pump, there are also sodium channels and potassium channels. These membrane proteins allow sodium and potassium, respectively, to pass through the membrane. They are normally closed, but when the decaying electronic impulse travels along the nerve cell tail, it causes the sodium channels to quickly open. Sodium ions outside the cell then come streaming into the cell down the electro-chemical gradient. As a result, the voltage drop is reversed and the decaying electronic impulse, which caused the sodium channels to open, is boosted as it continues on its way along the nerve cell tail.

When the voltage goes from negative to positive inside the cell, the sodium channels slowly close and the potassium channels open. Hence the sodium channels are open only momentarily, and now with the potassium channels open, the potassium ions concentrated inside the cell come streaming out down their electro-chemical gradient. As a result the original voltage drop is reestablished.

This process repeats itself as the electronic impulse travels along the tail of the nerve cell, until the impulse finally reaches the end of the nerve cell. Although we’ve left out many details, it should be obvious that the process depends on the intricate workings of the three membrane proteins. The sodium-potassium pump helps set up the electro-chemical gradient, the electronic impulse is strong enough to activate the sodium channel, and then the sodium and potassium channels open and close with precise timing.

How, for example, are the channels designed to be ion-selective? Sodium is about 40% smaller than potassium so the sodium channel can exclude potassium if it is just big enough for sodium. Random mutations must have struck on an amino acid sequence that would fold up just right to provide the right channel size.

The potassium channel, on the other hand is large enough for both potassium, and sodium, yet it is highly efficient. It somehow excludes sodium almost perfectly (the potassium to sodium ratio is about 10000), yet allows potassium to pass through almost as if there were nothing in the way.

Nerve cells are constantly firing off in your body. They control your eyes as you read these words, and they send back the images you see on this page to your brain. They, along with chemical signals, control a multitude of processes in our bodies, and there is no scientific reason to think they gradually evolved, one mutation at time.

Indeed, that idea contradicts everything we know from the science. And yet this is what evolutionists believe. Let me repeat that: evolutionists believe nerve cells and their action potential designs evolved one mutation at time. Indeed, evolutionists believe this is a proven fact, beyond all reasonable doubt.

It would be difficult to imagine a more absurd claim. So let’s have a look at the details of this line of thinking. Here is a recent paper from the Royal Society, representing the state of the art in evolutionary thinking on this topic. The paper claims to provide a detailed explanation of how early evolution produced action potential technology.

Sounds promising, but when evolutionists speak of “details,” they have something slightly different in mind. Here are several passages from the paper which reveal that not only is there a lack of details, but that the study is thoroughly unscientific.

We propose that the next step in the evolution of eukaryote DCS [membrane depolarization (through uncontrolled calcium influx), contraction and secretion] coupling has been the recruitment of stretch-sensitive calcium channels, which allow controlled influx of calcium upon mechanical stress before the actual damage occurs, and thus anticipate the effects of membrane rupture.

The recruitment of calcium channels? And exactly who did the recruiting? Here the authors rely on vague terminology to paper over a host of problematic details of just how random mutations somehow performed this recruiting.

To prevent the actual rupture, the first role of mechanosensory Ca++ channels might have been to pre-activate components of the repair pathway in stretched membranes.

“To prevent”? Let’s spell out the logic a little more clearly. The authors are hypothesizing that these calcium channels evolved the ability to pre-activate the repair pathway “to prevent” actual rupture. By spelling out the logic a bit more clearly, we can see more easily the usual teleology at work. The evolution literature is full of teleology, and for good reason. Evolutionists are unable to formulate and express their ideas without it. The ever-present infinitive form is the tell-tale sign. Aristotelianism is dead—long live Aristotelianism.

As another anticipatory step, actomyosin might have been pre-positioned under the plasma membrane (hence the cortical actomyosin network detected in every eukaryotic cell) and might have also evolved direct sensitivity to stretch … Once its cortical position and mechanosensitivity were acquired, the actomyosin network could automatically fulfil an additional function: cell-shape maintenance—as any localized cell deformation would stretch the cortical actomyosin network and trigger an immediate compensatory contraction. This property would have arisen as a side-effect (a ‘spandrel’) of the presence of cortical actomyosin for membrane repair, and quickly proved advantageous.

An “anticipatory step”? “Pre-positioning”? Actomyosin “evolved” sensitivity to stretch? The position and mechanosensitivity “were acquired”? The network could “fulfil an additional function”? Sorry, but molecular machines (such as actomyosin) don’t “evolve” anything. There is more teleology packed into these few sentences than any medieval tract. And for good measure the authors also add the astonishing serendipity that this additional function “would have arisen as a side-effect.” That was lucky.

Once covering the cell cortex, the actomyosin network acquired the ability to deform the cell by localized contraction.

The actomyosin network “acquired the ability” to deform the cell by localized contraction? Smart move on the part of the network. But may we ask just how did that happen?

