When cheer leading supersedes fact-checking.

Feathers on a Bird or Dinosaur Tail? The Media Are Certain; the Scientific Evidence Less So
Evolution News & Views 

A section of a 99-million-year-old feathered tail discovered in a chunk of amber in Myanmar belongs to a juvenile dinosaur, a coelurosaur, not a bird. The media are certain of it. The actual evidence is more ambiguous. National Geographic pounds the pulpit for a feathered dino:

First Dinosaur Tail Found Preserved in Amber
The tail of a 99-million-year-old dinosaur, including bones, soft tissue, and even feathers, has been found preserved in amber, according to a report published today in the journal Current Biology.

While individual dinosaur-era feathers have been found in amber, and evidence for feathered dinosaurs is captured in fossil impressions, this is the first time that scientists are able to clearly associate well-preserved feathers with a dinosaur, and in turn gain a better understanding of the evolution and structure of dinosaur feathers.

...

The semitranslucent mid-Cretaceous amber sample, roughly the size and shape of a dried apricot, captures one of the earliest moments of differentiation between the feathers of birds of flight and the feathers of dinosaurs.

...

The presence of articulated tail vertebrae in the sample enabled researchers to rule out the possibility that the feathers belonged to a prehistoric bird. Modern birds and their closest Cretaceous ancestors feature a set of fused tail vertebrae called a pygostyle that enables tail feathers to move as a single unit.

The reason that they claim it is a dinosaur and not a bird is because this is supposedly from a "long-tailed" individual. Most birds with bony tails are short-tailed, meaning they have fewer vertebrae in their tail compared to dinosaurs. Under ten vertebrae, perhaps only six or seven, would be the norm for a bony-tailed bird.

So what do they think about the number of vertebrae in this amber fossil? They say the living individual "likely" had more than 25 vertebrae.

But this is a matter of inference, because, as the paper admits, the soft tissue in the fossil is so undifferentiated from the bone that it is very difficult to tell what is tissue and what are vertebrae. As the paper puts it in technical language:

SR X-ray μCT scanning of DIP-V-15103 revealed that soft tissues have a density insufficiently different from the partially replaced skeletal elements to permit X-ray imaging and virtual dissection of osteology alone. Consequently, many diagnostic and comparative osteological details remain obscured.
At most, they can see clear evidence of only two vertebrae in this tail. From that they extrapolate that it had more than 25:

However, two vertebrae are clearly delineated ventrally (Figures 1F-1H). Extrapolating lengths of these vertebrae, the preserved tail section contains at least eight full vertebrae and part of a ninth.
So when they extrapolate from the two visible vertebrae, they get nine. That would certainly not preclude the creature from being a bird. In fact, some fossil birds had up to 20 to 23 vertebrae. As another paper states:

Archaeopteryx retained an ancestral caudal vertebral count of between 20 and 23. The next most basal bird, Jeholornis, from the Jiufotang Formation of China and dated at approximately 120 million years old, was also long-tailed, and had 22 caudal vertebrae that are nearly identical to those of Archaeopteryx.
If it did have up to 20 to 23 vertebrae, it could still be a bird. Yet again it's not clear exactly how many vertebrae this tail had because too much of it is missing.

The paper goes on:

Even with the skin adpressed to the bony surface, no features other than the grooved ventral sulci of two centra are clearly visible. This lack of topography suggests that the vertebrae lack prominent neural arches, transverse processes, or hemal arches. Therefore, the preserved segment is only a small mid to distal portion of what was likely a relatively long tail, with the total caudal vertebral count not reasonably less than 15, and likely greater than 25.
So they claim that the shape of the vertebrae suggests that what they are seeing is from the middle of the tail, and the actual tail was much longer. They admit that most features are not "clearly visible." Given that you can barely distinguish soft tissue from bone in this fossil, their inferences go too far.

Indeed while researcher Ryan McKellar tells Science Daily that "the feathers definitely are those of a dinosaur not a prehistoric bird," the paper itself is more circumspect, saying "it can likely be excluded from the long-tailed birds" (emphasis added). The Supplemental Information that goes with the paper includes the notable statement:

[T]here is a distinctive ventral groove on the caudal centra of the specimen, which is widely distributed among non-avialan theropods but which has yet to be reported in avialans (though the possibility of its presence in the two known long-tailed birds Archaeopteryx and Jeholornis cannot be excluded).
As a final note, one could argue that the age of the fossil (about 99 Ma) suggests that this individual lived long after known long-tailed bony-tailed birds. According to this paper, the most recent long-tailed bony-tailed bird lived about 122 million years ago.

That would be a very weak argument, however, since evolutionists regularly tolerate chronological gaps in the fossil record much greater than 20 million years. In fact they do this in their dinosaur-to-bird hypothesis.

After all, the dinosaurs that they claim supposedly gave rise to birds lived about 125 million years ago, but true birds like Archaeopteryx lived as far as about 150 million years ago. That's a major time gap. So if one were to propose that perhaps the long-tailed birds known from ~122 million years ago survived until ~99 million years ago, you would not be extrapolating fossil lineages any more than they already do.

In any case, all praise is due to the researchers for discovering and presenting this beautiful fossil with its unmistakable feathers. Probably no known feathers this old have ever been preserved in such gorgeous detail.


But unfortunately we have so little material, and the bone is so difficult to distinguish from the soft tissue, that any strong claims about this tail should be greeted with skepticism. This paper will not be the last word on the nature of the animal that sported this wonderful tail.

Optimal and then some.

Respect for Kinesin Grows
Evolution News & and Views December 10, 2015 5:39 PM 



The Discovery Institute video "Workhorse of the Cell: Kinesin" premiered last year on YouTube. Since then, additional facts about these molecular motors have come to light. Some highlights:

Relay Handoff

Kinesin-II, one of the extended family of kinesin motors, is involved in a "relay race" on a micro-miniature scale. It demonstrates how different families of molecular motors cooperate. This one works in synergy with other cargo-carrying motors in the important complex function known as "intra-flagellar transport" (IFT) that builds and maintains cilia and flagella. An important example occurs in the neurons of the eye.

O'Hagan and Barr, writing for Nature Cell Reports, describe "A motor relay on ciliary tracks" between kinesin-II and another motor. It turns out that kinesin-II is the marathoner running up the neuron into the crowded transition zone (TZ), where it "hands off" its cargo a sprinter named OSM-3 that runs it up to the cilium tip.

Peterman, Scholey and colleagues have now discovered a previously unappreciated complexity in the cooperation of anterograde motors using advanced techniques ....

