The design debate through the looking glass

Design through the Looking Glass

Evolution News & Views 

You don't have to hold an amino acid up to a mirror to see its mirror image. Amino acids (except for one, glycine) come in pairs, like gloves, on the real-world side of the looking glass. So do the sugars used in DNA and RNA; they are assigned a "handedness" based on conventional rules of describing their orientation in 3-D space. In all other physical respects, chemical and thermodynamic, they are identical in their activity. This makes them difficult to separate.

The phenomenon is known as chirality. The chiral "isoforms" are called enantiomers of each other. Left-handed enantiomers are preceded byL- (from Latin levo) as in L-alanine, while right-handed enantiomers are preceded by D- (fromdextro) as in D-ribose. A mixture of both hands is said to be racemic, or heterochiral. A pure mixture of one hand is called homochiral.

With only rare exceptions, all living things use just one "hand" of these molecular gloves: left-handed amino acids in proteins, and right-handed sugars in nucleic acids. How this came about has long been a mystery, as four Chinese scientists from Tsinghua University in Beijing explain in Nature Chemistry:

Despite biology's seemingly limitless diversity and the vastness of its territories that permeate into virtually every corner of the Earth, at the fundamental level of biochemistry, all known forms of life are narrowly defined by a single version of molecular machinery based on L-amino acids and D-ribose nucleic acids. Although rare examples of the use of D-amino acids, such as D-aspartic acid in animal brains, and L-sugars, such as L-arabinose in plants, do exist, the central dogma and most of the biological macromolecules have followed the homochirality established by life's earliest ancestors. Processes that led biology onto this particular chiral path have remained largely elusive, even though experimental evidence for breaking the mirror symmetry has been reported and many theoretical models have been proposed.[Emphasis added.]

As it stands, no experimental or theoretical model explains the origin of life's homochirality by natural processes. Some experimenters have produced a slight enantiomeric excess of one hand or the other, but usually with non-biological chemicals, and nothing approaching the purity of life's chiral molecules. Proteins and nucleic acids cannot work with mixed handedness. A single wrong-handed building block is enough to destroy DNA, RNA, and proteins. As we saw last year, checkpoints ensure that life's building blocks remain homochiral.

This purity of handedness baffles materialists, because their causal toolkit only includes natural law and chance. The probability of getting a single-handed polymer from racemic ingredients is comparable to getting a string of coin tosses coming up all heads. The longer the sequence, the more improbable it becomes -- quickly swamping the chance hypothesis. Yet as Wang et al. state, our knowledge of natural laws isn't helping solve the problem.

Recently, an in vitro selected catalytic RNA capable of incorporating nucleotides in a cross-chiral fashion without enantiomeric cross-inhibition was reported. The fact that no known laws of physics and chemistry preclude biology's use of either of the two chiral systems, mirror-image twins of one another, has led to an intriguing question as to whether a parallel mirror-image world of biology running on a chirally inverted version of molecular machinery could be found in the universe or be created in the laboratory.

Turning from origins to application, they describe their initial attempts to create mirror-image life:

We reasoned that towards synthesizing a mirror-image biological system, an imperative step would be to reconstitute a chirally inverted version of the central dogma of molecular biology with D-amino acid enzymes and L-ribose nucleic acids--although reconstituting a mirror-image, ribosome-based translation systemthrough the total synthesis of all the ribosomal RNA (rRNA) and protein building blocks is still beyond the current technology, the totalchemical synthesis of (small enough) mirror-image polymerases might be feasible. Here we set out to synthesize such a mirror-image polymerase and to test if two steps in the central dogma, the template-directed polymerization of DNA and the transcription into RNA, can be carried out in a synthetic mirror-image molecular system (Fig. 1a).

(For present purposes, we won't dispute the central dogma, although biologist Jonathan Wells has written extensively on its problems.)

These scientists did, in fact, succeed in getting some template-driven polymerization and transcription of opposite-handed amino acids. It was very slow, but it demonstrates that, in principle, life could exist in a mirror image of itself. Alice through the looking glass would appear identical to her mirror image, but would not be able to eat opposite-handed food!

Commenting on this work for Nature, Mark Peplow explains why synthetic mirror-image biomolecules have desirable properties:

In principle, looking-glass versions of these molecules should work together in the same way as normal ones -- but they might be resistant to attack by conventional viruses or enzymes that have not evolved in a looking-glass world.

That makes mirror-image biochemistry a potentially lucrative business. One company that hopes so is Noxxon Pharma in Berlin. It uses laborious chemical synthesis to make mirror-image forms of short strands of DNA or RNA called aptamers, which bind to therapeutic targets such as proteins in the body to block their activity. The firm has several mirror-aptamer candidates in human trials for diseases including cancer; the idea is that their efficacy might be improved because theyaren't degraded by the body's enzymes. A process to replicate mirror-image DNA could offer a much easier route to making the aptamers, says Sven Klussmann, Noxxon Pharma's chief scientific officer.

Wang et al. took the smallest known polymerase enzyme, just 174 amino acids long, and laboriously constructed a right-handed counterpart. They succeeded in getting it to extend a primer from 12 nucleotides to 18 nucleotides in 4 hours. Getting it to 52 nucleotides took 36 hours -- a "glacial pace," Peplow remarks. Nevertheless, it was an important discovery. Both the normal and mirror-image enzymes worked independently, without interference, when mixed in the same test tube.

The Design Inference

The researchers admit it would be a "daunting task" to build a mirror-image version of a ribosome where translation could take the left-handed RNA and translate it into a right-handed protein. Building a "looking glass cell" is a far-off dream. At this stage, though, we can draw some conclusions about chance and design.