Based on the genomic study of the protist Naegleria which has a biphasic life cycle (alternating between an amoeboid and a flagellated phase), amoeboid locomotion has been proposed to be ancestral for eukaryotes. It might have evolved in confined interstitial environments, as it is particularly instrumental for cells which need to move through small, irregularly shaped spaces by exploratory deformation.

Amoeboid locomotion evolved “as it is particularly instrumental.” No infinitive form but this is no less teleological. Things don’t evolve because they are “instrumental.” What the authors fail to inform their readers of is that this would require an enormous number of random mutations.

One can hypothesize that, if stretch-sensitive calcium channels and cortical actomyosin were part of the ancestral eukaryotic molecular toolkit (as comparative genomics indicates), membrane deformation in a confined environment would probably trigger calcium influx by opening of stretch-sensitive channels, which would in turn induce broad actomyosin contraction across the deformed part of the cell cortex, global deformation and cell movement away from the source of pressure.

The concept of a “molecular toolkit” is standard in evolutionary thought, and another example teleological thinking.

One can thus propose that a simple ancestral form of amoeboid movement evolved as a natural consequence of the scenario outlined above for the origin of cortical actomyosin and the calcium–contraction coupling; once established, it could have been further elaborated.

Amoeboid movement evolved “as a natural consequence,” and “once established” was “further elaborated”? This is nothing more than teleological story-telling with no supporting evidence.

It is thus tempting to speculate that, once calcium signalling had gained control over primitive forms of amoeboid movement, the same signalling system started to modify ciliary beating, possibly for ‘switching’ between locomotor states.

Calcium signaling “gained control” and then “started to modify” ciliary beating “for ‘switching’ between locomotor states”? The “for switching” is yet another infinitive form, and “gained control” is an active move by the calcium signaling system. Pure, unadulterated, teleology.

Possibly, in ancestral eukaryotes calcium induced a relatively simple switch (such as ciliary arrest, as still seen in many animal cells and in Chlamydomonas in response to high Ca++ concentrations), which was then gradually modified into more subtle modulations of beating mode with a fast turnover of molecular actors mediated by differential addition, complementation and loss.

“Calcium induced a relatively simple switch”? Sorry, ions don’t induce switches, simple or otherwise. And the switch “was then gradually modified into more subtle modulations”? Note how the passive voice obviates those thorny details. The switch “was modified” conveniently omits the fact that such modification would have to occur via random mutation, one mutation at a time.

Alternatively, control of cilia by calcium could have evolved convergently—but such convergence would then have been remarkably ubiquitous, as there seems to be no eukaryotic flagellum that is not controlled by calcium in one way or another.

“Could have evolved convergently”? And exactly how would that happen? At least the authors then admit to the absurdity of that alternative.

Unfortunately, they lack such sensibility for the remainder of the paper. As we saw above, the paper is based on a sequence of teleological thinking. It falls into the evolutionary genre where evolution is taken, a priori, as a given. This going in assumption underwrites vast stretches of teleological thought, and cartoon-level story telling. Not only is there a lack of empirical support, but the genre is utterly unscientific, as revealed by even a mildly critical reading.

And needless to say, the paper does absolutely nothing to alleviate the problem we began with. The many leaps of logic and reasoning in the paper reveal all manner of monumental changes evolution requires to construct nerve cells and the action potential technology. We are not looking at a narrative of minute, gradual changes, each contributing to the overall fitness. Many, many simultaneous mutations are going to be needed. Even a conservative minimum number of 100 simultaneous mutations leads to the untenable result of a one in 10^800 chance of occurring.

It’s not going to happen. Religion drives science, and it matters.

Here is How Evolutionists Respond to the Evidence

Unresponsive

Mutations are rare and good ones are even more rare. One reason mutations are rare is because there are sophisticated error correction mechanisms in our cells. So according to evolution random mutations created correction mechanisms to suppress random mutations. And that paradox is only the beginning. Because error correction mechanisms, as with pretty much everything else in biology, require many, many mutations to be created. If one mutation is rare, a lot of mutations are astronomically rare. For instance, if a particular mutation has a one-in-a-million (one in 10^6) chance of occurring in a new individual, then a hundred such particular mutations have a one in 10^600 chance of occurring. It’s not going to happen.

How do evolutionists reckon with this scientific problem?

First, one common answer is to dismiss the question altogether. Evolution is a fact, don’t worry about the details. Obviously this is not very compelling.

Second, another common answer is to cast the problem as a strawman argument against evolution, and appeal to gradualism. Evolutionists going back to Darwin have never described the process as “poof.” They do not, and never have, understood the process as the simultaneous origin of tens or hundreds, or more mutations. Instead, it is a long, slow, gradual process, as Darwin explained:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case […] Although the belief that an organ so perfect as the eye could have been formed by natural selection, is enough to stagger any one; yet in the case of any organ, if we know of a long series of gradations in complexity, each good for its possessor, then, under changing conditions of life, there is no logical impossibility in the acquirement of any conceivable degree of perfection through natural selection

The Sage of Kent could find “no such case”? That’s strange, because they are ubiquitous. And with the inexorable march of science, it is just getting worse. Error correcting mechanisms are just one example of many. Gradualism is not indicated.

