Darwinism Vs.the real world XXXIV

The Kidney's Irreducibly Complex Systems
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.

If a unicellular organism is like a microscopic island that can get what it needs and get rid of what it doesn't need through its surrounding water, the body, consisting of trillions of cells, is like a huge land mass that must move what it needs and doesn't need in and out of its interior so it can survive. The cells of the body need the right amount of oxygen and carbon dioxide to work right, so the lungs, at the direction of the respiratory center in the brain, take care of that.

They also need to have the right amount of water, sugar, salt, and other nutrients, which is taken care of by the gastrointestinal system, at the direction of the nervous system. And to transport what it needs into and out of its continental mass of cells, the body uses the cardiovascular system to move blood containing these chemicals to where they need to go so they can be on- or off-loaded.

Evolutionary biologists are good at imagining how the molecular structures for life may have come about, as long as they don't have to reckon with the objective standards those structures must meet to keep the cells and the body alive. To survive within the laws of nature, the cell must be able to control its volume and chemical content. So too, for the body to survive within the laws of nature, it must also control its volume and chemical content.

Stephen Meyer has described the complexity of the cell, the numerous systems within it, and what they must do for it to work properly. But each cell, no matter where it is located, is blind to the overall needs of the body. We have seen this in how the water content and blood levels of sodium, potassium, calcium, and nitrogen (protein) affect organ function and body survival. The common pathway the body uses to control all of these chemical parameters leads through the kidney.

The functioning unit in the kidney is the nephron, and there are about one million per kidney. The nephron filters fluid out of the blood by squeezing it through a specialized capillary system called the glomerulus. The kidneys filter about 7.5 liters of fluid, with its chemical content, out of circulation per hour. This fluid enters tubules, which wind their way through the tissue of the kidney on its way to becoming urine. As the fluid moves along the cells lining, the tubules reabsorb or secrete different chemicals to the degree that is necessary for body survival.

The body is always taking in different amounts of various chemicals through the gastrointestinal system, while simultaneously losing them through metabolism. Therefore, the ongoing chemical needs of the body are always in flux and the kidneys must constantly adjust to these changes by changing how much of a given chemical they keep or release from the body through the urine. We will look at the five vital chemicals mentioned above, water, sodium, potassium, calcium, and nitrogen, and explain how the body, through the kidneys, adjusts them to stay alive.

Evolutionary biologists may be good at describing how kidneys look and imagining how they evolved, but they never seem to mention how they work or what they would have had to do to keep the transitional organisms they belonged to alive.

Water is vital for life and is the commonest molecule in the body, making up sixty percent of its weight. Two-thirds of the body's water is inside the cells and one third is outside, either between the cells or inside the blood. If the body loses one-quarter of its water (10 liters), it dies. Since the kidneys filter 7.5 liters of fluid per hour this means that if they didn't take back any of it, the body would die in about ninety minutes.

Water can move freely in and out of the cell, so cell volume reflects the body's water content. In general, if the body's water content is below normal, then the volume of its cells will be below normal as well. The hypothalamus contains shrink-sensitive cells that can detect this drop in cell volume. These osmoreceptors react to worsening cell shrinkage by making more Anti-Diuretic Hormone (ADH) be released. ADH travels in the blood and attaches to specific receptors on certain tubules within the kidneys and tells them to bring more water back into the body from the urine in production. By using osmoreceptors in the brain, ADH, and its specific receptors on certain kidney tubules, the body is able to take of control of its water content.

Sodium is vital for life and dissolves in the body's water as an Na+ ion. The fluid outside the cells contains about ninety percent of the body's total sodium and is ten times more concentrated than the fluid inside the cells. Since water generally follows Na+ ions wherever they go in the body, this means that the relatively high concentration of sodium in the fluid outside the cells is responsible for not only its water content but also the blood volume. Much like water, if the body loses about one-quarter of its sodium, it dies. The amount of sodium in the blood is so high that the 7.5 liters of fluid the kidneys filter out per hour contains about one-half of the body's total sodium. If the kidneys didn't take back any of this filtered sodium, the body would die in about a half hour.