Peplow confirms that homochirality remains a vexing problem. He surely would have said otherwise if a likely non-random cause were known.

In their research paper, the Tsinghua researchers also present their work as an effort to investigate why life's chirality is the way it is. This remains mysterious: it may simply be down to chance, or it could have been triggered by a fundamental asymmetry in nature.

But Steven Benner, at the Foundation for Applied Molecular Evolution in Alachua, Florida, says it's unlikely that creating a mirror form of biochemical life could shed any light on this question. Almost every physical process behaves identically when viewed in a mirror. The only known exceptions -- called 'parity violations' -- lie in the realm ofsubatomic physics. Such tiny differences would never show up in these biochemical experiments, says Benner.

Benner and Peplow just conceded that natural law cannot explain homochirality. To a materialist, that leaves chance. For a short polypeptide of 100 amino acids to have formed by chance would be ½ x ½ x ½ ... 100 times: 1 chance in 2100, which is approximately 1 in 1030. There aren't enough probabilistic resources to make this likely to happen in a primordial soup of racemic amino acids. But then, even if it did, homochiral DNA or RNA would have to form independently out of its own racemic building blocks. There's just no realistic chance of success in a materialistic world. Intelligence, by contrast, can easily select one hand over the other; consider how quickly an eight-year-old could sort a pile of coins into heads and tails.

Another conclusion from this paper is that homochirality as observed in life is contingent: i.e., it could exist in the opposite mirror-image form. There is no chemical or thermodynamic reason why proteins must be left-handed as opposed to right-handed, or why nucleic acids must be right-handed as opposed to left-handed. The experiments show that chemical reactions can proceed just as well in a mirror-image world. When a choice has been made one way to the exclusion of other possibilities, and it is beyond the reach of chance, it gives indication that intelligence has embedded information into the system.

Finally, these researchers demonstrate empirically how intelligence can embed information into a system. They purposefully selected building blocks of one hand to construct their polymerase. They had a goal, and a means of reaching it. If we rightly judge their work as a product of intelligent design -- as glacially slow as it was -- how much more the products of a cell that work rapidly and accurately, using machinery at a level of sophistication beyond our ability to imitate?

It's logical. If a system on the far side of the looking glass is intelligently designed, then the system on the near side is also intelligently designed. Only a fun-house mirror could distort that conclusion.

Universal common ancestry in the hotseat II

The Vitellogenin Pseudogene Story: Unequally Yolked

Ann Gauger

Synteny refers to how well chromosomal sequences from different species align with one another. Genes can be in the same general order and location between species, for example rat and mouse, or chimp and human. If they align well, evolutionists take the alignment as evidence for common ancestry. Sometimes, the gene sequences may be interrupted by deletions or insertions, and stop codons, which prevent the gene from making functional protein.

These "inactivated" genes are calledpseudogenes, and are taken by evolutionists as further evidence for common descent. Their presence is explained as the remnants of once functional genes broken by mutation and no longer needed by the organism.

"Why should a designer litter the genome with so much trash?" the evolutionists say.

One particular story that combines ancient pseudogenes and synteny to argue for common descent is circulating on the web, right now. See here for comments yesterday by Evolution Newson "Functional Pseuodogenes and Common Descent." The story is several years old, but it's popular because it seems to confirm the old evolutionary idea that our long ago ancestors were egg-laying creatures that then evolved to live-bearing placental mammals. And it's being challenged because of new evidence coming from ENCODE and other genome projects.

Egg-bearing animals use proteins called vitellogenins to transport nutrients in their egg yolk. Each vitellogenin is a very long complicated protein composed of many exons (stretches of DNA that must be copied into RNA and then spliced together into one contiguous piece before being translated into vitellogenin). An article by Dennis Venema lays out the supposed story: humans retain the remnants of DNA that used to code for egg yolk proteins called vitellogenins. Since humans don't lay eggs, the argument goes, these "vitellogenin" pseudogenes, now long since mutated into near unrecognizability, must be inherited from common ancestors who did lay eggs. Venema claims that all three human "vitellogenin" pseudogenes, VIT1 through VIT3, show traces of sequence similarity to the functioning vitellogenin genes of the chicken.

All of this argument depends on three ideas: 1) we share common ancestry with egg laying animals, 2) any sequence similarity is due to ancestry not function, and 3) there was just one function for the vitellogenin gene, and that was making vitellogenin. Any function now is due to secondarily evolved function.

This story is based on a 2008 paper by Brawand et al. that discusses yolk proteins in egg-laying animals and mammals. In that paper they identified the region of the chicken genome where vitellogenin genes are located, then found the similar regions in humans, dogs, and various marsupials and platypus, to see if vitellogenin pseudogenes could be found in the right syntenic neighborhoods.

Patches of sequence similarity to the chicken genome that might be interpreted as pseudogenes can be found in syntenic regions of marsupial genomes. Evidence for vitellogenin pseudogenes in human and dog genomes, on the other hand, is very weak. It is practically nonexistent for vitellogenin genes VIT2 and VIT3 (it is not statistically significant compared to the genomic background). The remaining gene, VIT1, has two patches of similarity in its putative former coding sequence, according to a supplemental figure in the paper.

The best of them is a patch 150 bases long (out of 42,637 total bases for the gene!) that has roughly 50 percent identity, by my estimation, and a few deletions to help make things match up. According to the authors, there is a 95 percent chance that the amount of similarity between VIT1 for humans and dogs, and the chicken VIT1, is not due to random chance -- but that's just at the borderline for statistical significance. (They don't specify exactly what sequences they were comparing, so I am guessing it was the one whose sequence they reported in the paper.)