They find that kinesin-II acts as an import motor that transports cargos from the distal dendrite into the ciliary TZ (Fig. 1). Because the TZ is cluttered with obstacles such as Y-link attachments, kinesin-II (with its tendency to frequently detach from microtubules) may easily sidestep obstructions, switching to an adjacent microtubule protofilament to continue on its path to deliver cargo to the PS [proximal segment]. A similar model of obstacle avoidance was proposed to function in axons, in which kinesin-2 binds the same cargo as kinesin-1 to allow the complex to sidestep around Tau protein obstacles.

The authors then observed gradual acceleration of IFT in the PS, accompanied by a gradual decrease in abundance of kinesin-II and concurrent increase in OSM-3 (KIF17) (Fig. 1). The acceleration resulting from changing the ratio of kinesin-II to OSM-3 did not match previous predictions from in vitro data. Instead, a biased contribution model, in which OSM-3 outcompetes kinesin-II ten-fold, fitted the acceleration observed in vivo. These results suggested a 'handover zone' in the PS, in which kinesin-II gradually hands over its transport duties to the faster and more processive OSM-3, which then acts as an efficient long-range motor to bring IFT complexes to the ciliary tip. [Emphasis added.]

Noting that different kinds of cilia in various species have different families of motors acting together, the authors describe "an emerging theme" in IFT research. They sugest that "kinesin-II plays an essential role in ciliogenesis, whereas accessory motors are associated with specializations in ciliary form and function." Many debilitating diseases are known to occur from mutations in IFT.

It's amusing how they used the word "evolution" only one time. "Why did evolution add another anterograde motor when heterotrimeric kinesin-II seems capable of doing the job alone in algae?" As it turns out, this relay race is an efficient way to get the job done. Kinesin-II and OSM-3 each have their strengths, and each one is matched for its environment. Then, at the ciliary tip, another molecular motor -- dynein -- takes cargo back down.

The paper by Scholey and Peterman and colleagues in Nature Cell Biology doesn't have anything to say about evolution. Instead, the scientists explain why "functional differentiation" provides the best way to get cargo delivered on time:

Dissociated kinesin-II motors undergo rapid turnaround and recycling to the ciliary base, whereas OSM-3 is recycled mainly to the handover zone. This reveals a functional differentiation in which the slower, less processive kinesin-II imports IFT trains into the cilium and OSM-3 drives their long-range transport, thereby optimizing cargo delivery.

Kinesin-II is no slouch as a runner. In our video, it appears to walk slowly and deliberately, but remember: the narrator says it can take a hundred steps a second. The researchers seem to like the word "optimize," using it four times in all, such as:

We propose that the functional differentiation of kinesin-II and OSM-3 into an import motor and transport motor, respectively, optimizes sequential steps of anterograde IFT to build the cilium. The system thus exploits each kinesin-2's specific motor properties and requires that the number of motors on the cargo, that is, the IFT train, is well orchestrated, resulting in a gradual exchange of the different motors to ensure reliable handover of cargo (Fig. 7). In a broader context, the deployment of similar, same-polarity yet functionally differentiated motors may represent a common strategy for optimizing intracellular transport.

"Optimize" is a design term. Evolutionists, by contrast, are fond of "tinkering," wherein natural selection supposedly cobbles together parts just to get by. Which word is a better match to the observations?

Myosin Mimicry

Another walking motor is myosin, which walks along actin filaments instead of microtubules. Bioengineers at Emory University weren't quite able to imitate its motion, but they did improve on previous attempts by inventing a DNA-based motor that rolls like a wheel. At first, the news from Emory makes it sound like they bested nature:

"Unlike other synthetic DNA-based motors, which use legs to 'walk' like tiny robots, ours is the first rolling DNA motor, making it far faster and more robust," says Khalid Salaita, the Emory University chemist who led the research. "It's like the biological equivalent of the invention of the wheel for the field of DNA machines."

But then they have nothing but praise for natural myosin:

The field of synthetic DNA-based motors, also known as nano-walkers, is about 15 years old. Researchers are striving to duplicate the action of nature's nano-walkers. Myosin, for example, are tiny biological mechanisms that "walk" on filaments to carry nutrients throughout the human body.

"It's the ultimate in science fiction," Salaita says of the quest to create tiny robots, or nano-bots, that could be programmed to do your bidding. "People have dreamed of sending in nano-bots to deliver drugs or to repair problems in the human body."

So far, however, mankind's efforts have fallen far short of nature's myosin, which speeds effortlessly about its biological errands. "The ability of myosin to convert chemical energy into mechanical energy is astounding," Salaita says. "They are the most efficient motors we know of today."

The engineer makes this blunder in his reasoning, though:

"Our DNA-based motor can travel one centimeter in seven days, instead of 20 years, making it 1,000 times faster than the older versions," Salaita says. "In fact, nature's myosin motors are only 10 times faster than ours, and it took them billions of years to evolve."

For one thing, myosins are present in the earliest cells we know of, so it didn't take them "billions of years to evolve." For another, if he applied intelligence to build a cheap mimic, wouldn't that be evidence that the superior product required an intelligent cause?

Molecular Ruler

We see myosin at work in another role described in a paper in Nature Communications: helping maintain the cytoskeleton. There's an "evolutionarily conserved" group of "Rho-associated coiled-coil kinases" (ROCK) that "are essential regulators of the actin cytoskeleton" on which myosins travel. The authors give us a glimpse into the precarious balance of motors that keep a cell's membrane intact:

The ability of cells to change shape underpins physiological processes from embryonic development through pathogen clearance in the immune system. The plasma membrane of cells exhibits high mechanical resistance yet permits enormous changes in cell shape. This apparent paradox is resolved by a dynamic network of actin and myosin filaments beneath the plasma membrane that forms the cortical cytoskeleton. Stress fibres, bundles of actin fibres and myosin II motors traverse the cell between focal adhesions that anchor the cell in the extracellular matrix. Actomyosin contraction against these anchors generates the force required for shape change and cell motility. Phosphorylation of regulatory myosin light chain (RMLC) stimulates myosin activity, leading to contractile force generation. The Rho-associated coiled-coil kinases (ROCK) are essential for the maintenance and integrity of stress fibres in the cell by directly and/or indirectly phosphorylating RMLC. A null mutant of the Drosophila Rok gene or deletion of ROCK1 or ROCK2 in mice results in prenatal lethality.

Their diagrams show that ROCK acts as a "molecular ruler" due to the length of its coiled coil. "This represents a new type of spatial control, and hence a new paradigm for kinase regulation."