Since blood volume is dependent on water content and water content is dependent on sodium content, this means that the wall motion that takes place as blood flows into a blood vessel or chamber is a reflection of the body's sodium content. One set of sensors, called mechanoreceptors, detect this wall motion within the kidneys, where blood enters to be filtered, and another is in the walls of the atria. The sensory cells in the kidneys release a hormone, called renin. The amount of renin released is inversely related to how much wall motion the sensors detect. The more the walls stretch, indicating more blood volume, the less renin is sent out, and the less the walls stretch, indicating less volume, the more renin is sent out. In contrast, the atrial cells send out a hormone, called Atrial Natriuretic Peptide (ANP), in an amount that is directly related to how much wall motion they detect. The more the walls stretch, indicating more blood volume, the more ANP is sent out, and vice versa.

Renin results in the formation of a hormone called angiotensin II which binds to specific receptors in the adrenal glands and tells them to release another hormone called aldosterone. Aldosterone travels to the kidneys and attaches to specific receptors on the cells lining some of its tubules. This tells them to bring more sodium back into the body. So, the less blood volume, the more renin, resulting in more angiotensin II and aldosterone, and more sodium the kidneys reabsorb. In contrast, the more blood volume, the more ANP attaches to specific receptorson the same tubules in the kidneys and tells them to release more sodium. In other words, the effects of renin and ANP counterbalance each other. By using mechanoreceptors in the kidneys and atria, renin and ANP and specific aldosterone and ANP receptors on certain kidney tubules, the body is able to take of control of its sodium content.

Potassium is also vital for life and dissolves in the body's water as a K+ ion. The fluid inside the cells contains about ninety-eight percent of the body's total potassium and is over thirty times more concentrated than the fluid outside the cells. The relatively low K+ ion level in the fluid outside the cells must be maintained within a very narrow range to make sure the difference between the electrical charge inside and outside the cell allows for proper heart, nerve, and muscle function. The relative amount of potassium in the blood is a lot lower than it is for sodium, and if the kidneys did not bring any of it back from the 7.5 liters of fluid it filters per hour, the body would die in about a day.

The body uses sensors in specialized cells within the adrenal glands to detect the ratio between the K+ and Na+ ion concentration in the blood. If the ratio rises, due to an increase in K+ ion concentration or a decrease in Na+ ion concentration, these cells send out more aldosterone. Conversely, if the ratio drops, due to a decrease in K+ ion concentration or an increase in Na+ ion concentration, it sends out less aldosterone.

Aldosterone travels in the blood and attaches to specific receptors on the cells lining certain tubules in the kidneys and tells them to release K+ ions out through the urine and bring Na+ ions back in. More aldosterone, due to an increase in the ratio between K+ ions and Na+ ions, makes more K+ ions leave the body and more Na+ ions come back in. Less aldosterone, due to a decrease in this ratio, makes less K+ ions leave the body and less Na+ ions come back in. By using receptors that detect the ratio between K+ and Na+ ions in the adrenals and aldosterone and its specific receptor on certain tubules in the kidneys, the body is able to take control of its potassium content.

Calcium is vital for life and the bones of the body house over ninety-nine percent of its content. However, the remaining one percent is just as important for survival. Calcium dissolves in the body's water as Ca++ ions and its concentration in the blood is about ten thousand times more than within the cell. Besides creating the skeleton, bone also acts as a reservoir for the calcium needs of the body, which include heart, nervous, glandular, muscle function, and clotting. The total content of calcium is over one thousand milligrams and if the kidneys did not bring back any of it from the 7.5 liters of fluid that it filters per hour, the body would lose its entire supply in about two months.

The cells of the four parathyroid glands have sensors that can detect the calcium level in the blood. In response to a drop in serum calcium, they release more parathormone (PTH). PTH travels in the blood and not only makes the bone release more Ca++ ions into the circulation but tells the kidneys to activate Vitamin D so the gastrointestinal tract can absorb more calcium. It also attaches to specific receptors within the tubules and tells them to bring more calcium back into the body. By using calcium sensors, PTH, and its specific receptors in the kidneys, the body is able to take control of its calcium content.


Nitrogen is mainly present in the amino acids that make up the proteins of the body. Protein metabolism produces a highly toxic nitrogen-containing molecule called ammonia, which the liver converts into less toxic urea to be released from the body through the kidneys. The amount of fluid filtered by the glomeruli of the kidneys is called the Glomerular Filtration Rate (GFR) and is normally about 125 mL/min (7.5 liters/hr). The body's ability to keep its blood level of nitrogen-containing substances under control is directly related to its kidney function.