So what if the similarity is statistically significant? What apparent similarity there is could well be due to an overlapping gene with an entirely different function that is present in that stretch of sequence in the chicken, marsupial, dog, and human genomes. (I am guessing it is present in the other genomes -- I know it is present in humans.) Indeed, there is evidence of another gene with other possible functions in that region of the genome. As reported byTomkins:

...the alleged vtg [vitellogenin] fragment in human is not a pseudogene remnant at all, but a functional enhancer element in the fifth intron of a "genomic address messenger" (GAM) gene. This GAM gene produces long noncoding RNAs that have been experimentally shown to selectively inhibit the translation of known target genes, a majority of which are implicated in a variety of human diseases. Messenger RNAs from this gene are also expressed in a variety of human brain tissues. The alleged 150 base vtg sequence contains a variety of highly conserved mammalian transcription factor binding domains, nucleosome depleted open-active chromatin, is hypo-methylated, associates with RNA polymerase 2 in long-range chromatin interactions, and binds the Mafk transcriptional regulator. These combinatorial data clearly show that it is a functional enhancer element in a GAM gene expressed in the human brain -- strongly challenging the idea that this sequence is an egg-laying pseudogene genomic fossil.The long non-coding RNAs mentioned above are widely believed to have many important regulatory functions in the cell. They are implicated in long- and short-range interactions between genes, the way the DNA loops, whether genes are sequestered or not -- all these things and more are affected.

Let's summarize some of the main points we have discussed:

1. A similar arrangement of genes exists among mammalian genomes and the chicken genome in the neighborhood of the chicken vitellogenin genes, with the very important exception that in mammals, the vitellogenin genes are either absent or pseudogenized.
2. This similar order could be due to ancestry or functional reasons.
3. In humans the evidence for a vitellogenin pseudogene fragment is very weak.
4. It is possible that any sequence similarity there might be due to a shared function, because of the regulatory gene that exists in the same region. (This despite Venema's disparaging comments to the contrary. See above.)
5. If the sequence similarity is due to function, then it need not indicate common ancestry, or the former presence of an egg-laying protein in the human genome --
6. That is, if there is sufficient sequence similarity to make the claim in the first place.
7. Claiming exaptation, à la Venema, is a post hoc argument based on the prior assumption of common descent. It goes like this:
1. There is sequence similarity to vitellogenins in the human genome.
2. It must be due to common descent.
3. There is evidence of another possible function for the sequence.
4. It must have evolved as a secondary function, because we know that it was originally vitellogenin.
8. Claiming a functional reason for the similarity is a creationist dodge.
9. Claiming exaptation sounds like a dodge to me.

Universal common ancestry in the hotseat.

Functional Pseuodogenes and Common Descent

Evolution News & Views 

V.J. Torley and our colleague Cornelius Hunter have continued their discussion about common descent, a subject on which, as John West notes, advocates of intelligent design don't all agree. Airing such disagreements, if done in a respectful and substantive manner, is of course a healthy thing. Writing at Uncommon Descent, Dr. Torley raises an interesting point, directed at Dr. Hunter and citing theistic evolutionist Dennis Venema:

In the comments to one of your posts, you thanked a reader for linking to an article stating that the protein vitellogenin confers several beneficial effects upon bees, in addition to being used to make egg yolks. Humans possess a broken copy of the gene which makes this protein; they no longer need it. So my final question is: why do you not consider this gene to be vestigial -- especially when Dr. Jeffrey Tomkins's claim that the remaining gene [vitellogenin] fragments in human beings are functional has been soundly refuted by Dr. Dennis Venema?

Actually, if you read Venema's response to Tomkins, Venema appears to concede Tomkins's central point that the VIT1 gene could be functional. Here's what Venema writes:

He [Tomkins] argues that the 150 base pair fragment of VIT1 is "not a real pseudogene" but rather regulatory DNA for an unrelated gene -- DNA that functions to direct where and when another gene is transcribed. This gene falls into a class of genes known as "long non-coding RNAs" -- genes that are transcribed into RNA but do not code for proteins. These genes are thought to arise quite easily over the course of evolution, and many are thought to have little or no function (for a good but technical review, see here). Specifically, the VIT1 fragment Tomkins acknowledges sits in an intron of this gene (part of the gene that is spliced out of the RNA copy after it is transcribed from DNA). Tomkins summarizes the evidence -- such as it is -- that suggests this sequence might have a regulatory function. If this fragment is a functional part of an unrelated gene, he argues, it makes sense to understand it as the result of special creation, rather than the evolutionary remnant of a once-functional VIT1 gene in the lineage leading to humans.

Tomkins has presented evidence that the VIT1 pseudogene sits in part of an intron that is transcribed and produces long non-coding RNAs of the type we know often have function. What does Venema say next? Does he contest this evidence for functionality? No. According to Venema the "major problem" with Tomkins's argument isn't the evidence for functionality in the VIT1 pseudogene. Rather, he focuses on critiquing a false dichotomy that Tomkins has supposedly advanced:

The major problem with this argument is that it subscribes to a false dichotomy: that this sequence is either a VIT1 pseudogene fragment or a functional part of another gene. From an evolutionary perspective, there is no issue with it being both. Part of evolutionary theory is the expectation that occasionally some sequences, after losing their original function, may come under natural selection to be repurposed to another function. The technical term for this process is exaptation, and many examples of it are known. Certainly a long, non-coding RNA gene could arise at this location in the human genome and this sequence could be exapted as a regulatory sequence -- but there is no hint of admitting this possibility in Tomkins' work. Once again we are reminded that he is not writing for a scientifically informed audience, but rather for a lay audience that will not know about the possibility of exaptation and expect him to provide evidence that it is not a factor in this situation. Rather, it seems enough to Tomkins to suggest that the sequence is functional -- and that this alone will be enough for him to convince his readership that this fragment is "not a real pseudogene."