They try to make a case for ROCK evolving at the origin of multicellularity, but it's little more than speculation. "Given the role of ROCK in regulating actin dynamics at focal adhesions, it is tempting to speculate that the emergence of ROCK together with the integrin-mediated signalling machinery was a crucial event in metazoan evolution." Exactly how machinery "emerges" by blind processes is not clear. One thing is clear: it is "evolutionarily conserved throughout the animal kingdom." In fact, it is "remarkably well conserved across more than 600 million years of evolution." That's hardly something to make an evolutionist cheer. We'll take their concluding automotive analogy instead. It sounds more like design.

Our findings indicate that the activity of the Rho kinases is regulated by the spatial positioning of kinase and substrate in the cell, much like the clutch in a car engine determines whether the car is in gear or not. The engine, or kinase, is always running, but the car, or cell, doesn't move unless the clutch, or substrate, is engaged. This represents a new paradigm in kinase-substrate regulation, whereby substrate specificity and corresponding activity are simply governed by the precise spatial positioning of enzyme and substrate.

So there you have it. Cells are inhabited by molecular motors and engines with precision parts operating under tight regulations. Now you can watch our video animation with a little more appreciation for what these amazing molecular machines do for all life, including you.

Jehovah's Justice prevails

Why accepting I.D may not necessitate an embrace of the supernatural.

ID for Materialists:
January 25, 2016 Posted by Barry Arrington under Intelligent Design

Teleology in biology is unavoidable.  Dawkins was surely correct when he wrote that “Biology is the study of complicated things that give the appearance of having been designed for a purpose.”  He even characterized that appearance as “overwhelming.”  Of course, Dawkins does not believe living things were designed, and his entire project has been to convince his readers that the overwhelming appearance of design is an illusion.

The problem with the “it is all a grand illusion” position is that as science has progressed – even in the relatively short time since Dawkins wrote those words in 1987 – it has become increasingly more difficult to believe.  Advances in our understanding of genetics have revealed a semiotic code of staggering elegance and complexity, the replication of which is far beyond the ability of our best computer programmers.  The more we know about the cell, the more it becomes apparent that it is a marvel of nano-technology.  Origin of life researchers, when they are honest, admit that even the most simple life is miraculously complex, and the likelihood of living things having arose spontaneously through chance interactions of matter is vanishingly small.  I could go on, but you get the picture.

What is an honest materialist to do?  One approach is to jettison materialism altogether, as famous former arch-atheist Antony Flew did.  Flew insisted that while he did not believe in a personal God, he was nevertheless driven to deism by advances in origins of life science.  He wrote that “[t]he philosophical question that has not been answered in origin-of-life studies is this: How can a universe of mindless matter produce beings with intrinsic ends, self-replication capabilities, and ‘coded chemistry’?”  That question remains unanswered.

Another approach is to retain one’s materialism while positing the existence of yet-undiscovered natural telic laws.  This is the approach Thomas Nagel took in his Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature is Almost Certainly False.  It occurred to me recently that this approach may well be the most likely way for honest, curious and courageous materialists to accept the evidence on its own terms and at the same time find common ground with ID proponents.

RDFish is one of the most voracious proponents of materialism (which he prefers to call monist physicalism) ever to appear in these pages.  In one of his comments he argued that biological ID is committed to dualism.  I responded by arguing that while biological ID is certainly consistent with metaphysical dualism, it is not necessarily tied to it, and it can be accepted even by physicalist monists.  See here.

In the linked post I argued that a physicalist monist can accept a version of ID through the following reasoning:

Design, meaning the capacity to arrange matter for a purpose, exists as a category of causation.
The capacity to arrange matter for a purpose can be reduced to any force that is capable of arranging matter in the present so that it will have an effect in the future.
There are at least two candidates for causal forces that have the capacity to arrange matter for a purpose. (a)  intelligent agents who have an immaterial mental capacity; (b) an impersonal non-conscious yet-to-be-discovered natural telic force.
The monist rejects the existence of intelligent agents with immaterial mental capacities, because the existence of such agents obviously entails dualism.
Instead, the monist can resort to the natural telic force.
If such a natural telic force exists, the existence of design as a category of causation is no obstacle to accepting the truth of monist physicalism.
This get us to:

If monist physicalism is true and a natural telic force exists, it is nevertheless possible objectively to infer design.
Therefore, design may be inferred under monist physicalism using the explanatory filter.
Therefore, ID does not depend on dualist metaphysical assumptions and can be accepted by a monist.
Which brings us back to Nagel.  In his book Nagel argued that Neo-Darwinism has failed to account for the data and is therefore almost certainly false.  But Nagel is an inveterate atheist and he is unwilling to give up on atheistic monism.  For Nagel, rejecting Neo-Darwinism does not entail embracing a dualist conception of ID.  Instead, he has posited what can be called a monist conception of ID by proposing the existence of natural telic laws.

In his book Being as Communion Bill Dembski writes that Nagel’s conception of teleology is completely consistent with ID writ large:

Nagel proposes to understand teleology in terms of natural teleological laws.  These laws would be radically different from the laws of physics and chemistry that currently are paradigmatic of the laws of nature.  And yet, as we shall see, such teleological laws fit quite naturally within an information-theoretic framework . . . his proposal, given in Mind and Cosmos . . . connects point for point with the account of information given in this book.  Indeed, Nagel’s teleological laws are none other than the directed searches (or alternative searches) that are the basis of Conservation of Information . . . of this book.

When orthodox Christian theist Bill Dembski says that he and vigorously atheistic materialist Thomas Nagel hold views that can – at a fundamental level – be reconciled, the rest of us should sit up and take notice.  And Dembski is not alone among theists in noting how Nagel’s views are compatible with their tradition broadly construed.  Christian philosopher Edward Feser writes:

[Nagel] rightly suggests that theists ought to be open to the idea of immanent teleology of the Aristotelian sort.  He may not be aware that medieval theologians like Aquinas were committed to precisely that.

Of course, Aquinas believed in the immanent teleology inherent in all things.  The only difference between Aquinas and Nagel is that Aquinas believed that God infused those things with immanent teleology; whereas Nagel believes the teleology results from a natural telic law.  But for our purposes isn’t the obvious teleology – that even Dawkins recognizes while denying – the important thing, at least as an initial question about the objective nature of things?

If theists and materialists can agree about the objective existence of teleology in nature, can we not also agree that – at least while we are doing science – questions about the ultimate provenance of that teleology can be held in abeyance?

I see a number of advantages of this approach for both sides.  For the materialists, the advantages are obvious.  They will be able to accept on face value the common sense conclusion their materialism has until now forced them to deny.  Teleology exists.  And at the same time they will not be forced to allow Lewontin’s dreaded “divine foot” in the door, because a “natural telic law” is not even an agent, far less a divine (or even conscious) agent.  For theists, as I have argued all along, ID can be adopted to both a monist and a dualist metaphysics.  And I, when I am not doing science, will continue to argue that God is the best candidate for the provenance of the teleology.  At the same time, by allowing for the possibility of a natural telic law, we ID proponents will not have the doors of science slammed in our face on account of the “creationism in a cheap tuxedo” argument.