Especially in people with long-standing hypertension and diabetes, worsening kidney function causes the level of urea and other nitrogen-containing substances to rise. In fact, when the GFR is less than ten percent of normal, severe weakness, nausea, and confusion are common symptoms. In addition, there is often retention of sodium and water. This results in fluid build-up in the lungs, which in turn can cause shortness of breath and high levels of potassium, both of which can lead to cardiopulmonary arrest. It is at this time that a person may be considered for dialysis, which artificially cleans the blood of urea and other nitrogen-containing substances and stabilizes its water, sodium, and potassium levels.

The kidney may not be as sophisticated as the brain or the liver, but it definitely has a lot of roles to play when it comes to human life. Each of the control systems mentioned above is irreducibly complex in that all of the parts must be present for it to do its job. And to get the job done right so the body can survive within the laws of nature requires a natural survival capacity -- an inherent knowledge of what is required.

The word intelligence comes from the Latin words inter and lego which means to choose between, to choose one outcome from all possible outcomes. Most people would look at the complicated structure of the kidney and what it takes for the body to control its water content and blood levels of sodium, potassium, calcium, and nitrogen, and conclude that an intelligent agent, a mind, was at work here.


Funny thing about intelligence though; you must have it in order to detect it. One hopes, in the near future, students will learn the truth about how life really works, and not just how it looks, and with this knowledge see the inadequacy of neo-Darwinism as an explanation for biological origins.

universal common ancestry in the hot seat VII

The Placenta Problem: How Common Descent Fails
Ann Gauger 

Editor's note: For previous replies by Dr. Gauger to Dr. Torley in this series, see here, here, and here.

Philosopher Vincent Torley (and Washington University's Professor Josh Swamidass) have been trying to persuade me that common descent is the only rational view to affirm, the only intellectually consistent and respectable choice. What they don't seem to realize is that I see the evidence for common descent. I know its strength. The reason I doubt common descent is not because of the ways that it succeeds, but the ways that it fails.

Writing at Uncommon Descent, Torley poses the following challenge in "Consider the Opossum," thinking to trap me into either accepting the argument for common descent as the only evidence-based conclusion, or denying the evidence in order to escape the logic:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?

Do I accept Torley's logic? Yes. Do I think common descent is explanatory (A) and design is not (B)? No. Do I think that common descent is predictive (A) and design not (B)? No. The reason is that the syllogisms cut both ways. Design is both explanatory and predictive, particularly when dealing with pattern breaking observations in biology, where common descent doesn't work as an explanation. Thus the onus of proof is not on design alone, as Professor Swamidass thinks, but on common descent as well.

Let me show you. According to the theory of common descent, all true mammals are supposed to have descended from a common ancestor with a placenta. This is a trait common to all mammals. However, it has been a puzzle for some time that placentas differ in the form they take among different mammalian clades.

In the year 2000, French researcher Thierry Heidmann and coworkers found that genes derived from endogenous retroviruses (ERVs) appear to have been coopted to perform an essential role in placental formation. These genes, which resemble the ERV envelope gene env, make a protein that originally promoted fusion of the virus with its host cell's membrane, but now acts to promote fusion of membranes between the embryo and the lining of the uterus. These "repurposed" proteins are called syncytins. They are essential for placental formation, yet are of independent origin in different kinds of mammals -- primates have one kind, mice another, rabbits, cows, and carnivores yet others. They are clade-specific. In fact, in 2015 a functional syncytin was found in several marsupials, extending the presence and essential function of the protein to all placental mammals examined. All syncytins are lineage-specific, meaning that each mammalian clade has its own syncytin, with a unique sequence and location in the genome. They must have inserted themselves (or been placed there) after the separation of the mammals into different clades! This means there must have been multiple independent acquisitions of these syncytins to participate in an essential process that is common to all mammals. Why should there be unique syncytins in each clade?

What we have to explain is the unique and independent group-specific cooption of syncytins for a function that is essential for placental development, a feature common to all mammalian groups. Six independent origins for the placenta! There is no evidence of a grand ancestral syncytin shared by all groups that was later replaced by other syncytins, so the common descent explanation of the placenta in mammals fails.