Of course Venema is correct that finding function for this pseudogene is no refutation of Darwinian evolution. But his focus on this point distracts from the main issue here. And what's that?

The main issue is that evolutionists havecommonly argued that non-functionality in shared pseudogenes is what provides evidence for common ancestry. They argue that God would not put "broken" shared DNA in multiple speciesand thus this must be evidence for common ancestry over intelligent design (or special creation, or whatever). We've seen many theistic and atheistic evolutionists treat pseudogenes in precisely this manner:

• Richard Dawkins writes that "genomes are littered with nonfunctionalpseudogenes, faulty duplicates of functional genes that do nothing." (Richard Dawkins, A Devil's Chaplain: Reflections on Hope, Lies, Science, and Love (New York: Mariner Books, 2004), 99, emphasis added.)
• Kenneth Miller writes that the "human genome is littered with pseudogenes, gene fragments, 'orphaned' genes, 'junk' DNA, and so many repeated copies ofpointless DNA sequences that it cannot be attributed to anything that resembles intelligent design. " (Kenneth Miller, "Life's Grand Design," Technology Review, 97 (February/March, 1994): 24-32, emphasis added.)
• Francis Collins and Karl Giberson write in The Language of Science and Faith that pseudogenes are "broken," and it is "not remotely plausible" that "God inserted a piece of broken DNA into our genomes." In their view, pseudogenes shared across different species establish "conclusively that the data fits a model of evolution from a common ancestor." (Karl Giberson and Francis Collins, The Language of Science and Faith: Straight Answers to Genuine Questions(InterVarsity Press, 2011), 49, emphasis added.)
• Darrel Falk writes that one "might be tempted suggest that the reason why God put a deletion into the ape lineage is because it would make the gene more ideally suited to carrying out its purposes in apes. That might well have been a valid argument if this was afunctioning gene. However, it is not. The gene has no function. " (Darrel Falk,Coming to Peace with Science (IVP Academic, 2004), 188, emphasis added.)
• Denis Alexander writes: "[O]ur own genomes are loaded with 'pseudogenes,' stretches of DNA that are so similar to functional genes that there is no doubt where they came from, yet so full of mutations that they are functionally incapable of making protein, as can be shown experimentally in the laboratory" (Creation or Evolution, p. 112). He goes on to say that "pseudogenes ... have lost their function" (p. 204), calling them " derelict genetic fossils" (p. 205) or a "dysfunctional gene" (p. 206). He even calls them "nonfunctional genes" (p. 119).
• Even Venema makes a big deal about the idea that pseudogenes are non-functional: "Pseudogenes (literally, 'false genes') are gene sequences that have been inactivated by mutation that persist in the genome as nonfunctionalsequences. ... once inactivated, a pseudogene accumulates mutations only slowly because the proofreading mechanisms that govern DNA replication do not distinguish between functional and nonfunctional DNA sequences." (Emphasis added.)

In fact, in that same article, Venema goes on to say this specifically about the vitellogenin pseudogene. Immediately after calling pseudogenes "nonfunctional," he gives the example of the vitellogenin pseudogene:

The human genome thus contains the mutated remains of a gene devoted to egg yolk formation in egg-laying vertebrates at the precise location predicted by shared synteny derived from common ancestry.

So Venema calls pseudogenes "nonfunctional," gives the "vitellogenin pseudogene" as his primary example, and then goes on to use the supposed nonfunctionality of the vitellogenin pseudogene as evidence against intelligent design and for common ancestry.

He says much the same on BioLogos's website where he uses similar language to say that "pseudogenes are remnants of once-functional genes" and repeatedly calls them "non-functional." (See here and here.) And again he uses the vitellogenin pseudogene as an example, citing "the mutated remains of the vitellogenin gene."

Now Venema argues that the vitellogenin "pseudogene" in humans simply lost its original function and is now being used for a different function. Perhaps, he might argue, even if we are using the vitellogenin "pseudogene" for some function, the fact that we aren't using it to make egg yolk shows that we inherited it from a common ancestor we shared with chickens. This too would be a misguided argument.

First, proteins often have multiple domains that allow a protein to interact with different molecules in different contexts within a cell. At best, the human vitellogenin "pseudogene" only represents a small fraction of the chicken version of the gene. One could initially surmise that the fragment (or fragments) of the vitellogenin "pseudogene" that humans have (and use for some function) may not be the part (or parts) crucial only for making egg yolk in chickens. We may be using it for a non-egg-yolk related function that's also found in chickens.

But in this case, according to Tomkins (2015), the human "vitellogenin pseudogene" seems to be producing a long non-coding RNA (lncRNA), not a protein. LncRNAs are known to have all kinds of functional roles in humans, and are especially known to be involved in gene regulation. In this more likely case, perhaps the chicken vitellogenin gene produces not only egg yolk-related proteins, but also RNAs that haveother roles or functional interactions in chickens. We may be using our "vitellogenin pseudogene" for a similar RNA-based function or interaction that chickens do. For example, perhaps in addition to producing a protein, the chicken vitellogenin gene also produces RNAs with some regulatory role, and humans use our version of the "vitellogenin gene" for some similar RNA-based regulatory role. Indeed, Venema's discussion of the human "vitellogenin gene" seems to admit that something like this could be a possibility.