The better choice.

liberty,equality,brotherhood?

Currently Turned Against Pro-Lifers, French Totalitarian Impulse Can Easily Jump Oceans
David Klinghoffer 

Years ago when I was younger and more strident, I had a dinner conversation with a woman friend who, I realized too late, I didn't know quite as well as I thought. I should have understood that abortion isn't something to discuss like any other casual meal topic. I was stating a pro-life view when she suddenly put down her fork and left the restaurant. I found her crying outside and that was the end of the evening.

Was it asinine of me not to grasp that a woman, any woman, might have a painful personal history relevant to the subject that I as a man could not have? Yes. There's a time and a place for everything, and there are more or less sensitive ways to talk about abortion and human life. Lucky for me, though, this was New York City in the 1990s and not France in 2016.

On the heels of censoring a TV ad meant to discourage women from aborting Down syndrome children, the French Senate and National Assembly have gone further and voted to criminalize online pro-life activism. For applying "moral and psychological pressure," making women feel guilty, no matter how sensitive you are in applying this moral pressure, you could face prison and fines!

Alexandra DeSanctis reports at National Review:

The French Senate today adopted a bill criminalizing the posting of pro-life information online, a measure that was passed by the French National Assembly just last week. Violators face a maximum of two years in prison and over $30,000 in fines. The measure makes it a crime for pro-life individuals or activists to obstruct a woman's lawful decision to have an abortion, or to cause her guilt after the fact.

...

[T]he bill defines obstruction not only as the physical effort to block an abortion clinic, for example, but also "psychological obstacles..."

...

[M]any analysts agree that the bill will be interpreted to criminalize any person or website that posts information regarding alternatives to abortion, or even that espouses the Christian belief that the church considers abortion to be immoral. [Emphasis added.]

On the radio, Dennis Prager makes the important point that we wrongly see liberalism and leftism as being on some kind of continuum. Not so. The world could benefit from more genuine liberals. Leftism, on the other hand, is distinguished by its totalitarianism. In this case, the totalitarianism is wedded to scientism, the belief that science unmoored from other sources of values should reign supreme, including in defining which opinions may or may not be lawfully expressed.


This is scary, not because we live in France but because ideas like this are contagious and easily cross oceans. Do you doubt for a minute that some of our homegrown true believers that science has all the answers would love to hold the law more firmly in their grasp to wield against skeptics like us?

Modern medicine v. Darwin.

LSU Ophthalmologist Commends a "Design Approach" in Appraising Supposedly Vestigial Organs
Ann Gauger


Sometimes when our worldview is wrong, we miss important things. The Darwinian point of view in particular may lead to false assumptions. A doctor, Alan B. Richards, who teaches at the Health Sciences Center at Louisiana State University, writes to us with an example. He describes a part of the eye that many consider to be vestigial, that is, an evolutionary holdover from the past that now supposedly serves no function. He points out that viewing the tissue in question as vestigial can lead to serious mistakes. Because it actually serves a purpose, surgeons who are ignorant of that purpose can inadvertently cause damage.

Writes Dr. Richards:

Here are a couple of observations from the world of medicine regarding the dangers of a purely Darwinist approach.

I have read several sources about the plica semilunaris in the eye, and even among intelligent design advocates, no one seems to explain this misunderstood part of the body.

I am a pediatric ophthalmologist and I teach residents how to perform eye muscle surgery. The plica semilunaris is the curvilinear pinkish tissue in each person's eye nasally. According to neo-Darwinian advocates, the tissue is a useless holdover from evolution, a vestigial tissue of the nictitating membrane in other mammals. Residents, who are generally a bright bunch, routinely quote this "truth" to me each year. Thus, residents tend to be careless with this tissue unless taught properly.

When performing surgery for esotropia ("crossed eyes"), one must be very careful with the plica semilunaris. The tissue can easily be improperly attached too far temporally, as at the end of surgery the plica looks much like the normal conjunctiva that covers the eye (plica is modified conjunctiva).

I explain to the residents that the plica is needed to allow the eye to move outward or temporally, and sewing the plica in the wrong location can not only result in a dreadful red appearance to the eye, but the eye can be drawn inward.

In the first few years of my practice, I saw an unfortunate Vietnamese gentleman, who had immigrated to the USA during the upheaval in Southeast Asia ("boat people"). He had a benign growth on the nasal portion of his eyes (a pterygium). The operation to remove this lesion is usually straightforward, but whoever performed his surgery neglected the plica and sewed the plica semilunaris too far temporally, resulting in very crossed eyes and double vision. Understandable upset, I had to perform eye muscle surgery (strabismus surgery) to restore his vision to normal.

Since the residents may not consider me an authority on the subject of ocular anatomy, I give this this quote from Dr. Darlene A. Dartt, Associate Professor of Ophthalmology at Harvard Medical School in Duane's Clinical Ophthalmology, a well respected standard text on all aspects of ophthalmology, the first comprehensive ophthalmology text in the USA. (Thomas Duane, the editor, was chairman of ophthalmology at Wills Eye Hospital in Philadelphia, where I trained, the second-ranked ophthalmology program in the USA. Also, he was a former chairman of the American Medical Association's ophthalmology section and edited two standard reference works, Clinical Ophthalmology and The Biomedical Foundations of Ophthalmology.)

These words are from Chapter 2, "The Conjunctiva-Structure and Function":

The plica semilunaris is a crescent-shaped fold of conjunctiva that is situated medially and conjoins the bulbar conjunctiva with the caruncle and lacrimal portion of the eyelids (Fig. 3). It is located in the superior fornix at the junction of extending downward, surrounding the limbus to end in the inferior fornix. It extends 3 to 6 mm laterally from the caruncle. The nictitating membrane present in some animals is the counterpart to the plica, and is a partial or complete third eyelid. Although humans do not have a nictitating membrane, occasionally smooth muscle fibers may be present that are innervated with sympathetic nerves. Goblet cells are present in the plica either singly or in clusters. In humans, the plica functions as the opposite of a fornix; that is, if the conjunctiva were to directly join the eyelids to the globe, the globe and eyelids would both be restricted in movement. The fornix provides for a fold of conjunctiva that may be extended or retracted as the globe moves. Extension occurs because of fibrous slips that connect the fornix to its extra ocular rectus muscle. As the muscle contracts, the globe rotates and the adjacent conjunctiva is retracted. This occurs above, laterally, and below the globe, but not medially, which would not allow the lacrimal puncta to drain the lacrimal lake. On abduction the plica tends to unfold and flatten, whereas on adduction it is drawn posteriorly and is unfolded by the fibrous slips that extend to the plica and caruncle from the medial rectus. While it never completely unfolds, extreme adduction of the plica causes it to form a true fornix. As this occurs, a small movement of the globe occurs as a result of the retraction of the medial canthal tendon. This keeps the lacrimal puncta properly positioned with the lacrimal lake. The puncta now dips into the lacrimal strip to allow continuous drainage despite the position of the globe. In addition, the plica helps to maintain the lacrimal lake in its proper position and location in the puncta.