I repeat: distinct syncytins for cows, carnivores, rodents, primates, rabbits, and even tenrecs (a species thought to retain features of primitive mammals). We all recognize these clades based on their traits -- cows are different from carnivores, which are different from rodents, which are different from chimpanzees. Even nursery school children can tell the difference. And they are all thought to have descended from a common ancestor, the proto-mammal. Well, apparently, these well-defined clades of mammals make their placentas using analogous but distinct proteins. This perhaps explains why the placentas of each clade differ in their structures. But it flies in the face of the idea that all mammals are descended from a single kind of ancestor with a single kind of placenta.

I'll quote a review paper on syncytins. These are the people who discovered syncytins, and they have done great work. Yet they are forced into a corner by their own work and the idea of common descent. I have italicized the key features of syncytins that must be explained, and bolded the explanations offered:

... syncytins are 'new' genes encoding proteins derived from the envelope protein of endogenous retroviral elements that have been captured and domesticated on multiple occasions and independently in diverse mammalian species, through a process of convergent evolution. Knockout of syncytin genes in mice provided evidence for their absolute requirement for placenta development and embryo survival, via formation by cell-cell fusion of syncytial cell layers at the fetal-maternal interface. These genes of exogenous origin, acquired 'by chance' and yet still 'necessary' to carry out a basic function in placental mammals, may have been pivotal in the emergence of mammalian ancestors with a placenta from egg-laying animals via the capture of a founding retroviral env gene, subsequently replaced in the diverse mammalian lineages by new env-derived syncytin genes, each providing its host with a positive selective advantage.

Rather than postulating six independent, random capture events in placental development, they are now postulating at least one more, a founding syncytin leading to a primitive placenta, then the other syncytins to replace that one in each lineage. Each replacement must have had a clear selective advantage as time went on to make the replacement possible, and each must be the outcome of a random series of events. To say it again, the common descent prediction is that there must have been a founding syncytin in the first mammal with a placenta, or something else that functioned in syncytin's place, in order for the primitive placenta to arise and subsequently be passed to all mammalian clades. For which there is no evidence, and may never be.

Can common descent explain the unexpected observation of six independent origins for the placenta? No. Could it predict it? No.

Common design has an explanation, but not one that will be palatable to my interlocutors. The designer used the same idea six different times to produce the same outcome in six different "designs" (clades). That's another way of saying all these clades have the same outcome, the placenta, but achieved by independent uses of the same idea.

This can be stated as a general principle. Design predicts that we should find other examples where there are similar but independent ways of performing an essential function or of solving a common biological problem. The means may differ between groups, but the outcome is the same across groups. Or to put it another way, multiple independent paths converge on a common solution. There are many examples of this known already, at the molecular and organismal level. It's known in evolutionary terms as convergent evolution, but I'll call it convergent design.

Convergent design is to be expected under the design hypothesis because the designer is not constrained by an evolutionary tree. He can reuse ideas that work in one setting in a different place. In fact, he can mix and match his methods to get to any outcome he wants. I am thinking of echinoderms (sea stars and sea urchins) that look alike as adults but get there by very different developmental paths, or two very different animal groups that come up with similar molecular solutions to create a new function, echolocation.

Convergent design is clearly observable across biology but has no evolutionary mechanism. There are proposed reasons for it but no demonstration. I can hear in my head the arguments of evolutionary biologists: intrinsic constraints, canalization, living in similar environments or ecological niches, you have no demonstration either...

So then maybe the answer comes down to probability.

In considering these alternative explanations, ask yourself, how likely is it that a retrovirus would infect, invade the germ line (the cells that make eggs and sperm), then insert itself at random in locations in the genome that are expressed in the developing embryo or primitive uterus at the proper time, then promote fusion of membranes to permit the formation of a placenta, with all this happening at least six separate times in the six lineages tested so far? We should also make clear, expressing a syncytin by itself is unlikely to be enough to make a placenta, which is a complex organ requiring interactions between mother and embryo, and the ability to exchange nutrients and oxygen.

Let me close by posing Torley's questions to him, concerning syncytins:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?


Evidence for and against common descent. It's not nearly so open and shut a case as some believe, unless there is an a priori commitment to materialistic explanations.

Electric bacteria for design.

By Jasmin Fox-Skelly

 

Some microbes have developed the ultimate stripped-down diet. They do not bother with food or oxygen. All they need to survive is pure electrical energy.
They often live in muddy seabeds or along the banks of rivers. Finding them is easy: biologists can coax them out of hiding by sticking an electrode into the sediment. The bacteria nearest to the electrode will even grow biological equivalents of electrical wires out of their bodies, so that other microbes further away can hook up to the electricity source. It is effectively a living power grid.
What's more, it appears that we can all benefit from this microscopic grid. Among other things, it might provide an effective way to deal with toxic waste and other forms of environmental pollution.
 