What if computer manufacturers were required to have a useful, functional electronic device at each step in the manufacturing process? With each new wire or solder, what must emerge is a “long series of gradations in complexity, each good for its possessor.”

That, of course, is absurd (as Darwin freely confessed). From clothing to jet aircraft, the manufacturing process is one of parts, tools, and raw materials strewn about in a useless array, until everything comes together at the end.

The idea that every single biological structure and design can be constructed by one or two mutations at a time, not only has not been demonstrated, it has no correspondence to the real world. It is just silly.

What evolution requires is that biology is different, but there is no reason to believe such a heroic claim. The response that multiple mutations is a “strawman” argument does not reckon with the reality of the science.

Third, some evolutionists recognize this undeniable evidence and how impossible evolution is. Their solution is to call upon a multiverse to overcome the evidence. If an event is so unlikely it would never occur in our universe, just create a multitude of universes. And how many universes are there? The answer is, as many as are needed. In other words, when confronted with an impossibility, evolutionist simply contrive a mythical solution.

Forth, another common response that evolutionists make is to appeal to the fitness of the structure in question. Biological designs, after all, generally work pretty well, and therefore have high fitness. Is this not enough to prove that it evolved? For evolutionists, if something helps, then it evolves. Presto.

To summarize, evolutionists have four different types of responses to the evidence, and none of the responses do the job.

Religion drives science, and it matters.

Early Complexity: A Case Study of Evolutionary Theory

No Matter How Perplexing

Nature does not make jumps. That old canon of natural history, as Darwin called it, goes back centuries and was heartily endorsed and adopted by evolutionary theory. Here are representative quotes from Origin, 1st edition, explaining important this doctrine was to Darwin:

I have been astonished how rarely an organ can be named, towards which no transitional grade is known to lead. The truth of this remark is indeed shown by that old canon in natural history of "Natura non facit saltum." We meet with this admission in the writings of almost every experienced naturalist; or, as Milne Edwards has well expressed it, nature is prodigal in variety, but niggard in innovation. Why, on the theory of Creation, should this be so? [194]

On the theory of natural selection we can clearly understand the full meaning of that old canon in natural history, "Natura non facit saltum." This canon, if we look only to the present inhabitants of the world, is not strictly correct, but if we include all those of past times, it must by my theory be strictly true. [206]

The canon of "Natura non facit saltum" applies with almost equal force to instincts as to bodily organs. [210]

the canon in natural history, of "natura non facit saltum" is applicable to instincts as well as to corporeal structure, and is plainly explicable on the foregoing views, but is otherwise inexplicable,—all tend to corroborate the theory of natural selection. [243]

As natural selection acts solely by accumulating slight, successive, favourable variations, it can produce no great or sudden modification; it can act only by very short and slow steps. Hence the canon of "Natura non facit saltum," which every fresh addition to our knowledge tends to make more strictly correct, is on this theory simply intelligible. We can plainly see why nature is prodigal in variety, though niggard in innovation. But why this should be a law of nature if each species has been independently created, no man can explain. [471]

In these and other passages Darwin explained the fundamental evolutionary view and prediction that evolution and natural selection produce gradual change with no sudden changes or jumps.

At this point, more than a century and a half later, that fundamental prediction of evolution has been falsified so many times by the empirical evidence it is a wonder there is anyone left believing in the theory.

One way that this prediction has been falsified, among many, is in the finding of early complexity. Evolutionists of course expected that the history of life would reveal a gradual increase in complexity. But as I have discussed many times here, life does not fit this evolutionary expectation. Instead the very earliest life forms reveal high complexity.

For example, as science writer (and evolutionist) Amy Maxmen explains, Amoebas contain hundreds of times more DNA than humans, and this “just didn’t make sense.”

amoebas date back farther in time than humans, and simplicity is considered an attribute of primitive beings. It just didn’t make sense.

The amoeba versus human comparison was just one example of how genome size contradicts evolutionary theory. What about the number of genes? Here again, evolution makes a clear prediction, as Maxmen explains:

Simple, early organisms would have fewer genes than complex ones, they [evolutionists] predicted

And here again, the evolution prediction was demolished by the science. For example, evolutionists were surprised to find sea anemones have more genes than insects, in spite of arising earlier. That, admits Maxmen, “meant animals might have been genetically complex from the start.”

These sorts of findings also contradict the evolutionary tree. Your high school biology book said that the new genetic data perfectly corroborated the traditional morphological data. Evolutionists have triumphantly celebrated the confirmation that the molecular sequence data provided to pre-existing evolutionary trees.