The bold type and underlining are my emphasis: properly the nictitating membrane is the counterpart or analog to the plica; calling the plica vestigial ignores its function. (How does one prove an organ has no function, without very, very careful study?) While the plica is not as important as some other portions of the eye (e.g., the retina, the optic nerve), the structure still serves an important function.

Thus, a design approach (whether or not one accepts common ancestry, directed theistic evolution (highly recommend "Evolution of Living Organisms" by Pierre-P Grasse), or sudden or progressive creation) results in clearer thinking than the approach that man is a result of random accidents and full of useless organs.

Alan B. Richards, MD
Clinical Assistant Professor
LSU Health Sciences Center
Shreveport, LA

Assuming non-function, or in this case, vestigiality, seems to be the default position of neo-Darwinism. When a biological structure seems useless, or it seems to be broken, and yet it appears to be derived from a similar structure in other organisms, the leap is made to say that the thing under study is evolutionary detritus that has not been completely removed by natural selection.

We have seen this viewpoint before. Junk DNA and pseudogenes, for example, have been considered to be evolutionary leftovers that are non-functional. You can even see the assumption in the names these genetic elements were given. But as time goes on, more and more functions are being discovered for junk DNA and pseudogenes.


The intelligent design intuition, in contrast, is to assume function, that things are there for a purpose, and are not merely some evolutionary holdover. I wonder how many "functionless" things like the plica semilunaris will be found to have function after all, once we begin to look more carefully using a design perspective.

The big deal re:The Royal society's peek under darwinism's hood

Why the Royal Society Meeting Mattered, in a Nutshell

Evolution News & Views

We devoted considerable attention to last month's Royal Society meeting in London. Otherwise, the three-day conference on "New Trends in Evolutionary Biology" was kept rather quiet in the media.

Oh, there were a few reports. Writing for the Huffington Post, science journalist Suzan Mazur complained of a lack of momentousness: "[J]ust what was the point of attracting a distinguished international gathering if the speakers had little new science to present? Why waste everyone's time and money?" On the other hand, a write-up in The Atlantic by Carl Zimmer acknowledged a sense of strain between rival claques of evolutionists: "Both sides offered their arguments and critiques in a civil way, but sometimes you could sense the tension in the room -- the punctuations of tsk-tsks, eye-rolling, and partisan bursts of applause."

Mild drama notwithstanding, why should anyone care about this meeting?

Despite the muffled coverage, the meeting was still significant in a number of ways. First, remember that the Royal Society is arguably the world's most august scientific body. Its founders included Robert Boyle and it was later headed for 24 years (1703-1727) by Isaac Newton -- a fact that is hard to forget when they have his death mask on prominent display in a glass case. Portraits of Boyle and Newton on the walls look down from above. The historical connections lent a certain weight by themselves to the proceedings.

That such a thoroughly mainstream scientific organization should now at last acknowledge problems with the received neo-Darwinian theory of evolution is also obviously notable. Indeed, from our point of view, though presenters ignored, dismissed, or mocked ID, not realizing the number of design-friendly scientists in the audience, the proceedings confirmed something ID advocates, including Stephen Meyer and others, have been saying for years.

Consider, for example, Meyer's provocative claim in the Prologue to Darwin's Doubt:

The technical literature in biology is now replete with world-class biologists routinely expressing doubts about various aspects of neo-Darwinian theory, and especially about its central tenet, namely the alleged creative power of the natural selection and mutation mechanism.

Nevertheless, popular defenses of the theory continue apace, rarely if ever acknowledging the growing body of critical scientific opinion about the standing of the theory. Rarely has there been such a great disparity between the popular perception of a theory and its actual standing in the relevant peer-reviewed science literature.

The opening presentation at the Royal Society conference by one of those world-class biologists, Austrian evolutionary theorist Gerd Müller, underscored exactly Meyer's point. Müller opened the meeting by discussing several of the fundamental "explanatory deficits" of "the modern synthesis," that is, textbook neo-Darwinian theory. (Discovery Institute's Paul Nelson recounted Müller's remarks here, on which in part we base the following.) According to Müller, the as yet unsolved problems include those of explaining:

Phenotypic complexity (the origin of eyes, ears, body plans, i.e., the anatomical and structural features of livings);

Phenotypic novelty, i.e., the origin of new forms throughout the history of life (for example, the mammalian radiation some 66 million years ago, in which the major orders of mammals, such as cetaceans, bats, carnivores, enter the fossil record, or even more dramatically, the Cambrian explosion, with most animal body plans appearing more or less without antecedents); and finally

Non-gradual forms or modes of transition, where you see abrupt discontinuities in the fossil record between different types.

As Müller has explained in previously published work (with Stuart Newman), although "the neo-Darwinian paradigm still represents the central explanatory framework of evolution, as represented by recent textbooks" it "has no theory of the generative."1 In other words, the neo-Darwinian mechanism of mutation and natural selection lacks the creative power to generate the novel anatomical traits and forms of life that have arisen during the history of life. Yet, as Müller noted, neo-Darwinian theory continues to be presented to the public via textbooks as the canonical understanding of how new living forms arose -- reflecting precisely the tension between the perceived, and actual, status of the theory that Meyer described in Darwin's Doubt.

Yet, the most important lesson of the Royal Society conference lies not in its vindication of claims that our scientists have made, gratifying as that might be to us, but rather in defining the current problems and state of research in the field. The conference did an excellent job of defining the problems that evolutionary theory has failed to solve, but it offered little, if anything, by way of new solutions to those longstanding fundamental problems.

Much of the conference subsequent to Müller's talk did discuss various other proposed evolutionary mechanisms. Indeed, the prime movers in the Royal Society event, Müller, along with James Shapiro, Denis Noble, and Eva Jablonka -- the "Third Way of Evolution" crowd -- have proposed repairing the explanatory deficits of the modern synthesis by highlighting evolutionary mechanisms other than random mutation and natural selection. Much debate at the conference centered around the question of whether these new mechanisms could be incorporated into the basic population genetics framework of neo-Darwinism, thus making possible a new "extended" evolutionary synthesis, or whether the emphasis on new mechanisms of evolutionary change represented a radical, and theoretically incommensurable, break with established theory. This largely semantic, or classificatory, issue obscured a deeper question that few, if any, of the presentations confronted head on: the issue of the origin of genuine phenotypic novelty -- the problem that Müller described in his opening talk.

