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.

Separating tool from toolmaker.

No, Your Brain Isn't a Three-Pound Meat Computer
Brendan Dixon

In all the latest sound and fury over Artificial Intelligence -- Will some future Terminator run us over like ants (as Michio Kaku worries)? Must we act quickly to prevent the rise of an evil AI overlord (per Elon Musk)? -- one notes an important, if unstated, assumption: Computers can be intelligent like humans are intelligent. If so, well, perhaps Kaku, Musk, and others are right to stoke fear and thus propel us to action to avert disaster.

On the other hand, if it's not possible, then, like a well-timed magician's trick, the fear-mongering may have us looking for one kind of problem even as we wholly miss another.

Now Roger Epstein, former editor of Psychology Today and an active researcher, writes at Aeon to reject the assumption that the brain works like a computer in any way ("The Empty Brain"):

But here is what we are not born with: information, data, rules, software, knowledge, lexicons, representations, algorithms, programs, models, memories, images, processors, subroutines, encoders, decoders, symbols, or buffers -- design elements that allow digital computers to behave somewhat intelligently. Not only are we not born with such things, we also don't develop them -- ever.

. . .

Computers, quite literally, process information -- numbers, letters, words, formulas, images...Humans, on the other hand, do not -- never did, never will.

Calling the brain, as some have, a three-pound computer made of meat presses the metaphor too far. Epstein recalls other metaphors, all now rejected, drawn from the technology of their day. He predicts the day will come, and is coming, when we'll look back and consider the "brain is a computer" metaphor quaint.

Metaphors always trail what is; the best of them still leave behind much of what we are. Metaphors, and models give us a convenient shorthand, but when flipped around to proscribe what we are, they mislead and delude. Computers do not play games like humans play games. Computers do not create like humans create. Computers, at their most fundamental level, do not even solve computational problems like humans solve computational problems.

Computers are machines we've made, into which we can put reformulated pieces of ourselves. They are a tool, not a replacement. And they most certainly are not electronic versions of whatever it is that goes on inside our heads. Epstein continues:

Misleading headlines notwithstanding, no one really has the slightest idea how the brain changes after we have learned to sing a song or recite a poem. But neither the song nor the poem has been "stored" in it. The brain has simply changed in an orderly way that now allows us to sing the song or recite the poem under certain conditions.

If Epstein is correct, and I believe he is, then the entire AI endeavor, at least in its most extreme forms, will fail. We will not succeed at downloading our minds onto a computer. We will not succeed at creating a computer whose (so called) intelligence is anything like ours. Machines will not suddenly become self-aware and sweep humanity aside.

What should give us pause, however, is that a flawed metaphor inspiring false fears will lead us to miss the real problems with AI and the true magnitude of our own minds. AI works because we deposit portions of our intelligence, recoded into the algorithms a computer can use, into the machines. As with any complex endeavor in which our off-the-cuff guesses are often incorrect, the results of these algorithms can elude our guesses and may produce solutions we might otherwise have missed. This fact in itself demonstrates that whatever a computer is doing, it is not the same thing we do in our own heads.

But since those algorithms capture, at best, only a small portion of our intelligence, they have edges or boundaries, places where they fail because the machine has gone outside the map we coded into it. AlphaGo, which defeated a world-ranked Go player, made a few moves that were not just poor or weak, but were of the what-the-heck-were-you-thinking variety. Why? Because it wasn't thinking: It was following a map, an algorithm, even if a self-adjusting one, and found itself lost once it passed borders.

AI machines are more a form of mimicry than anything even approaching intelligence. That we're better at creating mimicking machines does not change the reality that these machines, like Polly requesting a cracker, do their work without understanding a single word uttered.

We need metaphors to talk about complex things. But when we replace the real with a model, we lose that which we were originally trying to understand.


The real problem with AI, then, is not the prospect of Terminator, but, instead, the likelihood of our blindly depending on machines, lulled to trust them by bad metaphors. The danger is that computers will fail us, and possibly do so in very bad ways.