But that celebration was premature. In fact, study after study have found there is no such corroboration. In fact, as I have documented many times, morphological data across the species contradict the evolutionary tree (i.e., they do not fall into an evolutionary common descent pattern), and the new molecular data simply continued that trend.

Then molecular analyses did something else. They rearranged the order of branches on evolutionary trees. Biologists pushed aside trees based on how similar organisms looked to one another, and made new ones based on similarities in DNA and protein sequences. The results suggested that complex body parts evolved multiple times and had also been lost.

In other words, the scientific data contradict the theory. The result is that evolutionists have had to concoct increasingly complex and bizarre epicycles to try to explain the data. This includes complex structures evolving, then disappearing, then re-evolving, all in the same lineage, as well as independently evolving in a separate lineage. As Maxmen explains:

Furthermore, the idea that complex parts like a brain and nervous system—including nerve cells, synapses, and neurotransmitter molecules—could evolve separately multiple times perplexes evolutionary biologists because parts are gained one at a time. The chance of the same progression happening twice in separate lineages seems unlikely—or so biologists thought.

This is a tautology. Whatever we observe, evolution somehow created it, no matter how ridiculous the narrative becomes. An unfair criticism? Consider Maxmen’s conclusion:

When new data suggests a rearrangement, it must be considered no matter how perplexing the conclusion seems.

In other words, the plausibility of evolution is not a consideration. No matter “how perplexing” are the data, we must find a way to force fit it into the theory.

Religion drives science, and it matters.

Embryonic Development Reveals Staggering Complexity

Oh My

I recently cited a paper on the evolution of embryonic development and how the evidence contradicts evolutionary theory and common descent. Even the evolutionists, though in understated terms, admitted there were problems. Evolutionary analyses are “reaching their limits,” it is difficult to “conclude anything about evolutionary origins,” genetic similarities “do not necessarily imply common ancestry,” and “conserved regulatory networks can become unrecognizably divergent.” In other words, like all other disciplines within the life sciences, embryonic development is not working. The science contradicts the theory.

But there is much more to the paper, and as a reader noticed, the authors give a rather blunt admission of the magnitude of the problem, not often seen in the literature:

One of the main reasons for Duboule’s pessimism about the return of the EvoDevo comet is the staggering complexity and diversity of cellular and developmental regulatory processes. The configuration space for realistic models of such systems is vast, high dimensional, and potentially infinitely complex.

Staggering complexity? Staggering diversity? The configuration space is vast and high-dimensional?

And it is potentially infinitely complex?

And we are to believe this is the product of random mutations?

Religion drives science, and it matters.

About That RNA World Hypothesis

It Just Doesn’t Make Sense

Given its widespread popularity and acceptance you might not have realized that the so-called RNA-World hypothesis suffers from some dramatic problems. At the top of the list is the rather awkward fact that there is, err, no evidence for it. While skeptics have pointed this out for years, we now see evolutionists coming clean on this inconvenient truth as well. To wit, here is how Peter Wills and Charles Carter open their recent BioSystems paper:

The RNA World is a widely-embraced hypothetical stage of molecular evolution, devoid of protein enzymes, in which all functional catalysts were ribozymes. Only one fact concerning the RNA World can be established by direct observation: if it ever existed, it ended without leaving any unambiguous trace of itself.

Even this is a bit of an understatement. Because without the prior assumption of evolution, which can and has underwritten a wide range of speculation, there is precisely zero reason to believe this wild hypothesis. No organisms have ever been discovered that demonstrate the RNA World hypothesis in action. Nor have scientists ever constructed any such organisms in their laboratories. This is not too surprising because no one has even produced anything remotely close to a detailed design of how such organisms could function.

Wills and Carter also point out negative evidences such as catalysis (RNA enzymes lack the ability to function over a wide range of temperatures) and the “impossible obstacles” to the hypothetical yet necessary transition from the RNA World to something resembling today’s extant cells. As Carter explains:

Such a rise from RNA to cell-based life would have required an out-of-the-blue appearance of an aaRS [aminoacyl-tRNA synthetase]-like protein that worked even better than its adapted RNA counterpart. That extremely unlikely event would have needed to happen not just once but multiple times—once for every amino acid in the existing gene-protein code. It just doesn’t make sense.

Indeed, it just doesn’t make sense. And yet in spite of these obvious problems, the RNA World has been a textbook staple, presented as a plausible and likely example of how early life evolved.

Religion drives science, and it matters.

How Embryonic Development Bears on Evolution

Follow the Theory

In order for evolution to have occurred, the intricate embryonic development stages of species must have evolved. Indeed, the developmental pathways of the species would be crucial in such a process. If we are to believe the evolutionary claim that the species spontaneously arose, then untold embryonic development pathways must have somehow undergone massive change. But while evolutionists expected the study of such evolution of development to yield great insight into the evolutionary process and history, it has underwhelmed. This shortcoming is well known, as exemplified in this 2015 paper:

First, traditional comparative approaches to the evolution of development—whether focused on the morphological or on the molecular/genetic level—are reaching their limits in terms of explanatory power.