Electricity-eating microbes might sound like something straight out of a science fiction novel. In fact their behaviour is not quite as exotic as it might first appear.

                
All lifeforms on Earth – even humans – must harness energy if they are to remain alive. This energy comes in the form of electrons, the same tiny negatively-charged particles that create a current when they zip around electrical wires in a circuit.
We humans, along with most other organisms on this planet, get our electrons from sugars in the food that we eat. In a series of chemical reactions that happen inside our cells, the electrons are released, and ultimately flow into oxygen – the same oxygen which we have just breathed in through our lungs. That flow of electrons is what powers our bodies.
This means that the challenge for all creatures is the same. Whether the organism is a single-celled bacterium or a blue whale, it has to find a source of electrons, and a place to dump them to complete the circuit.
But what happens when there is no oxygen to dump your electrons onto?
Many organisms live in low-oxygen environments and so must use alternative electron dumps. For some, that means "breathing" metals instead of oxygen.
In 1987 Derek Lovley and his lab at the University of Massachusetts stumbled across the first of these bacteria on the banks of the Potomac River near Washington DC.
The microbes, called Geobacter metallireducens, were getting their electrons from organic compounds, and passing them onto iron oxides. In other words they were eating waste – including ethanol – and effectively "breathing" iron instead of oxygen.
Of course, this is not breathing as we would recognise it. For one thing, bacteria do not have lungs. Instead, the bacteria pass their electrons to metal oxides that lie outside the cell.
They do this through special hair-like wires that protrude from the cell's surface. These tiny wires act in much in the same way that copper wire does when it conducts electricity. They have been dubbed "microbial nanowires".

 

Geobacter bacteria are able to survive on energy sources entirely unavailable to most lifeforms.

They are even able to effectively "eat" pollution. They will convert the organic compounds in oil spills into carbon dioxide, or turn soluble radioactive metals like plutonium and uranium into insoluble forms that are less likely to contaminate groundwater – and they will generate electricity in the process.
In fact, some even see a future in which microbial fuel cells power devices like smartphones using seaweed, urine or sewage as their only food source: the ultimate in recycled energy.
In 1988, a year after Lovley's discovery, microbiologist Kenneth Nealson of the University of Southern California found a second electron-excreting bacterium.He was investigating a strange phenomenon in Oneida Lake in New York State. The lake contains manganese, which reacts with the oxygen in the air to form manganese oxide.
However, Nealson did not find as much manganese oxide as he was expecting. Some of it was missing. The culprit, it turns out, was Shewanella oneidensis.
This bacterium breathes oxygen when it is available, but in the muddy banks of the lake where oxygen is scarce it instead passes its electrons directly onto manganese oxide, producing a stream of electricity. It can do the same thing with other metals like iron.
Just how the bacteria were doing this was a mystery until very recently.
Under the microscope, Shewanella appear to have long thin hair-like extensions of their outer membrane. These filaments were at first thought to conduct electrons along them like a copper cable, much like Geobacter. However, it turns out that the long filaments are only conductive when dried out in a lab.
Instead Shewanella appear to shuttle electrons out of their cells using transport molecules called flavins and "stepping stone" proteins embedded in the outer membrane called cytochromes.

So far we have only talked about bacteria that produce electricity when they breathe. But these electron-excreting microbes are not the only ones that researchers have found.
While most organisms get their electron fix from carbohydrates, some bacteria can harvest electrons in their purest form. They can effectively "eat" electrons from minerals and rocks. In a way, they are getting their electrical energy straight from the socket.
Annette Rowe, a graduate student of Nealson, has found six new bacterial species on the ocean floor that can live off electricity alone. All are very different to one another, and none of them is anything like Shewanella or Geobacter.Rowe took samples of sediment from the seabed in Catalina Harbour off the Californian coast, brought them back to the lab and inserted electrodes into them. She then varied the voltage of the electrodes to see whether the bacteria in the sediment would "eat" electrons from the electrode, or discharge electrons on to it.
She found that, when no other food source was available, the bacteria would happily take electrons directly from the electrodes. In their natural habitat, the bacteria likely take their electrons directly from iron and sulphur in the seabed.
Examples of electron-eating bacteria found by Rowe include Halomonas, Idiomarina, Marinobacter, and Pseudomonas of the Gammaproteobacteria, and Thalassospira and Thioclava from the Alphaproteobacteria.