On the Darwinian establishment's tyranny of authority

As Eric Hedin Earns Tenure, It's Time to Set the Record Straight -- Again
Sarah Chaffee


Up until 2013, Eric Hedin, a Ball State University associate professor of astronomy and physics, taught an interdisciplinary honors course called Boundaries of Science. The course explored intelligent design, among other topics. Biologist Jerry Coyne and the Freedom From Religion Foundation caught wind of this and complained, accusing Hedin of proselytizing and teaching Christianity. Hedin was investigated, and Ball State cancelled the course, while releasing a statement prohibiting the teaching of intelligent design as science.

Obviously, nobody aiming at a career in science would wish to be at the center of attention like that, and Hedin's critics knew it. They set out to intimidate him and other scientists with an interest in ID.

Though Hedin's future looked iffy at the time, he has now earned tenure. That's the good news. The bad news is that his milestone was greeted with reporting in the media that recycled inaccurate, damaging claims from the original controversy, claims that had already been firmly refuted. Inside Higher Ed, for one, repeats obvious errors about Hedin and his course that require setting the record straight once again.

First, Inside Higher Ed reporter Colleen Flaherty gives credence to false claims that Hedin proselytized. She notes:

Eric Hedin, the associate professor of astronomy and physics at Ball State University who was investigated in 2014 for allegedly teaching intelligent design, has earned tenure. That's despite claims that he was proselytizing in a science class and the university's strong affirmation of the scientific consensus around evolution in light of the allegations.

...

The foundation said it did not object to the premise of the honors science seminar, described in the syllabus as an investigation of "physical reality and the boundaries of science for any hidden wisdom within this reality which may illuminate the central questions of the purpose of our existence and the meaning of life. Rather, the organization said it objected to the course "as taught," based on reports that Hedin was proselytizing and endorsing a Christian viewpoint over others presented. As a public university, Ball State could be in violation of its obligation to separate church and state, the foundation said. [Emphasis added.]

In an article at the time, John G. West, the Center for Science & Culture's Associate Director, noted:

[T]he complaint against Hedin did not identify any student who was willing to complain on the record against Hedin. Instead, it merely highlighted a few anonymous (and ambiguous) comments from RateMyProfessor.com, a website that doesn't even verify whether those posting comments are in fact college students, let alone whether they ever took courses from the professor in question.

Furthermore, according to documents released by Ball State, students reported that the course was evenhanded:

"I'm an agnostic and I find absolutely nothing wrong with... [Professor Hedin's] teachings; ... as far as intelligent and thought-provoking discussions go, [Hedin's Boundaries of Science course]... is one of the most INNOVATIVE classes I have had during my time at Ball State. I lean more towards scientific evidence than anything else, but being an intelligent, curious, and open-minded individual, I appreciate all of the discussions that this class has had and all of the new ideas I have come to understand. There is nothing wrong with this class, and I would recommend it to anyone, no matter what their religious beliefs are."

"I took the honors physics course taught by Dr. Hedin in the spring of 2011. While learning about scientific concepts such as quantum mechanics, black holes, the formation of stars, and other topics, Dr. Hedin's instruction challenged me in a way that my other university classes did not. This course made me a better learner. It allowed me to become much more competent in these complex scientific areas of study and prompted me to become an individual who is committed to learning more about these topics in my own time. At times, in the classroom, students would pose questions which were related to spiritual concepts, but Dr. Hedin merely facilitated discussion giving EVERY single student an opportunity to provide input. Furthermore, Dr. Hedin goes above and beyond the actions of a typical college educator."

Inside Higher Ed's reporter puts unverified student reports, damaging to Hedin's reputation, front and center in her article, while ignoring positive reviews.

Second, Hedin's course, as described in the syllabus and approved by the university, fulfilled course expectations. Boundaries of Science (HONRS 296) was an interdisciplinary honors course, not a narrowly focused science course. The stated purpose of HONRS 296 courses at Ball State is to "emphasize relationships of the sciences to human concerns and society." In line with this, Hedin covered a wide range of topics relevant to the boundaries of science, including human consciousness, intelligent design, evolution, debate on the place of naturalism, perspectives on the relationship between science and faith, and the nature of science. The course centered on physics, cosmology, and astronomy, but delved into biology and more. Hedin did not teach creationism -- the religious view that the earth was created several thousand years ago.