Except that this is an overstatement. To say that comparative approaches “are reaching their limits in terms of explanatory power” is to suggest that there was, at one time, some significant level of explanatory power provided. That would be a very optimistic interpretation of the data.

The paper continues:

The more we learn about the evolution of pattern-forming gene networks, or the ontogeny of complex morphological traits, the more it becomes clear that it is less than straightforward to conclude anything about evolutionary origins or dynamics based on such comparisons alone.

“Less than straightforward”? Let’s be clear—a more accurate descriptor would be “impossible.” In fact, the evidence does not reveal an evolutionary history, but rather is supported by the theory. Evolutionary theory does not follow the data, as Huxley prescribed, but rather the data follow the theory.

The paper continues:

On the one hand, homoplasy or convergent evolution abounds at all levels of investigation. One of the most lauded major insights of EvoDevo is that a common toolkit of genes and signaling pathways is reused over and over again to create a large diversity of different body plans, shapes, and organs.

Most lauded major insights? That would be the mother of all euphemisms. Evolutionists are always rationalizing devastating contradictions as teachable moments, and here we have yet another example. To cast the nonsensical finding of a “common toolkit” as a “major insight” is laughable.

This becomes clear as the paper continues:

Because of this, similarities in gene expression patterns or morphological structure often do not necessarily imply common ancestry, since they may as well reflect the frequent reuse of the same regulatory or morphogenetic modules.

Profound similarities “do not necessarily imply common ancestry.” We have now entered a Lewis Carroll world, as Sober would put it. The whole point of evolution was that such similarities revealed and mandated common descent. But now, we have the exact opposite, as similarities cannot be due to common descent, but must have arisen independently. And this is an “insight”? A fundamental prediction is demolished and evolutionists do not skip a beat. This is not science.

But it gets worse:

On the other hand, developmental system drift allows conserved networks to change considerably in terms of their component genes and regulatory interactions without changing the phenotypic outcomes such systems produce. This means that even functionally conserved regulatory networks can become unrecognizably divergent at the molecular and genetic level, especially across large evolutionary time spans.

We have now reached the height of absurdity. First, profound developmental similarities were found which could not be ascribed to common descent. Now we find that those developmental pathways which can (theoretically) be ascribed to common descent are profoundly different.

When will this bad dream end? The science contradicts the theory. Over. And over. And over. And over.

It never ends. Religion drives science, and it matters.

[h/t: El Hombre]

Allmon and Ross Demolish Evolution

It Gets Worse

Last time we saw, in a new paper, evolutionists Warren Allmon and Robert Ross reformulate the argument for evolution from homologous structures. The paper makes several mistakes, but is important because it is a rare case of evolutionists (i) recognizing the religion in evolutionary thinking, and (ii) trying to do something about it. In this case the religion is in the claim that God would not have created non optimal homologies (such as vestigial structures). Allmon and Ross attempt to remove the religion by restating the claim as: God did not have to create such homologies. It is good that evolutionists are finally recognizing the religion, after having been in denial for so many years. But Allmon and Ross’ solution fails on several counts.

The first failure of Allmon and Ross’ solution is that it strips the power of the argument. The traditional religious arguments (i.e., God would not create those structures) at least had the virtue of providing a strong argument for evolution. Granted it was a religious argument, and granted one had to agree with that particular religion. And granted it ignored the problems of process and pattern (more below on that). And granted it turned evolution into, as Elliott Sober hinted, a “Lewis Carroll world in which down is up,” because the argument required evidence that is unlikely on evolution. The more unlikely, the better. Such is the logic of evolution’s religion. But after all those caveats, at least it provided a strong argument for evolution.

With design refuted, evolution had to be true, no matter how many problems it had. But with Allmon and Ross’ reformulation, design is not refuted. Now the advantage for evolution is not that the alternative is false or even highly unlikely, but that the alternative does not specify what we observe whereas evolution does. Allmon and Ross triumphantly conclude their new formulation is a powerful argument for evolution. They apparently think their reformulation is merely a minor tweak, and that their new argument is just as strong as the traditional argument. It isn’t. There is no free lunch. What Allmon and Ross fail to understand is that this is a much weaker argument.

But it gets worse.

The second failure of Allmon and Ross’ solution is that it never did get rid of the religion as they had hoped. Allmon and Ross naively assume that the claim God may or may not create these homologies is merely an obvious point of fact. This is a deep subject into which Allmon and Ross have rushed in, but suffice it to say that it is not at all clear that God can go with either world. Leibniz undoubtedly would disagree. The Lutheran polymath would argue that because of His perfection and other attributes, God cannot just create any old world. The bottom line, and one which Allmon and Ross are blissfully naïve of, is that like it or not, claims about God are religious.