In either case, our "vitellogenin pseudogene" and the chicken version would turn into a mere example of homologous DNA performing a homologous functions -- something we see all the time in biology and which can be explained by common design just as easily as by common descent. It doesn't appear that the specific function of our "vitellogenin gene" has been explored yet, and this would be an interesting question to investigate. The hypotheses offered here could very well turn out to be true.

But doesn't have to be the case, however, to defeat the vitellogenin argument for common ancestry. That's because, as a second point, even if humans are using our "vitellogenin gene" for entirely different purposes than chickens do, this still doesn't provide evidence for common ancestry. Why? Because we often see in technological designs that similar parts can be used for very different purposes. A plastic ring in one design might be used for blowing bubbles, but in another it helps seal the connections between two pipes. Or a plastic container in an outboard boat motor holds fuel, but in another technological design it holds dishwashing liquid. Using similar parts for different purposes is easily accommodated by common design.

Moreover, when we in biology see this sort of phenomenon -- similar parts performing different functions -- it is usually taken as evidence against common ancestry, not for it, as the textbook Explore Evolution notes:

In another surprising twist, biologists have also discovered many cases in which the same genes help to produce different adult structures. Consider, for instance, the eyes of the squid, the fruit fly, and mouse. The fruit fly has a compound eye, with dozens of separate lenses. The squid and mouse both have single-lens camera eyes, but they develop along very different pathways, and are wired differently from each other. Yet, the same gene is involved in the development of all three of these eyes.

According to neo-Darwinian theory, the development of non-homologous structures should be regulated by non-homologous genes. So, many biologists were taken aback to discover that non-homologous eyes (from an insect, a mollusk, and a vertebrate) could be regulated during their development by homologous genes, like Pax-6. Stephen Jay Gould called this discovery, "...unexpected under usual views of evolution...."

To summarize, biologists have made two discoveries that challenge the argument from anatomical homology. The first is that the development of homologous structures can be governed by different genes and can follow different developmental pathways. The second discovery, conversely, is that sometimes the same gene plays a role in producing different adult structures. Both of these discoveries seem to contradict neo-Darwinian expectations.

(Explore Evolution, Second Edition, pp. 44-45)

Thus, examples where homologous genes perform non-homologous functions are said to provide a conundrum for common ancestry; it would be a mistake to cite similar DNA being used for different purposes as evidence forcommon ancestry.

But this speculation about the function of the human "vitegellenin" gene is an aside, because if we look at the arguments that are actually being made and what we already know to be true, the argument from vitegellenin for common ancestry is defeated. Here is what's really going on:

1. Evolutionists have often claimed that DNA elements like the VIT1 pseudogene are "non-functional."
2. Evolutionists claim that these pseudogenes provide special evidence for evolution because God would not create different species with shared non-functional DNA in the same location. Therefore, they argue, pseudogenes must be evidence for shared ancestry.
3. Tomkins presented evidence that the VIT1 "pseudogene" is indeed functional in humans.
4. Evolutionists responded not by disputing Tomkins's evidence for functionality in the human VIT1 "pseudogene." Rather, they shifted the argument, saying in effect, "Well, common ancestry/evolution isn't refuted simply by finding a function or a pseudogene."

One might reply to point (4) as follows: We never said that functional pseudogenes refute evolution. But functional pseudogenes do in fact refute a central part of a major argument that evolutionists have made against ID and forcommon ancestry. Venema does not seem to contest the evidence that Tomkins cites showing that the vitellogenin "pseudogene" is functional. Although Venema does not explicitly concede the point, by its very nature his argument is one that accepts its functionality.

No, the evidence raised by Tomkins suggesting vitellogenin "pseudogene" functionality in humans poses a major problem for those who make the case that the vitellogenin pseudogene provides compelling evidence for common ancestry. Tomkins's argument has hardly been "soundly refuted" by Venema.

File under "well said" XXVI

You have enemies? Good. That means you've stood up for something, sometime in your life. Winston Churchill

A clash of titans XVIII

A rude awakening from the European Dream?Pros and Cons

Will the poor always be with us?Pros and Cons.

The pink slip for Mendel?

Teach students the biology of their time
An experiment in genetics education reveals how Mendel’s legacy holds back the teaching of science, says Gregory Radick.


Historians study the causes and consequences of past events, but also consider alternative scenarios. What might have happened, for example, if Britain had stayed out of the war in Europe in 1914? Science historians also ask such counterfactual questions, and the results can be surprisingly instructive.Take genetics. The past year has seen prolonged celebrations of the work of Gregor Mendel, linked to the 150th anniversary of the paper that reported his experiments with hybrid peas. Mendel’s experiments are central to biology curricula across the world. By contrast, the criticisms levelled at Mendel’s ideas by W. F. R. Weldon, Linacre professor at the University of Oxford, UK, are a footnote.

From 1902, Weldon’s views brought him into increasingly bad-tempered conflict with Mendel’s followers. In basic terms, the Mendel­i­­­­ans believed that inherited factors (later called ‘genes’) determine the visible characters of an organism, whereas Weldon saw context — developmental and environmental — as being just as important, with its influence making characters variable in ways that Mendelians ignored. The Mendelians won — helped by Weldon’s sudden death in 1906, before he published his ideas fully — and the teaching of genetics has emphasized the primacy of the gene ever since.The problem is that the Mendelian ‘genes for’ approach is increasingly seen as out of step with twenty-first-century biology. If we are to realize the potential of the genomic age, critics say, we must find new concepts and language better matched to variablebiological reality. This is important in education, where the reliance on simple examples may even promote an outmoded determinism about the power of genes.