Inside Higher Ed also regurgitates the Freedom From Religion Foundation's complaint that the "partial syllabus" for Hedin's course included works by intelligent design proponents and other "Christian apologists who lack any scientific credentials whatsoever," such as C. S. Lewis.

In actuality, the two main texts were a book by Oxford University's John Lennox, a mathematician whom West describes as "a scholar who explicitly rejects Biblical creationism," and a mainstream textbook by Mark A. Garlick, a PhD in astrophysics, covering cosmic history from the Big Bang to the origins of life. A bibliography of optional additional materials included works from a diverse set of philosophical and religious (and anti-religious) perspectives that students could choose to consult -- or not -- at their own discretion.

Inside Higher Ed also repeats inaccuracies from then-Ball State President Jo Ann Gora's public statement:

"Intelligent design is overwhelmingly deemed by the scientific community as a religious belief and not a scientific theory," and the question was not one of academic freedom, but one of academic integrity, she said. "To allow intelligent design to be presented to science students as a valid scientific theory would violate the academic integrity of the course as it would fail to accurately represent the consensus of science scholars."

This statement contains several errors. The point about "consensus" science is not a valid way to judge intelligent design; instead, it is often an excuse not to examine the evidence. Intelligent design is not a religious belief -- it does not draw from any sacred text. On the contrary, intelligent design uses the scientific method to reach its conclusions. Here is a brief summary of ID, according to Casey Luskin, former Center for Science & Culture Research Coordinator:

Intelligent design is a scientific theory that holds some aspects of life and the universe are best explained by reference to an intelligent cause. Why? Because they contain the type of complexity and information that in our experience comes only from intelligence.

As a result, intelligent-design theorists begin by studying how intelligent agents act when they design things. Intelligence is a process, or a mechanism, which we can observe at work in the world around us. Human designers make a great dataset for studying how intelligent agency works.

When we study the actions of humans, we learn that intelligent agents produce high levels of complex and specified information (CSI). Something is complex if it's unlikely, and specified if it matches some independent pattern.

...

By assessing whether natural structures contain the type of complexity -- high CSI -- that in our experience comes only from intelligence, we can construct a positive, testable case for design.

And what happens when we study nature? Well, the past 60 years of biology research have uncovered that life is fundamentally based upon:

A vast amount of complex and specified information encoded in a biochemical language;

A computer-like system of commands and codes that processes the information.

Molecular machines and multi-machine systems.

But where in our experience do things like language, complex and specified information, programming code, or machines come from? They have one and only one known source: intelligence.

For further information on the scientific theory of intelligent design and related matters, see our resource list of "Essential Readings."

Finally, despite Dr. Gora's assertion, academic freedom was indeed the primary issue at stake in Hedin's case. We have dealt with this extensively elsewhere.


Despite claims from the Freedom From Religion Foundation and other activists, Hedin in fact has a fine record as both a scientist and a teacher, and he deserved fairer treatment from Inside Higher Ed. It would have been much more fitting to celebrate his tenure, than to dig up unsubstantiated accusations from the past.

Past the hand waving at the engineering of the nuclear membrane

What It Takes to Build a Nuclear Membrane
Evolution News & Views

In the cartoon depictions of cells we often see, the nucleus looks about as complicated as a balloon. It's drawn as a thin membrane bubble surrounding the chromosomes. The balloon pops when the cell divides, then the cell blows new balloons around each daughter cell's DNA. What could be simpler?

Authors in Current Biology give a reality check by describing in detail the structure of the nuclear membrane. It's mind-boggling how sophisticated it is -- and they don't even get into the most mind-boggling part: the nuclear pore complexes that let cargo in and out. (At the risk of redlining the boggle-meter, we'll save that subject for another time.)

In their "Quick Guide to Lamins," Wei Xie and Brian Burke introduce us to the complexities of the critically important proteins that make up the nuclear membrane. First of all, what are lamins?