But it gets worse. Much worse.

Not only did Allmon and Ross utterly misapprehend and expose the homology argument, they have, in fact, altogether demolished evolutionary theory. Remember, with their reformulation it becomes utterly crucial that evolution predicts what we observe. In other words, evolution must predict the pattern of similarities and differences we observe across the species. This is because their new formulation was that while design can explain a common descent pattern or other patterns, evolution is narrowly restricted to the common descent pattern.

With that the two Harvard trained Epicureans just inadvertently blew up evolution. This is because what we actually observe is not the common descent pattern.

The actual comparisons between the species have contradicted the common descent pattern over and over. It is, as we have documented here so many times, not even close.

If evolution predicts the common descent pattern, then by modus tollens, evolution is false.

Religion drives science, and it matters.

Evolutionists: Our Findings Suggest That Similarities in Bilateria Evolved Independently

Not Even Wrong

This week one of the top scientific journals in the world published what would seem to be a ground breaking paper. The paper claims to have found evidence for the independent evolution of nervous system similarities across the Bilateria. As the abstract explains:

Our findings … suggest that the similarities in dorsoventral patterning and trunk neuroanatomies evolved independently in Bilateria.

By the end of the manuscript the authors are even more confident:

Therefore, the expression of dorsoventral transcription factors evolved independently from the trunk neuroanatomy at least in certain bilaterian lineages

This is a monumental claim, but there is only one problem: It is blatantly false. The paper’s findings did not “suggest” the evolution, independent or otherwise, of the transcription factor expression patterns. They certainly did not demonstrate, show or find such an incredible conclusion.

It would be difficult to overstate how misleading this paper is. It provided literally zero evidence for any such evolution. Nothing. Nada.

There simply is no such scientific evidence in the paper. The claim that they found that the expression of dorsoventral transcription factors evolved independently in certain bilaterian lineages is not even wrong.

Let’s be clear about this. I am not saying their claim is weak. I am not saying their claim is faulty. I am not saying they failed to make their case conclusively. The problem is they don’t have any case at all.

We cannot criticize the science because, well, there is no science. For a paper entitled “Convergent evolution of bilaterian nerve cords,” one would have expected at least some evidence and explanation for the evolution of bilaterian nerve cords.

Unfortunately papers such as this inform journalists and science writers. They report that scientists have now discovered yet another aspect of evolution. It is yet another example of how science proves evolution.

In fact, if one is looking for a meaningful takeaway, what the study did find is that the expectations of evolution—that nervous system similarities would align with the evolutionary tree—turned out to be, like so many other of evolution’s predictions—false. But that doesn’t fit the narrative.

Religion drives science, and it matters.

Protein Mutations Are Highly Coupled

A Rugged Fitness Landscape

A new study from Michael Harms’ laboratory at the University of Oregon finds that potential amino acid substitutions in protein sequences are highly coupled. That is, if one residue mutates to a new amino acid, the swap impacts the other possible substitutions—they now have a different impact on the protein tertiary structure. As the paper explains:

Proteins exist as ensembles of similar conformations. The effect of a mutation depends on the relative probabilities of conformations in the ensemble, which in turn, depend on the exact amino acid sequence of the protein. Accumulating substitutions alter the relative probabilities of conformations, thereby changing the effects of future mutations. This manifests itself as subtle but pervasive high-order epistasis. Uncertainty in the effect of each mutation accumulates and undermines prediction. Because conformational ensembles are an inevitable feature of proteins, this is likely universal.

This coupling leads to a “profound unpredictability in evolution,” and the authors conclude that “detailed evolutionary predictions are not possible given the chemistry of macromolecules.”

This finding seems to confirm what many evolutionists have said for decades—that evolution is a contingent, not law-like, process:

These [macro]evolutionary happenings are unique, unrepeatable, and irreversible.” – Theodosius Dobzhansky, 1957.

Laws and experiments are inappropriate techniques” for explaining evolutionary events and processes. – Ernst Mayr

What science needs are “plausible scenarios for a fully material universe, even if those scenarios cannot be currently tested.” – Victor Stenger, 2004

any replay of the tape would lead evolution down a pathway radically different from the road actually taken. – Stephen Jay Gould

All of this is in direct contradiction to the science, which reveals undeniable patterns in biology that have been repeated over and over. From the pervasive instances of convergence, recurrence, and all kinds of other “ence’s”, to the non adaptive patterns discussed by Michael Denton, the biological is anything but haphazard or random. Clearly, the same solution, for whatever reason, is used repeatedly across a wide range of species, in various patterns.

This is a clear falsification of an evolutionary expectation expressed across many years, and widely held by a consensus of experts.