Many more electron-loving bacteria have now been found. In fact all you have to do is stick an electrode in the ground and pass electrons down it, and soon the electrode will be coated with feeding bacteria. Experiments show that these bacteria essentially eat or excrete electricity.
The holy grail of electricity-loving bacteria would be having a species that could both eat and excrete electrons, and so could exist entirely on electricity alone without any other energy source
According to Lovley, that grail has already been discovered. Some species of Geobacter, he says, can both directly transfer electrons to electrodes and also directly accept electrons from them.
In 2015, we learned that electron-eating and electron-excreting microbes can actually team up and pass electrons between each other, wiring themselves into a common electrical grid.
At the bottom of the ocean lie vast reserves of methane, released by microbes feeding on the remains of dead algae and animals as they sink down from the surface. If the methane escaped into the atmosphere the gas would exacerbate global warming, but luckily a consortium of microbes seem to keep it in check.
Different species of bacteria and archaea – ancient single-celled microbes similar to bacteria in many ways – team up to degrade the methane before it can get the surface.Gunter Wegener from the Max Planck Institute for Marine Microbiology in Bremen wondered how the process worked. He collected samples of the microbes
, which live at temperatures of 60C on the ocean floor, and put them under a scanning electron microscope.
The microscope revealed thin wire-like structures protruding from the bacterial cells. Although only a few nanometres wide, the wires were several micrometres long, which is much longer than the cells themselves.
It seems that the bacteria use these nanowires to hook up with the archaea.
The archaea feed on electrons from methane, oxidising the gas to generate carbonate. They then pass the electrons on to their partner bacteria along the nanowires, which act like power cables. Finally the bacteria deposit the electrons onto sulphate, producing energy that the cell can use in the process.
The researchers have now identified the genes that coded for the production of these nanowires. It is only when methane is added as an energy source that the genes are switched on and the nanowires form between bacteria and archaea.
This ancient form of electronic cooperation between the two types of microbe may have evolved billions of years ago, when the Earth's atmosphere was oxygen-free.
"One of the most interesting developments in the area of microbes eating and breathing electrons is the concept of direct interspecies electron transfer," says Lovley. "This is when microorganisms wire themselves together to share electrons, permitting them to carry out reactions that neither would be able to carry out individually."
Lovley and his lab have also discovered other communities of bacteria that are able to pass electrons directly to each other.

In the lab, Lovley showed that two species of Geobacter – G. metallireducens and G. sulfurreducens – survive by forming a conductive network of nanowires, through which electrons can be shuttled. G. metallireducens takes electrons from ethanol and then passed them directly to G. sulfurreducens using this electrical grid.                     
Cable bacteria live on sea floors and river beds where there is little oxygen. Without oxygen, they have nowhere to donate their electrons.
In a more extreme version of this process, some bacteria can link up to form long "cables".To cope with this the cable bacteria, which belong to the family Desulfobulbaceae, form chains, one cell in diameter, extending thousands of cells and distances of several centimetres – a huge distance for a bacterium only 3 or 4 micrometres long – until they finally reach a habitat with oxygen.
The first bacterium in the chain, which lives in a low-oxygen habitat, takes electrons from sulphide and passes them onto the next bacterium. This bacterium then passes the electrons on to the next cell, and so on until the final bacterium in the chain can finally pass the electrons onto oxygen.
This means that bacteria living in seabed mud where no oxygen penetrates can access oxygen dissolved in the seawater above simply by "holding hands" with other bacteria. Running along the chains of bacteria are ridges that connect the cells together, possibly allowing electrons to flow between them.
Other bacteria rely on rocks and minerals to do all the hard work for them when it comes to eating and dumping electronsBacteria have been seen to attach themselves to conductive materials, such as the iron-rich mineral magnetite, in order to pass electrons between each other through the magnetite. It is thought that chains of magnetite can form, bridging the gap between the electron-donating and the electron-accepting bacteria.
The environments these bacteria occupy may seem exotic, but electron-eating and -breathing microbes can also be found in more familiar settings.
For instance, they have been discovered in the digesters that convert brewery wastes to methane. Inside one such brewery, Geobacter metallireducens was directly transferring electrons to another bacterium, Methanosaeta harundinacea, which was then passing the electrons on to carbon dioxide.
It is even possible that microorganisms in the human gut electrically interact with cells in the gut lining.Just why have the bacteria evolved this neat trick?Being able to survive on electrons alone is a smart way of coping when resources and food are scarce, as can be the case at the bottom of the ocean or deep underground. Here, there is not quite enough energy for an organism to grow, or compete, but there is enough for it to exist – just about.
If life exists on other worlds, such as Mars or Jupiter's moon Europa, it will probably be in similarly sparse environments. Astrobiologists searching for evidence of extraterrestrial life might be particularly interested in electricity-eating and electricity-excreting microbes.
Whether or not such alien life is ever found, electricity-eating and -excreting bacteria here on Earth are still a significant discovery. All you need to do is provide them with an electrode onto which they can "breathe" electrons, and they have the potential to steal electrons from toxic waste, oil spills and nuclear waste, cleaning up our waste and generating electricity in the process.
Not bad for simple single-celled organisms.BBC Earth