Lamins are structural proteins of the nuclear envelope that are unique to metazoans. Coelenterates, such as hydra, and the nematode Caenorhabditis elegans contain only a single lamin gene. Drosophila has two lamin genes and mammals have three. The lamin genes encode a repertoire of proteins that is augmented by alternative splicing. [Emphasis added.]
So right off the bat, only multicellular animals have lamin genes and proteins. Lamins are among the numerous new cell products, tissues, and organs that appeared without ancestors at the Cambrian explosion. This is confirmed by a 2012 paper that tries to describe the "Evolution of the lamin protein family":

The lamin/IF protein family seems to be restricted to the metazoans. In general, invertebrate genomes harbor only a single lamin gene encoding a B-type lamin. The archetypal lamin gene structure found in basal metazoans is conserved up to the vertebrate lineage.
This distinction with metazoans is curious, since all eukaryotes have a nucleus. Another 2012 paper claims to have found a "lamin-like" protein in a slime mold, but here in 2016, Xie and Burke make no mention of it, suggesting it isn't commonly thought of as an evolutionary precursor (and it just pushes the question further back: where did the slime mold get it?).

Development

The lamins represent the founding members of the intermediate filament (IF) superfamily, and are classed as type V IF proteins. Like all IF proteins, each of the lamins features a globular aminoterminal head domain followed by a central alpha-helical coiled-coil domain. This terminates in a second globular region that has at its core an immunoglobulin fold. In contrast to cytoplasmic IF proteins, each of the lamins contains a nuclear localization sequence that lies just downstream of the coiled-coil domain and is essential for directing the lamins into the nucleus, where they assemble into the nuclear lamina, a protein meshwork that is intimately associated with the nuclear face of the inner nuclear membrane (INM).
They have a zip-code tag that directs them to the nucleus, where they assemble into a meshwork. The membrane has layers: an inner membrane, an outer membrane, and an inter-membrane space. But that is only the beginning. Since mammal lamins are much more complicated and poorly understood, the authors talk about frog lamins, where scientists have been able to tease out some of the details.

Structure

Lamins "spontaneously assemble" into an "orthogonal network" of half-staggered filaments. At least that's what they do in a petri dish. Undoubtedly the process is more involved in the living cell, because "Numerous nuclear pore complexes are associated with this filament meshwork."

Function

Lamins provide both strength and flexibility to the nuclear membrane, and are responsive to the environment. If your lamins are working, be thankful. Bad things happen when they don't.

Forming a 10-20 nm filamentous layer beneath the INM, the mammalian nuclear lamina provides mechanical strength to the nuclear envelope. The nuclei of fibroblasts deficient in A-type lamins lose their normally smooth and round shape; instead irregularities, often severe, are observed. These irregularities are frequently associated with the appearance of nuclear membrane blebs and transient ruptures of the nuclear envelope (Figure 1). Intriguingly, motile cells and cells growing on rigid substrates upregulate A-type lamin expression. Conversely, cells on deformable substrates have reduced A-type lamin expression. It is likely that these differences represent a mechanism by which cells can adapt to changes in mechanical forces transmitted to the nucleus via the cytoskeleton....
It turns out that lamins are in communication with the cytoplasm and the outside world. And that's not all; they communicate with the inside of the nucleus as well:

In addition to their direct structural supporting functions, lamins associate with a number of other nuclear envelope components, including nuclear pore complexes and LINC (linker of the nucleoskeleton and cytoskeleton) complexes. The latter are composed of SUN domain proteins in the INM and the KASH proteins in the outer nuclear membrane (ONM). These proteins establish transluminal interactions within the perinuclear space, the gap that separates the INM and ONM. Through this interaction, SUN-KASH pairs represent links in a molecular chain that spans both nuclear membranes and physically couples the lamina and other nuclear structures to the cytoskeleton. In this way, LINC complexes may have essential roles in nuclear migration/ positioning and mechanotransduction in both health and disease.
The whole "balloon" that appeared so simple at the beginning is composed of several complexes in three layers, with parts that communicate longitudinally and parts that communicate transversely. All of this communicates with the meshwork outside the nucleus, the cytoskeleton. And besides all that, lamins are important players in what goes on inside the nucleus: so much so, that your lifespan might depend on what these proteins do.