But what if Mendelism had never come to dominate genetics in the first place? What if Weldon’s perspective had emerged as the winner in that historical battle, and his interactionism, allied to his vivid sense of how variable the real characters of real organisms are (never just yellow or green, round or wrinkled, or any other Mendelian binary), had become the core of the subject? This is where I, and colleagues, have tried to run an experiment.

In a recent two-year project, we taught university students a curriculum that was altered to reflect what genetics textbooks might be like now if biology circa 1906 had taken the Weldonian rather than the Mendelian route. These students encountered genetics as funda­mentally tied to development and environment. Genes were not presented to them as what inheritance is ‘really about’, with everything else relegated to ignorable supporting roles. For example, they were taught that although genes can affect the heart directly, they also affect blood pressure, the body’s activity levels and other influential factors, themselves often influenced by non-genetic factors (such as smoking). Where in this tangle, we ask them, is a gene for heart disease? In effect, this revised curriculum seeks to take what is peripheral in the existing teaching of genetics and make it central, and to make what is central peripheral.Our experimental group consisted of second-year humanities undergraduates. First-year biologists, who were taught the conventional approach, acted as our control. We saw a difference — those students taught the Weldon way emerged as less believing of genetic determinism, and, I suspect, better prepared to understand the subtleties of modern genetics. (The difference was statistically significant, but I hesitate to make much of that, given that numbers were small and there were differences between the groups. I am mindful, too, that it was Weldon who first drew attention to Mendel’s own problems with exaggerated statistics.)

With such experiments — bringing insights from the archive into the science classroom — the scientific past can inform and maybe even improve the scientific future. In turn, they suggest a broader vision of collaboration. To advance scientific knowledge, historians and philosophers of science should work in close proximity to scientists, not actually in the lab but right down the corridor. Then, investigations into neglected phenomena and debates that were shut down too soon might provide the spark to serve creative science.

What of Mendel? Some might complain that it is a poor anniversary gift to jettison him from his place of honour in the genetics curriculum. Let me suggest that this grumbling, although understandable, is misguided. If we want to honour Mendel, then let us read him seriously, which is to say historically, without back-projecting the doctrinaire Mendelism that came later. Study Mendel, but let him be part of his time.

Likewise, let our biology students be part of their time, by giving them a genetics curriculum fit for the twenty-first century. If we teach them about Mendel, we should do so not to fill them with slack-jawed wonder at his foundational achievement, but to help them to appreciate how even the most imaginative and rigorous science — and Mendel’s was first rate on both counts — bears the stamp of the historical circumstances of its making. To learn that lesson about past science is to bring a welcome level of self-awareness and critical self-reflection to the present.

On the evolution of a Darwinist.

The Evolving Dr. Schafersman (Again)
John G. West

Dr. Steven Schafersman, self-proclaimed "secular humanist" and head of Texan Citizens for Science, is once again insisting that "language by the anti-evolutionists about doubt or weaknesses or controversy involving evolution is just rhetoric. Doubts or weaknesses don't exist among scientists." Poor Dr. Schafersman needs to recheck some of his previous public statements, for despite what he says now, during the 2003 biology textbook adoption process in Texas he ultimately conceded that there are plenty of scientific controversies in modern evolutionary theory. As I pointed out in a podcast in January, Schafersman in 2003 did initially assert that there were no scientific controversies over evolution for textbooks to cover. But then he began to...well... evolve. By the time the adoption process was finished, Schafersman was admitting that there are in fact many scientific controversies raised by modern evolutionary theory, only he thought that students were too stupid to study them. Recounting Dr. Schafersman's evolving statements is a great way to expose the sham claim we've been hearing throughout this week that evolution has no weaknesses.

Below is a step-by-step account Dr. Schafersman's amazing evolution in 2003:

1. In his written testimony submitted to the Texas State Board of Education on July 9, 2003, Dr. Schafersman asserted categorically:

All the biology texts are factually accurate and free of errors concerning evolution; the books do not misrepresent any details of the modern scientific understanding of evolution, nor do they omit scientific information critical of evolution, because there isn't any such information, contrary to what you have led to believe. (emphasis added)
2. In his oral testimony before the Board on July 9, 2003, Dr. Schafersman made the same general point but added a slight, unexplained qualification:

There is no scientific controversy about the fact of evolution and, thus, no weakness concerning its occurrence. There are also no weaknesses about the theory of evolution at the level it is presented in these textbooks. [Transcript of Hearing on July 9, pp. 112-113] (emphasis added)
3. In the web version of Dr. Schafersman's written testimony of July 9, 2003, a more extensive qualification suddenly appeared (which was not in the version of his testimony he actually submitted to the Board). In his revised written testimony, Dr. Schafersman explicitly acknowledged that there are in fact "disagreements and controversies ('weaknesses') concerning evolutionary theory," but he implied they are only appropriate for professional researchers and graduate students to hear about:

There is no scientific controversy about the fact of evolution and thus no scientific weaknesses concerning its occurrence. There are also no weaknesses about the theory of evolution at the level it is presented in these textbooks. Disagreements and controversies ("weaknesses") concerning evolutionary theory are found at the frontiers of research and graduate education, not at the level of introductory biology textbooks. [originally posted at http://www.txscience.org/files/testimony.htm] (emphasis added)
4. Finally, in the web version of Dr. Schafersman's written testimony submitted to the Board for the Sept. 10, 2003 hearing, Dr. Schafersman acknowledged that there are in fact "many disagreements among scientists" about evolution, and he even conceded that learning about these disagreements need not be limited to just graduate students and researchers, but also some upper-division undergraduate students might be able to study them. Dr. Schafersman also provided a detailed list of what he regarded as the genuine scientific controversies over evolution. Notably, Schafersman's list included some of the key controversies previously raised by critics of evolution (such as the sufficiency of microevolution to explain macroevolution, and questions about the primacy of natural selection):

There are many disagreements among scientists about the correct nature or explanation of the evolutionary process. These should be studied in a university evolution class, usually taught in the senior year because of the great amount of prior biological knowledge needed to understand the issues. Their existence indicates that evolutionary science is a very healthy, active, and productive field. Here are some of them, including all the most contentious ones:
A. The sufficiency of microevolution to explain macroevolution v. the existence of specific macroevolutionary processes such as mass extinction, species selection, macromutation, etc.