Indeed, by the end of Day 3 of the meeting, it seemed clear to many of our scientists, and others in attendance with whom they talked, that the puzzle of life's novelties remained unsolved -- if, indeed, it had been addressed at all. As a prominent German paleontologist in the crowd concluded, "All elements of the Extended Synthesis [as discussed at the conference] fail to offer adequate explanations for the crucial explanatory deficits of the Modern Synthesis (aka neo-Darwinism) that were explicitly highlighted in the first talk of the meeting by Gerd Müller."

In Darwin's Doubt, for example, Meyer emphasized the obvious importance of genetic and other (i.e., epigenetic) types of information to building novel phenotypic traits and forms life. The new mechanisms offered by the critics of neo-Darwinism at the conference -- whether treated as part of an extended neo-Darwinian synthesis or as the basis of a fundamentally new theory of evolution -- did not attempt to explain how the information necessary to generating genuine novelty might have arisen. Instead, the mechanisms that were discussed produce at best minor microevolutionary changes, such as changes in wing coloration of butterflies or the celebrated polymorphisms of stickleback fish.

Moreover, the mechanisms that were discussed -- niche construction, phenotypic plasticity, natural genetic engineering, and so on -- either presupposed the prior existence of the biological information necessary to generate novelty, or they did not address the mystery of the origin of that information (and morphological novelty) at all. (Not all the mechanisms addressed were necessarily new, by the way. Niche construction and phenotypic plasticity have been around for a long time.)

Complex behaviors such as nest-building by birds, or dam construction by beavers, represent examples of niche construction in which some organisms themselves demonstrate the capacity to alter their environment in ways that may affect the adaptation of subsequent generations to the environment. Yet no advocate of niche construction at the meeting explained how the capacity for such complex behaviors arose de novo in ancestral populations, as they must have done if the naturalistic evolutionary story is true.

Rather, these complex behaviors were taken as givens, leaving the critical question of their origins more or less untouched. While there is abundant evidence that animals can learn and transmit new behaviors to their offspring -- crows in Japan, for instance, have learned how to use automobile traffic to crack open nuts -- all such evidence presupposes the prior existence of specific functional capacities enabling observation, learning, and the like. The evolutionary accounts of niche construction theory therefore collide repeatedly with a brick wall marked "ORIGINAL COMPLEX FUNCTIONAL CAPACITY REQUIRED HERE" -- without, or beyond which, there would simply be nothing interesting to observe.

Jim Shapiro's talk, clearly one of the most interesting of the conference, highlighted this difficulty in its most fundamental form. Shapiro presented fascinating evidence showing, contra neo-Darwinism, the non-random nature of many mutational processes -- processes that allow organisms to respond to various environmental challenges or stresses. The evidence he presented suggests that many organisms possess a kind of pre-programmed adaptive capacity -- a capacity that Shapiro has elsewhere described as operating under "algorithmic control." Yet, neither Shapiro, nor anyone else at the conference, attempted to explain how the information inherent in such algorithmic control or pre-programmed capacity might have originated.

This same "explanatory deficiency" was evident in the discussions of the other mechanisms, though we won't attempt to demonstrate that exhaustively here. We would direct readers, however, to Chapters 15 and 16 of Darwin's Doubt, where Meyer highlighted the way in which, not just neo-Darwinism, but also newer evolutionary mechanisms, including many discussed at the conference, fail to solve the question of the origin of information necessary to generate novelty. In those chapters, he reviewed a range of proposed fixes to the Modern Synthesis. He acknowledged and described the various advantages that many of these proposals have over neo-Darwinism, but also carefully explained why each of these mechanisms falls short as an explanation for the origin of the biological information necessary to build novel structures and forms of animal life. He quoted paleontologist Graham Budd who has observed: "When the public thinks about evolution, they think about [things like] the origin of wings....But these are things that evolutionary theory has told us little about."

Many fascinating talks at the Royal Society conference described a number of evolutionary mechanisms that have been given short shrift by the neo-Darwinian establishment. Unfortunately, however, the conference will be remembered, as Susan Mazar intimated in her coverage, for its failure to offer anything new. In particular, in our judgment, it failed to offer anything new that could help remedy the main "explanatory deficit" of the neo-Darwinian synthesis -- its inability to account for the origin of phenotypic novelty and especially, the genetic and epigenetic information necessary to produce it. These are still problems that evolutionary theory tells us little about.

Notes:

(1) Gerd Müller and Stuart Newman, On the Origin of Organismal Form (Cambridge, MA: MIT Press, 2003), p.7.

On the Nobel committee's design filter.

Behe: Nobel Prize for Chemistry Begs the Question of Intelligent Design

David Klinghoffer

The 2016 Nobel Prize for Chemistry recognized the intelligent design (what else would you call it?) of artificial molecular machines. These "nano" machines are impressive as technical achievements. Yet they are also exceedingly simple, "cute" but "useless," as  Nature reported that "some chemists" say. "We need to convince [researchers] that these molecules are really exciting," as one scientist remarked.

Writing at CNSNews , Discovery Institute biochemist Michael Behe makes the point that Darwin advocates don't want to hear. If scientists need to be "convinced" that nano machines are "exciting" and useful, the same is surely not true when it comes to the molecular machines familiar to biologists. That's the nanotechnolgy that make continuing existence possible for chemists, Nobel Laureates, and every living creature on the planet:

Many of the pioneers of the [nanotechnology] field drew inspiration from molecular machines discovered in biology such as the bacterial flagellum, a whip-like outboard motor that can propel bacteria through liquid. Yet the molecular machines laboriously constructed by our brightest scientists are Tinkertoys compared to the nanotechnology found in living cells. That may change -- with the expenditure of much effort and brain power the chemists' machines may be improved in the future. But right at this very moment sophisticated molecular robot walkers à la Star Wars are transporting critical supplies from one part of your cells to others along molecular highways, guided by information posted on molecular signposts. Molecular solar panels that put our best technology to shame are found in every leaf. Molecular computer control systems run the whole show with a reliability that exceeds that of, say, a nuclear reactor. What's more, unlike the artificial molecular machines that were painstakingly assembled by chemists, cellular molecular machines assemble themselves. As an astonished science writer once put it: "The cell's macromolecular machines contain dozens or even hundreds of components. But unlike man-made machines, which are built on assembly lines, these cellular machines assemble spontaneously from their protein and nucleic-acid components. It is as though cars could be manufactured by merely tumbling their parts onto the factory floor." Now those are smart materials!