It is clear that perturbations in nuclear lamina structure can strongly influence chromatin organization. This may lead to genome-wide changes in replication and transcription activities. As an example, 3D-SIM has revealed that 50% or more of telomeres are associated with the nuclear lamina. The interplay between telomeres and A-type lamins, in conjunction with lamina-associated polypeptide 2-alpha (LAP2-alpha), is thought to regulate cell proliferation and longevity.
Speaking of longevity, there's a strange and highly upsetting genetic disease called progeria. It turns kids old before their time; often they die of "old age" in their teens. That is an example of a laminopathy, one of two dozen lamin disorders that cause severe disability or death. A single point mutation in one lamin gene can cause progeria. Others cause muscular dystrophy or nerve damage, if the individual even survives to birth.

Final Thoughts

We've taken a brief look at proteins that appeared abruptly in the animal kingdom and remain highly conserved throughout life. Their amino acid sequences cannot tolerate mutations. They perform vital functions, both structurally and in interaction with other complexes. They have important roles in cell division and longevity. And these authors did not even get into the fantastic operation at mitosis, when this highly integrated membrane is systematically torn down and rebuilt in the two daughter cells in a matter of minutes.


In other words, one solution to simplistic speculation about evolution is to look closely at a particular phenomenon, with all its intricacies. The design is in the details.

Plankton takes the stand for design.

Oceans Full of Design
Evolution News & Views

Some look like miniature spaceships. Some look like tiny jewel boxes. Others look like miniature versions of shrimp. They constitute most of the biomass on the planet, regulate earth's carbon and oxygen, and provide food for fish, birds, and blue whales -- the largest animals to ever grace the earth. What are they? Collectively, we call them "plankton," a word meaning drifters. Such a catch-all term hardly does justice to their incredible diversity and importance to us all. A few recent papers are opening wider the black box of these wonderful plants (phytoplankton) and animals (zooplankton).

The Jewel Boxes: Diatoms

We discussed the diatoms and their delicate silica shells a couple of months ago, so we won't go into detail here. Suffice it to say that one of the papers we will look at confirms that these single-celled algae are useful as well as ornamental. "Among autotrophs, diatoms are commonly attributed to being important in carbon flux because of their large size and fast sinking rates."

The Spaceships: Rhizaria

Diatoms are not the only Baroque artists. Other microbes in the plankton community build even more elaborate 3-D shapes, notably the radiolarians and foraminifera. Not your ordinary amoebas, the Rhizaria share characteristics with the familiar blob-like protists, including pseudopodia, but they also construct "intricate mineral skeletal structures of opal (SiO2), celestite (SrSO4) or calcite (CaCO3)," David A. Caron says in Nature. Classification of these organisms continues to the present day.

Do you know the name and evolutionary affiliation of any of the most conspicuous groups of single-celled organisms in the world's oceans? Did you guess the Rhizaria, or one of the more familiar groups of plankton that make up this supergroup, such as the Radiolaria, Acantharia or Foraminifera? If you didn't, you're not alone -- until recently, neither did the vast majority of biological oceanographers. Biard et al. report on page 504 of this issue that the abundance and biomass of these enigmatic species in the ocean are much greater than previously recognized. In addition, Guidi et al. (page 465) reveal the extent of the Rhizaria's involvement in the export of carbon from the atmosphere to the ocean depths. [Emphasis added.]
Ernst Haeckel had many faults, but he provided one worthy achievement that continues to grace textbooks today. No, it's not his infamous embryos; it's a series of detailed drawings of Rhizarians he made from samples collected by the oceanic Challenger expedition of 1872-1876. The fantastic skeletons of these creatures have to be seen to be believed (searching on rhizaria+Haeckel quickly brings up the drawings). Caron shows a few of the colonial forms in his article. By "holding hands" with their pseudopodia, these animals can form large colonies. "Some species can even form cylindrical colonies approximately 1 cm in diameter and greater than 1 m in length," Caron notes.

While over-designed for Baroque symmetry and detail, Rhizarians are also useful. That's what Caron and the two papers he references focus on: "the vital export of carbon from upper ocean layers to the deep ocean." Without the help of these organisms reducing atmospheric carbon dioxide, where would the earth be today? And do they have to be so doggone beautiful to carry on that task? None of the papers explain how these amazing spaceships, cathedrals and geodesic domes evolved. To fill that gap, design scientists could take leadership over this vast research opportunity.