B. Disagreements about the tempo and mode of evolution under different circumstances: slow v. fast, gradual v. punctuated, before and after a mass extinction event, background evolution v. adaptive radiation, etc.

C. Adaptation of all features in evolution via natural selection v. features resulting from non-adaptive events and processes, such as correlation of growth, body constraints, neutral theory, genetic drift, etc.

D. The role of contingency and non-progression in evolutionary history v. evolutionary progress, improvement, and repetition due to convergent evolution.

E. Disagreements about the primacy of natural selection of individuals compared to other levels of the evolutionary hierarchy, such as gene selection, group selection, and species selection.

F. Nature v. Nurture, Genes v. Environment--this is the most divisive controversy. There are at least three positions: blank slate/human potential proponents v. sociobiologists and evolutionary psychologists v. biological determinists and IQ and race investigators.

G. The extent to which evolutionary theory can explain or account for human morality, religion, behaviors, self-awareness, free will, etc.

H. The reality or not of memes in the human population; memes are similar to genes, but are actually ideas or concepts that evolve throughout the human population and are affected by similar processes that affect genes, such as natural selection, genetic drift, founder effect, etc. Memes affect cultural evolution in the same way that genes affect physical evolution.
[originally posted at http://www.txscience.org/files/icons-revealed/index.htm ] (emphasis added)

5. So Dr. Schafersman eventually conceded that there are many scientific controversies over evolutionary theory, and he was even willing to allow some undergraduate students to study them. But he continued to oppose the right of high school students to learn about them. Why? To be blunt, he seemed to think that high school students are too dumb to understand scientific controversies. So in his view, even "Real scientific problems, controversies, etc., should not be included in introductory science textbooks." It's better for high school students to simply accept existing theory and learn not to question:

Scientific theories are too massive and established to expect any high school student to critique or question. The vast majority of high school students would not be able to perform such critiques in a scientific way. Scientific theories should be accepted as reliable knowledge in K-12 classes, and not made the object of questioning until they have the educational training necessary to do so, which consists of years of graduate study at universities.
Real scientific problems, controversies, etc., should not be included in introductory science textbooks, because they are almost always too difficult to understand and their presence would only lead to student confusion and frustration.

There are certainly problems, controversies, difficulties, and knowledge gaps with the modern theory of evolution--the explanation of how the mechanism of the evolutionary process operates over time--but for the reasons stated above, these topics are just too complex to be dealt with in high school. They almost never are, and the textbooks need not and usually do not cover them.

The concept of students learning about the 'strengths and weaknesses' in scientific 'hypotheses and theories' in high school is unscientific and pedagogically useless.

[originally posted at http://www.txscience.org/files/icons-revealed/index.htm] (emphasis added)


6. So who are the ones trying to "dumb-down" how biology texts cover evolution? Those who want textbooks to cover evolutionary controversies, or Darwinists like Steve Schafersman who think allowing students to learn about the strengths and weaknesses of existing theories (as mandated by Texas law) is "unscientific and pedagogically useless"?

Darwinism vs.the real world XXX

Calcium: Maintaining the Right Proportions
Howard Glicksman


Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series,  see here. Dr. Glicksman practices palliative medicine for a hospice organization.

Evolutionary biology is historical science. But that I mean it tries to explain the origin of life by looking only at what is needed to live and explaining it by guessing at historical circumstances. In contrast, physiology is operational science, in that, by looking at how what is needed to live functions within the physical and chemical laws of nature, it tries to explain how life actually works. But when it comes to question of the origin of life, non-operational science is important as well. In other words, it is important to consider what happens when what is needed to live is not functioning well enough to survive. Pathophysiology is "the physiology of disordered function," or the science that explains how the body malfunctions and dies. It is representative of non-operational science.

Natural history museums often display human skeletons alongside those of other animals. Without any discussion of the physiology and pathophysiology of bone and calcium metabolism, these exhibits seek to convince the unwary that life must have come about by chance and the laws of nature alone. In contrast, museums of science and technology display the skeletal remains of different inventions with the intermediate models that led up to the modern versions. By discussing the science behind the technology and the problems and failures encountered along the way, they demonstrate the intelligence used to create them. When it comes to how bones fit into the origin of life, natural history museums only use historical science to show how life looks, whereas when it comes to human ingenuity, museums of science and technology add operational and non-operational science to show how inventions work and don't work to prove their point.

My last article in this series showed that the molecular and cellular structure of bone is complex and that its relationship with the calcium metabolism makes it absolutely vital. The bone cells live within the bone they form. They include the osteoblasts, which take calcium from the tissue fluid surrounding the bone cells to form bone, and the osteoclasts, which break down and remove calcium from bone and deposit it into the bone tissue fluid. Ninety-nine percent of the body's calcium is within its bones and ninety-nine percent of the calcium within the bones is in a crystalline form called calcium hydroxyapatite.