But there is another problem with these protein findings. In addition to confirming the complexity and coupling of protein folding, the findings also seem to corroborate what theoretical and experimental studies have shown for years, that the fitness landscape of macromolecules in general, and proteins in particular, is rugged.

The problem of evolving a protein is difficult for several reasons. First, protein function drops off rapidly with only a few mutations. Very quickly a protein loses its function as you move away from the native sequence.

Second, random or starting sequences are stuck in a flat and rugged fitness landscape. There is little sign of a the kind of smooth and gradually increasing fitness landscape that would aid evolution’s enormous task of figuring out how proteins could evolve.

These problems are just getting worse, and this new finding a good example of that trend.

Religion drives science, and it matters.

Blindness in Cave Fish is Due to Epigenetics

Evolutionists Say “We See”

A recent paper out of Brant Weinstein’s and William Jeffery’s laboratories on eye development, or the lack thereof, in blind cave fish has important implications for evolutionary theory (paper discussed here). The study finds that the loss of eyes in fish living in dark Mexican caves is not due to genetic mutations, as evolutionists have vigorously argued for many years, but due to genetic regulation. Specifically, methylation of key development genes represses their expression and with it eye development in this venerable icon of evolution. But the finding is causing yet more problems for evolutionary theory.

Darwin appealed to the blind cave fish in his one long argument for evolution. It is a curious argument in many ways, and the first sign of problems was in Darwin’s presentation where he flipped between two different explanations. At one point he explained the loss of vision in the cave fish as an example of evolutionary change not due to his key mechanism, natural selection. Instead, the Sage of Kent resorted to using the Lamarckian mechanism or law of “use and disuse.” Privately Darwin despised and harshly criticized Lamarck, but when needed he occasionally employed his French forerunner’s ideas.

Elsewhere Darwin hit upon a natural selection-based mechanism for the blind cave fish, explaining that elimination of the costly and unneeded vision system would surely raise the fitness of the hapless creatures.

This latter explanation would become a staple amongst latter day evolutionary apologists, convinced that it mandates the fact of evolution. Anyone who has discussed or debated evolutionary theory with today’s Epicureans has likely encountered this curious argument that because blind cave fish lost their eyes, therefore the world must have arisen by itself.

Huh?

To understand the evolutionary logic, or lack thereof, one must understand the history of ideas, and in particular the idea of fixity, or immutability, of species. According to evolutionists, species are either absolutely fixed in their designs, or otherwise there are no limits to their evolutionary changes and the biological world, and everything else for that matter, spontaneously originated.

Any evidence, for any kind of change, no matter how minor, is immediately yet another proof text for evolution, in all that the word implies.

Of course, from a scientific perspective, the evidence provides precisely zero evidence for evolution. Evolution requires the spontaneous (i.e., by natural processes without external input) creation of an unending parade of profound designs. The cave fish evidence shows the removal, not creation, of such a design.

The celebration of such evidence and argument by Darwin and his disciples reveals more about evolutionists than evolution. That they would find this argument persuasive reveals their underlying metaphysics and the heavy lifting it performs. It is all about religion.

We are reminded of all this with the news of Weinstein’s new study. But we also see something new: The insertion, yet again, of Lamarck into the story. The irony is that the epigenetics, now revealed as the cause of repressed eye development in the cave fish, hearkens back to Lamarck.

Darwin despised Lamarck and later evolutionists made him the third rail in biology. Likewise they have pushed back hard against the scientific findings of epigenetics and their implications.

The environment must not drive biological change.

False.

Well such biological change must not be transgenerational.

False.

Well such inheritance must not be long lasting, or otherwise robust.

False again.

This last failure is revealed yet again in the new blind cave fish findings.

False predictions count. A theory that is repeatedly wrong, over and over, in all of its fundamental expectations, will eventually be seen for what it is.

The rise of epigenetics is yet another such major failure. Evolutionists pushed back against it because it makes no sense on the theory, and that means it cannot now be easily accommodated.

One problem is that epigenetics is complex. The levels of coordination and intricacy of mechanism are far beyond evolution’s meager resources.

It’s not going to happen.

Another problem is the implied serendipity. For instance, one epigenetic mechanism involves the molecular tags places on the tails of the DNA packing proteins called histones. While barcoding often seems to be an apt metaphor for epigenetics, the tagging of histone tails can influence the histone three dimensional structures. It is not merely an information-bearing barcode. Like the tiny rudder causing the huge ship to change course, the tiny molecular tag can cause the much larger packing proteins to undergo conformational change, resulting in important changes in gene accessibility and expression.

This is all possible because of the special, peculiar, structure and properties of the histone protein and its interaction with DNA. With evolution we must believe this just happened to evolve for no reason, and thus fortuitously enabled the rise of epigenetics.

Another problem with epigenetics is that it is worthless, in evolutionary terms that is. The various mechanisms that sense environmental shifts and challenges, attach or remove one of the many different molecular tags to one of the many different DNA or histone locations, propagate these messages across generations, and so forth, do not produce the much needed fitness gain upon which natural selection operates.