One of the reasons for their anonymity to oceanographers is the delicate morphologies of living specimens. These structures deteriorate badly as a result of the methods and preservatives that have routinely been used for collection and species identification. Some species contain no skeletal material, and in plankton samples their remains are often not recognizable. Substantial abundances of Rhizaria were detected by divers in the open ocean more than two decades ago, and are visible in earlier underwater images. However, truly global surveys have never been conducted.
The Mighty Migrating Micro-Shrimp

Illustra Media's documentary Flight: The Genius of Birds briefly mentions the annual bloom of plankton in the Weddell Sea that coincides with the arrival of the Arctic terns. In the bloom, the phytoplankton feed the zooplankton which set the table for birds, fish and mammals. Blue whales migrate to this Antarctic sea to scoop up the krill in their gigantic mouths.

Illustra's Design of Life films showcased the amazing animal migrations of butterflies, birds, salmon and sea turtles, but there are microscopic migrators you probably didn't know about. That's because scientists didn't know much about them, either. Among them are tiny shrimp-like crustaceans like copepods, amphipods and krill. Scientists at the Alfred Wegener Institute discovered something amazing about these little guys. They migrate hundreds of meters almost every day. The scientists spent three years studying this phenomenon.

The daily vertical migration of zooplankton -- often crustaceans with body lengths ranging from millimetres to centimetres -- is mainly triggered by the day-night cycle. In order to escape potential predators, they dive into the dark depths at sunrise and stay there during the day. After sunset, they once again rise to the upper layers to feed where the sunlight has allowed planktonic algae to grow. Until now, only short time snippets of the migration pattern of the zooplankton in the Southern Ocean existed. Because of its seasonal sea ice cover, many areas are not accessible by ship during the southern winter. At this time of year, biological network samples can only be taken intermittently.
The current study is based on data that was collected during three Polarstern expeditions and with deep-sea moorings deployed in the Southern Ocean between 2005 and 2008 within the framework of the LAKRIS project (Lazarev Sea Krill Study). As part of this study ADCPs were moored at three different geographical locations along the Greenwich meridian; the ADCPs send out sound waves at fixed intervals and cover an up to 500 metres deep water layer under the surface. While the strength of the echo provides information about the concentration of the zooplankton, the migration velocity can be calculated based on the Doppler shift of the sound frequency.

It was a pretty clever method of data collection. The only times crustaceans don't make the daily trip is during the spring bloom when their algae prey are so abundant, they need not worry about predators; or else, possibly, the predators can't see them as well at that season. Regardless, they don't seem to be passively riding currents, because the migration is timed to the threat and can be switched off.

As the Illustra films demonstrated, any migration requires navigation, energy planning and timing. To migrate 500 meters every day is a big task for a 5-millimeter animal. That's roughly 100,000 body lengths, like swimming 10 marathons a day. How do they do it? Is there an ID researcher that would like to explore these uncharted waters?

Final Thoughts

We've taken a brief look at microscopic organisms with a big job: regulating the carbon and oxygen cycles of the whole planet. They're implicated in nitrogen and phosphorus regulation as well. How did the earth get along before these amazing creatures "evolved"? Don't ask the evolutionists, because they didn't say.


Here's what makes earth stand out from all the exoplanets that the Kepler spacecraft is finding. It's not just water. It's not just air. Only the earth, as far as we know, is filled with functioning creatures that do what they do because of complex specified information -- the hallmark of intelligent design.

In defense of commonsense re:the design debate

Book by Douglas Axe Shows the Key to Understanding Origins Is the "Design Intuition" -- Pre-Order Now!
Evolution News & Views 

A remarkable thing about evolutionary theory is the way it demands that we deny our intuition at almost every step. Evolutionists then assure us that the science is all figured out, so we needn't trouble our silly heads about the relevant biology.

In a new book, Douglas Axe of Biologic Institute turns this standard assurance on its head. In Undeniable: How Biology Confirms Our Intuition That Life Is Designed, Dr. Axe restores the place of intuition alongside intellect in considering the question of life's origins.