Has nutritition science let cholesterol out of the dog house?

High cholesterol 'does not cause heart disease' new research finds, so treating with statins a 'waste of time'

Henry Bodkin

 

Cholesterol does not cause heart disease in the elderly and trying to reduce it with drugs like statins is a waste of time, an international group of experts has claimed.

A review of research involving nearly 70,000 people found there was no link between what has traditionally been considered “bad” cholesterol and the premature deaths of over 60-year-olds from cardiovascular disease.
Published in the BMJ Open journal, the new study found that 92 percent of people with a high cholesterol level lived longer.The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.
The results have prompted immediate scepticism from other academics, however, who questioned the paper’s balance.
High cholesterol is commonly caused by an unhealthy diet, and eating high levels of saturated fat in particular, as well as smoking.

It is carried in the blood attached to proteins called lipoproteins and has been traditionally linked to cardiovascular diseases such as coronary heart disease, stroke, peripheral arterial disease and aortic disease.
The authors have called for a re-evaluation of the guidelines for the prevention of cardiovascular disease and atherosclerosis, a hardening and narrowing of the arteries, because “the benefits from statin treatment have been exaggerated”.
The results have prompted immediate scepticism from other academics, however, who questioned the paper’s balance.
High cholesterol is commonly caused by an unhealthy diet, and eating high levels of saturated fat in particular, as well as smoking.

It is carried in the blood attached to proteins called lipoproteins and has been traditionally linked to cardiovascular diseases such as coronary heart disease, stroke, peripheral arterial disease and aortic disease.
Co-author of the study Dr Malcolm Kendrick, an intermediate care GP, acknowledged the findings would cause controversy but defended them as “robust” and “thoroughly reviewed”.
“What we found in our detailed systematic review was that older people with high LDL (low-density lipoprotein) levels, the so-called “bad” cholesterol, lived longer and had less heart disease.”
Vascular and endovascular surgery expert Professor Sherif Sultan from the University of Ireland, who also worked on the study, said cholesterol is one of the “most vital” molecules in the body and prevents infection, cancer, muscle pain and other conditions in elderly people.
“Lowering cholesterol with medications for primary cardiovascular prevention in those aged over 60 is a total waste of time and resources, whereas altering your lifestyle is the single most important way to achieve a good quality of life,” he said.
Lead author Dr Uffe Ravnskov, a former associate professor of renal medicine at Lund University in Sweden, said there was “no reason” to lower high-LDL-cholesterol.
But Professor Colin Baigent, an epidemiologist at Oxford University, said the new study had “serious weaknesses and, as a consequence, has reached completely the wrong conclusion”.
Another sceptic, consultant cardiologist Dr Tim Chico, said he would be more convinced by randomised study where some patients have their cholesterol lowered using a drug, such as a stain, while others receive a placebo.
He said: “There have been several studies that tested whether higher cholesterol increases the risk of heart disease by lowering cholesterol in elderly patients and observing whether this reduces their risk of heart disease.
“These have shown that lowering cholesterol using a drug does reduce the risk of heart disease in the elderly, and I find this more compelling than the data in the current study.”
The British Heart Foundation also questioned the new research, pointing out that the link between high LDL cholesterol levels and death in the elderly is harder to detect because, as people get older, more factors determine overall health.
“There is nothing in the current paper to support the author’s suggestions that the studies they reviewed cast doubt on the idea that LDL Cholesterol is a major cause of heart disease or that guidelines on LDL reduction in the elderly need re-valuating,” a spokesman said.