No one needs to labor to convince anybody that  kinesins  (walking transport proteins) are useful. It sounds like he's headed in a dangerous direction:

Here's a question that'll get you into trouble in a lot of places for asking it out loud: if brilliant scientists can manage to make only toy molecular machines, what does it take to make the sophisticated machinery of the cell? For the past several decades I and others have been arguing that the ultra-sophisticated systems at the foundation of life powerfully bespeak purposeful design -- and for the same reason that the much simpler machines made by Nobel prize winners do: it takes intelligence and planning to arrange multiple parts into a working machine.

Yeah, smart guy, but billions of years!

Critics retort that, given billions of years and the whole world to work with, Darwin's mechanism of random mutation and natural selection could do the job. But there's no good reason to think so. The best, most recent laboratory and field evolution experiments show that random mutation most often breaks or damages genes that already exist and, counterintuitively, that sometimes helps a species survive. Needless to say, a process which most often breaks genes isn't going to build much of anything.

What are you, Behe, some sort of creationist?

Another common objection I hear is that the conclusion that the molecular foundation of life was purposely designed has religious implications. But so what? Science is supposed to be a search for truth based on our best understanding of nature. Science isn't supposed to shy away from a conclusion just because it doesn't fit some people's philosophical preconceptions.

The sophisticated design of living nanotechnology exceeds by light years that of human nano-inventions. Yet evolutionists deny that the former offers scientific evidence of intelligent direction, even as the latter, child's play by comparison, obviously do. For reference, see the debate I highlighted yesterday on protein evolution between  Doug Axe and Keith Fox.

Dr. Behe's own work in illuminating the evidence for intelligent design is the subject of a new hour-long documentary,  Revolutionary: Michael Behe and the Mystery of Molecular Machines. It's available now on DVD or Blu-ray.

More waving away of evidence of design.

Evolving Protein-Protein Binding -- Not a Problem?

Cornelius Hunter 

Dennis Venema is a Fellow of Biology with BioLogos, where he writes a series of posts called "Letters to the Duchess" -- an allusion to Galileo's "Letter to the Grand Duchess Christina." In the past, I have looked at Professor Venema's articles on evidences for common descent (see here

 , 

 here

,

 here

 , 

 here

, 

 here

, and 

 here

).

In a recent  online discussion 

 with Venema, he made the erroneous claim that the mammalian immune system, with its search for, and production of, antibodies, is a good example of why evolving protein-protein binding sequences is not a problem. In fact the mammalian immune system is yet another enormous problem for the theory of evolution.

The mammalian immune system is not a good example because it is designed for this job of creating protein-protein binding sequences. It searches a well-defined design space extremely rapidly, and measures the success of its search experiments accurately and quickly. The fact that our immune system successfully designs antibodies in short order does nothing to address the problem of how random mutations occurring throughout the genome are supposed to have found myriad binding sequences, crucial for life. Venema also referred to another example that he has written about. Unfortunately this example also fails to demonstrate Venema's claim of "evolution producing a new protein-protein binding event."

The problem with evolving protein-protein binding is that too much gene sequence complexity is required to achieve the needed binding affinity. You could say it is an "all-or-none" type of problem.

One or two mutations will not generally do the job -- you usually need more mutations before the two proteins stick together very well. And stick together they must, on a massive scale, in order to perform their necessary tasks. Even the simplest, unicellular, organisms contain massive protein machines, consisting of dozens of different proteins binding together to perform crucial life functions.

The study Venema referred to did a beautiful job in confirming this "all-or-none" character of protein-protein binding sequences. The study showed that in order for a viral protein to perform a relatively simple switch from one protein to a very similar protein required four types of mutations. Anything less and no dice.

The twist in this study was that subsets of the four mutation types were apparently useful for a different function (strengthening the binding affinity to the original protein). So while in general the evolution of protein-protein binding sequences is astronomically difficult because too many simultaneous mutations are required, in this case the four mutation types could be accumulated, with useful benefit realized at some of the intermediate steps.

This is not a general result. It is not a revolutionary new finding that reverses our understanding of protein-protein binding sequences.

It confirms our knowledge, and adds a fascinating outlier case where the "all-or-none" character is circumvented by intermediate functions that fortuitously "push" the design in the right direction. As the study explains:

The "all-or-none" epistasis among the four canonical phage mutations implies that it would have been unlikely for the new function to evolve on the scale of our experiments, except for the lucky fact that some of the mutations were beneficial to the phage in performing their current function, thereby pushing evolution toward the new function.

The study provides no indication that the untold thousands upon thousands of protein-protein binding problems in molecular biology would enjoy this type of setup. And if they did, oh what a suspicious sign of design that would be.

Venema is mistaken in his attempt to recruit this study as a solution to the evolution of protein-protein binding sequences. Strangely, not only had Michael Behe provided his explanation of the study, but Venema was aware of it at the time of his writing. Venema explained that in his next article he would address Behe's explanation, but in fact Venema simply rehashed Behe's original explanation for why protein-protein binding is a problem for evolution. Venema did not address Behe's explanation but simply concluded that Behe's original explanation must be false because, after all, this new study demonstrates the evolution of just such protein-protein binding sequences.

This is an unfortunate misuse of a study that most readers will not understand. Venema has force-fitted the study into an evolutionary proof.

Additional Problems

In addition to the basic problem of serendipity, this confirmation of the "all-or-none" character of protein-protein binding sequences was possible only with a very contrived, designed, laboratory experiment. Simply put, a virus population was provided with a willing and well-fed host to live off. In the meantime, many more host targets awaited the virus population. So a few mutations helped the viruses infect the initial hosts, and mere single additional mutation then allowed the viruses to infect the second group of hosts.

It was, again, an entirely artificial, laboratory environment, that wasn't even intended to replicate a realistic evolutionary environment. Venema nowhere explained this.

Second, the study also discovered even more serendipity. Not only were there "luckily" intermediate fitness benefits, but the finding of the four mutations types also required certain mutations in the host genome. Without them, no dice.

Finally, it is worth noting that across the many different virus populations used in the experiment, the virus protein in question did not incur any synonymous mutations. The study attempted to explain this as a sign of selection:

First, all 248 independent mutations in the 51 sequenced J alleles were nonsynonymous, whereas the expected ratio of nonsynonymous to synonymous changes is 3.19:1 under the null model for the ancestral J sequence. This great excess is evident even if we include only the 82 nonsynonymous mutations in the 24 isolates that did not evolve the new receptor function.