Undeniable will be published on July 12 by HarperOne, but you can pre-order before then and participate in an exclusive, private conference call with Dr. Axe and talk- show host Michael Medved. You'll also receive digital versions of three complete books from Discovery Institute Press: Debating Darwin's Doubt, The Unofficial Guide to Cosmos, and Science & Human Origins. See here for easy instructions.Throughout his distinguished and unconventional career, engineer-turned-molecular-biologist Axe has been asking the questions that much of the scientific community would rather silence. Now, he presents his conclusions in this brave and pioneering book. Axe argues that the key to understanding our origin is the "design intuition" -- the innate belief held by all humans that tasks we would need knowledge to accomplish can only be accomplished by someone who has that knowledge. For the ingenious task of inventing life, this knower can only be God.

Starting with the hallowed halls of academic science, Axe dismantles the widespread belief that Darwin's theory of evolution is indisputably true, showing instead that a gaping hole has been at its center from the beginning. He then explains in plain English the science that proves our design intuition scientifically valid. Lastly, he uses everyday experience to empower ordinary people to defend their design intuition, giving them the confidence and courage to explain why it has to be true and the vision to imagine what biology will become when people stand up for this truth.

Armed with that confidence, readers will affirm what once seemed obvious to all of us -- that living creatures, from single-celled cyanobacteria to orca whales and human beings, are brilliantly conceived, utterly beyond the reach of accident.

Our intuition was right all along.

Douglas Axe is the director of Biologic Institute. His research uses both experiments and computer simulations to examine the functional and structural constraints on the evolution of proteins and protein systems. After a Caltech PhD he held postdoctoral and research scientist positions at the University of Cambridge, the Cambridge Medical Research Council Centre, and the Babraham Institute in Cambridge.

His work and ideas have been featured in many scientific journals, including the Journal of Molecular Biology, the Proceedings of the National Academy of Sciences, and Nature, and in such books as Signature in the Cell and Darwin's Doubt by Stephen Meyer and Life's Solution by Simon Conway Morris.

On surviving the Darwinian inquisition.

World Magazine Tells David Coppedge's Powerful Story

David Klinghoffer 

I had the privilege of getting to know David Coppedge a few years ago, leading up to the shameful resolution of his 2012 discrimination case against NASA's Jet Propulsion Lab. His story is among those that remind us intelligence design isn't only a scientific issue but one with serious civil rights implications as well.

See here for more background on the Coppedge case. In brief, the mild-mannered team lead computer administrator on the Cassini Mission to Saturn was viciously punished by JPL supervisors. His offense? Sharing information about ID, all in the most respectful, appropriate manner. Now his persecution and its aftermath are recounted in a moving article in World Magazine ("After a fiery trial").

Take a moment and read it. I'm glad to have stayed in touch with Coppedge since the court case in Los Angeles, so I'm familiar with some of what's related here. To call his experiences dramatic is an understatement. Here's how it began:

When JPL hired Coppedge in 1996 as a computer system administrator to help with the Cassini mission to Saturn (described by NASA as "the most ambitious effort in planetary space exploration ever mounted"), he was thrilled to land his dream job: Here he was, at the heart of cutting-edge science -- probing the heavens, discovering the great unknown, making history. As team lead, he constantly tried to excite his team members with the awareness they were part of something extraordinary.

He also occasionally offered DVDs about intelligent design to co-workers whom he knew. His goal wasn't to proselytize, he says, but to stir conversations, because "if the Darwinian picture is flawed, people ought to know the facts." He had one co-worker who would talk frequently about his interest in photography -- so why not share his own interest in the origin of life? If anyone expressed disinterest, he says, he immediately backed down. So Coppedge was flabbergasted when his supervisor told him "a number of people" had complained that he was "pushing religion" during work hours. His demotion came a month later.

There ensues the court battle, punctuated by mysterious debilitating headaches, a struggle with cancer, spiritual trial and renewal, even a near-deadly encounter with a flying insect. This is a remarkably resilient man. On top of everything else, his Facebook feed, which I follow, demonstrates his remarkable gifts as a nature photographer and his daring as an outdoorsman and adventurer across the wildernesses of the West.

His story has a happy ending, but then so does the Book of Job.

The thumb print of Jehovah II

The thumb print of Jehovah III

The thumb print of jehovah IV

File under "well said" XXV

God said: you must teach, as I taught, without a fee.
The Talmud

A clash of titans XVII

Modi's India at the edge of fascism?Pros and Cons.