The remaining one percent of bone calcium is dissolved as calcium phosphate in the tissue fluid that surrounds the bone cells. Since this bone tissue fluid is in direct contact with the capillaries, it acts as a bridge by which calcium can move between the circulation and the bone. Through the bone tissue fluid, the body is able to not only supply the bone with its calcium needs, but also provide for its ongoing calcium needs. In other words, through tissue fluid and circulation, the bones act as a reservoir for the calcium metabolism of the body. Let's look at the roles that non-bone calcium plays within the fluid inside and outside of the cells.

Just as sodium (Na+) and potassium (K+) become positively charged ions when dissolved in water, calcium becomes positively charged Ca++ ions in solution. The amount of Ca++ ions within a given amount of fluid is called the Ca++ ion concentration. Of the one percent of calcium outside the bones, only ten percent is present as Ca++ ions in solution outside the cells. This extracellular fluid includes the interstitial fluid, which surrounds the cells and the plasma in the blood. The remaining ninety percent of calcium outside the bones resides in the cells. However, most of this intracellular calcium is not dissolved in the cellular fluid (cytosol) but stored in many of its organelles. In fact, the concentration of Ca++ ions in the cytosol is about ten thousand times less than in the fluid surrounding the cells and in the blood. Since the kidneys constantly filter fluid, with its content of Ca++ ions, out of the circulation, if none of it could be brought back, the body would lose its total calcium content in about two months.

In addition to providing the calcium the bones need to protect the organs from injury and attachment for muscles so we can breathe, move around, and manipulate things, the Ca+ ions in the extracellular fluid are also vital for clotting. Without Ca++ ions in the blood, clotting would be impossible and every day injuries would be much more serious threats. However, there is another very important role the Ca++ ions outside the cells play, which affects all nerve and gland function, heart, and all other muscle function.

Nerve cells produce neurohormones and gland cells produce fluids, enzymes, and hormones. Under a controlled setting, these are released in response to an appropriate stimulus. For example, as noted previously, when the core temperature rises above normal, the sympathetic nerves release acetylcholine , telling the sweat glands to perspire. And when the blood glucose drops too low, the alpha cells in the pancreas release glucagon, telling the liver to release glucose from glycogen. Each of these actions takes place because of a specific signal. This signal is the sudden and massive movement of Ca++ ions into the nerve and gland cell through Ca++ ion channels caused by original stimulus (the rise in core temperature and the drop in blood glucose). This controlled, sudden, and massive influx of Ca++ ions into the cell is the universal signal telling the nerve cells to release their neurohormones and gland cells to release fluids, enzymes, and hormones.

Heart and other muscle cells work by contracting. This involves the contractile proteins within them interacting with each other in a specific way. When adequately stimulated, massive amounts of Ca++ ions enter the cytosol of the heart muscle cells from the surrounding fluid and are released from Ca ++ ion storage units (sarcoplasmic reticulum). This sudden rise of Ca++ ions allows the contractile proteins to interact and bring about contraction. The other muscle cells of the body work in a similar way. With adequate stimulation, they release massive amounts of Ca++ ions into the cytosol from the sarcoplasmic reticulum, making their contractile proteins interact to cause contraction. Just like for nerve and gland cells, it is this controlled, sudden, and massive influx of Ca++ ions into the cytosol that is the universal signal that brings about heart and other muscle cell function.

Controlled nerve, gland, heart and all other muscle function require that the ten thousand-fold difference between the Ca++ ion concentration outside and inside the cell be maintained. But, in trying to maintain this difference in Ca++ ion concentration, the laws of nature present the body with a dilemma. Diffusion is a law of nature that says chemicals in solution are always in motion and tend to move from an area of higher to lower concentration. Since Ca++ ions can diffuse across the plasma membrane, this means that diffusion tends to make Ca++ ions enter these cells. This movement into the cells would significantly increase the Ca++ ion concentration within them and if not opposed would make them non-functional.

If you read some of the earlier articles in this series you may have noticed that the dilemma that diffusion presents to the cell for Ca++ ions is similar to the one it faces for Na+ and K+ ions. The body solves that problem through millions of sodium-potassium pumps in the plasma membrane, which use energy to pump Na+ ions out of the cell while bringing K+ ions back in, against their natural tendency to go in the opposite directions. The innovation the cells use to overcome the natural force of diffusion so they can keep the Ca++ ion concentration in their cytosol ten thousand times less than what it is outside of them is the calcium pump.

There are calcium pumps within the plasma membrane of all of the cells of the body and within the sarcoplasmic reticulum of the heart and other muscle cells, which use energy to actively pump Ca++ ions out of the cytosol. In this way, the body maintains normal nerve, gland, heart, and all other muscle function.

Don't you think it would be good for natural history museums to include in their displays on human skeletons information about the cellular and molecular make-up of bones, their relationship with the calcium metabolism, and the importance of Ca++ ions inside and outside the cell? Then, when they use the similarities between human skeletons and the ones of other animals to claim that life must have come about by chance and the laws of nature alone, the accompanying questions will be apparent. Where did the osteoblasts and osteoclasts come from and in which order? Where did the calcium pumps come from and how do they know how much calcium to send out of the cell to allow for nerve, gland, heart and all other muscle function? That would be educating the public about how life works instead of just how it looks.


Next time we'll look at how the body acquires calcium. The process isn't as easy as it is for water, glucose, and salt. In fact, the mechanism involved is just one more reason to wonder how evolutionary biologists can continue to claim that life has come about by chance and the laws of nature alone.