This is suspicious. According to evolutionary theory, a lack of selection will be manifest in relatively few nonsynonymous mutations. So the ratio of normalized nonsynonymous mutations-to-normalized synonymous mutations (the so-called Ka/Ks ratio) will be less than unity. On the other hand, strong selection will be manifest in relatively many nonsynonymous mutations. So the Ka/Ks ratio will be greater than unity.

A high Ka/Ks ratio, and hence an inference of strong selection, should be due to relatively many nonsynonymous mutations. In this study, however, it is in the synonymous mutations where the surprise comes. There were zero. In other words, the Ka/Ks ratio is infinity. To pass this off simply as a sign of strong selection is not good science, even within the normal science of evolutionary theory.

It's irreducible complexity all the way down II

Newfound Genetic Code-in-Code Regulates Stress Response
Evolution News & Views 

There are 64 combinations in the genetic code (43), because there are four bases arranged in threes. Each triplet codon codes for one amino acid, of which there are 20 normally used in proteins. This mismatch of 64 versus 20 has been called degeneracy, and has long been a mystery. Some amino acids have a single codon, but others can be coded by up to six codons. Is this redundancy just a "frozen accident," as Francis Crick thought? Could there be functional reasons why a gene would specify one codon instead of another?

In the past, we examined growing evidence for function in the degeneracy. Last year we learned that different codons work at different rates, providing a "speed limit" mechanism for protein formation. In 2014, Casey Luskin wrote about how differing codons provide the cell with "translational pausing" that affects folding rates with phenotypic effects. The prior year, we saw that alternate codons have effects on circadian rhythms. In 2011, contributor Jonathan M. discussed additional evidences of fine-tuning in the mismatch. As Luskin said, "The theory of intelligent design predicts that living organisms will be rich in information, and thus it encourages us to seek out new sources of functionally important information in the genome."

Now we have another fulfillment of that prediction. Research at MIT has found a "Newly discovered genetic code [that] controls bacterial survival during infections" (emphasis added). This code-in-a-code makes use of the redundant codons for signaling bacteria to switch on their stress response strategy: "to enter a dormancy-like state that allows them to survive in hostile environments when deprived of oxygen or nutrients." The team led by Peter Dedon, a professor of biological engineering at MIT, found this out by working with Mycobacterium bovis.

Basically, the codons affect their corresponding transfer-RNAs (tRNA) in different ways. Notice first how complex the transfer RNA system is:

Once a tRNA molecule is manufactured, it is altered with dozens of different chemical modifications. These modifications are believed to influence how tightly the tRNA anticodon binds to the mRNA codon at the ribosome.
In this study, Dedon and colleagues found that certain tRNA modifications went up dramatically when the bacteria were deprived of oxygen and stopped growing.

Experimenting on the bacterium's response to anoxic conditions, the researchers wondered if alternate codons made a difference. They knew that "the amino acid threonine can be encoded by ACU, ACC, ACA, or ACG," so they went hunting for possible connections to the stress response.

One of these modifications was found on the ACG threonine anticodon, so the researchers analyzed the entire genome of Mycobacterium bovis in search of genes that contain high percentages of that ACG codon compared to the other threonine codons. They found that genes with high levels of ACG included a family known as the DosR regulon, which consists of 48 genes that are needed for a cells [sic] to stop growing and survive in a dormancy-like state.
When oxygen is lacking, these bacterial cells begin churning out large quantities of the DosR regulon proteins, while production of proteins from genes containing one of the other codons for threonine drops. The DosR regulon proteins guide the cell into a dormancy-like state by shutting down cell metabolism and halting cell division.

Here, then, is powerful evidence for different effects when the same amino acid is encoded by an alternate codon. The work by Dedon's team is published in Nature Communications, an open-access journal.

Apparently the ACG codon affects the "wobble" of its corresponding tRNA and how tightly the amino acid is bound. This, in turn, affects the translation efficiency in the ribosome, thus regulating the dosages of protein products. They began to see a method in the madness of degeneracy, evident in the phrase "coordinated system":

Codon re-engineering of dosR exaggerates hypoxia-induced changes in codon-biased DosR translation, with altered dosR expression revealing unanticipated effects on bacterial survival during hypoxia. These results reveal a coordinated system of tRNA modifications and translation of codon-biased transcripts that enhance expression of stress response proteins in mycobacteria.
In the conclusion, they elaborate on this coordinated system, stating that it represents another genetic code:

There is emerging speculation for the existence of a 'code of codons' based on gene-specific codon usage patterns that can regulate translation. Among possible mechanisms linking environmental changes to codon-biased translation, recent studies have shown that the dozens of modified ribonucleosides in tRNA form a dynamic system that responds to cellular stress. We have shown that stress-specific alterations in tRNA wobble modifications, which can expand or limit tRNA decoding capabilities, facilitate decoding of cognate codons that are over- or under-used in mRNAs, which enhances translational elongation and leads to the selective up- and downregulation of the codon-biased genes.
The news report from MIT doesn't hesitate to call this a "newly discovered genetic code" or "alternate genetic code" with functional significance, constituting "another layer of control, mediated by transfer RNA, that helps cells to rapidly divert resources in emergency situations." Another biochemist comments on the significance of the discovery:

"The authors present an impressive example of the new, emerging deep biology of transfer RNAs, which translate the genetic code in all living organisms to create proteins," says Paul Schimmel, a professor of cell and molecular biology at the Scripps Research Institute, who was not involved in the research. "This long-known function was viewed in a simple, straightforward way for decades. They present a powerful, comprehensive analysis to show there are layers and layers, ever deeper, to this function of translation."
That's right out of intelligent design's list of predictions. As powerful as the evidence was for design in the genetic code's translation mechanism mediated by tRNA, it wasn't powerful enough. Now scientists are beginning to view "layers and layers, ever deeper" in its sophistication. "It is really an alternative genetic code, in which any gene family that is required to change a cell phenotype is enriched with specific codons," Dedon says. And he believes this is not an isolated case. "The researchers have also seen this phenomenon in other species ... and they are now studying it in humans."

Interested in other recent papers with design implications? Check these out:

Boris Zinshteyn and Rachel Green, writing for Science, think about "When Stop Makes Sense." They investigate why, contra the "standard" genetic code, "stop codons" sometimes specify amino acids. "The answers to this puzzle," they say, "may provide insights into translation termination and gene regulation in all eukaryotes."


Sandra Wolin, writing in the Proceedings of the National Academy of Sciences, investigates RNA modification enzymes that act as chaperones, helping tRNAs fold into the proper shape. "Because nucleotide modifications can also stabilize RNA structure and influence folding pathways," she says, "it will be both exciting and challenging to tease out the relative contributions of each function and the ways in which the two roles intersect and reinforce each other."