The incredible epigenetics mechanisms are helpful only at some yet to be announced future epoch when the associated environmental challenge presents itself. In the meantime, selection is powerless and according to evolution the incredible system of epigenetics, that somehow just happened to arise from a long, long series or random mutations, would wither away with evolution none the wiser.

These are the general problems with epigenetics. In the case of the blind cave fish, however, there is possible explanation. It is a longshot, but since this case specifically involves the loss of a stage of the embryonic development, evolutionists can say that genetic mutations caused changes in the methylating proteins, causing them to be overactive.

This explanation relies on the preexistence of the various epigenetic mechanisms, so does not help to resolve the question of how they could have evolved. What the explanation does provide is a way for evolutionists to dodge the bullet presented by the specter of the cave fish intelligently responding to an environmental shift.

Such teleology in the natural world is not allowed.

So the evolutionary prediction is that these proteins will be found to have particular random changes causing an increase in their methylation function, in particular at key locations in key genes (i.e., the genes associated eye development).

That’s a long shot, and an incredible violation of Occam’s Razor.

My predictions are that (i) this evolutionary prediction will fail just as the hundreds that came before, and (ii) as with those earlier failures, this failure will do nothing to open the evolutionist’s eyes.

Religion drives science, and it matters.

World’s Oldest Tree is World’s Most Complex Tree

Makes Perfect Sense

We have often discussed the problem of “early complexity,” and how as we peer back in time—whether in the geographic strata or by phylogenetic reconstruct—things don’t get simpler. This makes no sense on evolution and this week’s news of a fossil specimen in northwest China, revealing and ancient, and highly complex, tree, just makes it worse. As one of the authors admitted:

This raises a provoking question: why are the very oldest trees the most complicated?

Fortunately evolution is a fact.

Welcome to Alt-Science

Expelled

Sometimes it’s obvious, as in the case of the scientific research paper that was rejected after it was accepted. While the paper was well accepted and given positive comments from peer reviewers, certain members of the editorial board of a seemingly scientific journal noticed that the results had negative implications for evolution. And so months after the editor had told the authors he was happy “to proceed with publication,” the paper suddenly was, “on further reflection and discussion,” summarily rejected.

And what exactly was the “discussion” about? That “the unspoken implication of the article is that, probabilistically, random undirected evolution is impossible.”

And that, dear scientists, is not allowed.

Random undirected evolution is, by definition, a fact. Break that ground rule, and pay the price. This isn’t about science or truth. This is the alt-science that seeks to control everything from publications and textbooks to careers and funding.

Religion drives science, and it matters.

But, But, But, … The Origin Of Life Was All But Solved!

“The origin of life is among the greatest open problems in science”

With everyone from the National Academy of Sciences to science writers such as Carl Zimmer proclaiming that the origin of life problem has essentially been solved, we wonder why we continue to find researchers, this time Yehuda Zeiri at Ben-Gurion University, admitting that:

Despite decades of research, how life began on Earth remains one of the most challenging scientific conundrums facing modern science.

and Sara Walker resorting to hope and luck:

The origins of life stands among the great open scientific questions of our time. While a number of proposals exist for possible starting points in the pathway from non-living to living matter, these have so far not achieved states of complexity that are anywhere near that of even the simplest living systems. A key challenge is identifying the properties of living matter that might distinguish living and non-living physical systems such that we might build new life in the lab. This review is geared towards covering major viewpoints on the origin of life for those new to the origin of life field, with a forward look towards considering what it might take for a physical theory that universally explains the phenomenon of life to arise from the seemingly disconnected array of ideas proposed thus far. The hope is that a theory akin to our other theories in fundamental physics might one day emerge to explain the phenomenon of life, and in turn finally permit solving its origins. […] If we are so lucky as to stumble on new fundamental understanding of life that allows us to solve our origins, it could be such a radical departure from what we know now that it might be left to the next generation of physicists to reconcile the unification of life with other domains of physics, as we are now struggling to accomplish with unifying general relativity and quantum theory a century after those theories were first developed.

But “hope” is not a good science strategy.

One sign of this problem is the proliferation of hypotheses, indicating, as we have pointed out many times, the lack of any good solution. Or as Alex Berezow a bit more bluntly puts it:

The origin of life is a profound mystery. Once life arose, natural selection and evolution took over, but the question of how a mixture of various gases created life-giving molecules that arranged into structures capable of reproducing themselves remains unanswered. Many theories have been proposed, some of which are popular (e.g., RNA World), and some of which are a far-fetched (e.g., aliens). Unlike politics, more ideas are not necessarily better; in science, a diversity of theories tends to betray the reality that scientists have no idea what's going on.

No idea what’s going on? It must be time for Jeremy England to find another Ilya Prigogine idea.