On Learning to disagree without being disagreeable.

In the Evolution Debate, Not Listening Happens in One Direction, Not Two

David Klinghoffer

 

An eloquent post from Terry Teachout, the Wall Street Journal theater critic, might as well be a commentary on Doug Axe's observations this morning ("Public Opinion Is the Ultimate Peer Review"). Teachout (whom I had the privilege of working with at National Review long ago) laments the divorce between cultures symbolized by Red and Blue states. He recalls a time before half the country was so fiercely committed to regarding itself as Enlightened while dismissing the other half as Benighted, hopelessly so, or worse. Anyway that's how I would characterize it.

Many, perhaps most Americans of my generation (I was born in 1956) lived in places whose residents included people who read, liked, listened to, and thought all sorts of things, and who voted differently, even unpredictably, on election day. As a result, we learned to get along with one another, and sometimes we even learned from one another. At the very least, we learned -- up to a point -- to be reasonably tolerant of each other's crotchets.
More and more, though, we don't live together and we don't listen to each other. As a result, the modest but real tolerance of the past is increasingly giving way to attempts at outright repression, or (more often, at least for now) [a] sniggeringly dismissive attitude...

He refers to a Washington Post story deploring a prominent person's well-known appetite for fast food:

This "news" story is, in its minor but nonetheless revealing way, illustrative of the condition that now increasingly prevails in American society, which is that those who disagree no longer have anything to say to each other. Fact-based argument has been replaced by reflexive contempt. Nor should this be in any way surprising. In a totally polarized political environment, persuasion is no longer possible: we believe what we believe, and nothing matters but class and power. We are well on the way to becoming a land of jerking knees.
Never before have I felt so strongly that Americans are talking past instead of to one another.

The dividing line extends from food to faith, from politics to science. Oh, most certainly it includes science. Doug Axe, in his post, responds to a Caltech commencement address by Atul Gawande, the surgeon and New Yorker staff writer. To someone like Gawande, these sentences by Dr. Axe are a counterintuitive shot across the bow: "People aren't stupid. Science is a public enterprise, and public acceptance has always been its most significant seal of approval."
The theme of Axe's forthcoming book, Undeniable -- How Biology Confirms Our Intuition That Life Is Designed, is the validity of ordinary intuition as a tool in judging science. That idea is anathema to Americans on the other side of the worldview divide that Terry Teachout describes. For them, people -- "mere people," as Axe puts it ironically -- are indeed stupid.
In fact the deplorable stupidity of half the population is a pillar of faith for the Enlightened. The Benighted show their benightedness by trying to have a conversation with the Enlightened, not realizing that their "conversation" partner isn't even listening. For the Enlightened, it often seems, "nothing matters but class and power."
We see this in the discussion, such as it is, of intelligent design versus unguided Darwinian evolution. In this debate about an ultimate question, the mystery of human and biological origins, for one side "Fact-based argument has been replaced by reflexive contempt."
I would only offer this addendum to Terry's observations, from our experience in the context of the evolution controversy. Scientists open to evidence for design offer abundant "fact-based arguments," only to be greeted by a "sniggeringly dismissive attitude." They are not talking past us. By that I mean, design advocates genuinely register and understand, even if they reject, arguments from the other side. The "reflexive contempt" does not operate equally in both directions.

universal common ancestry in the hot seat. VI

The Opossum's Tale: The Torley Saga, Cont.

Ann Gauger

Background: There has been an on-going discussion between Dr. Vincent Torley, a philosopher, and myself on the subject of pseudogenes, synteny, and common descent. These are technical terms and the arguments may seem abstruse, but the topic is important because of its implications. Those who hold to common ancestry accept that, at the very least, each major group of animals is descended from a common ancestor, and some hold that the common ancestry goes all the way back to the first cell. The question is whether we share common ancestry with chickens and opossums, and by implication, with chimpanzees. What we have been discussing for all these posts is this: How strong is the evidence that we have the remnants of an egg yolk protein, vitellogenin, in our genome? Do we come from an egg-laying ancestor?

 

In a post at Uncommon Descent, "Consider the Opossum," Vincent Torley took me to task for a number of reasons, but chief among them was that I ignored the evidence for synteny between the opossum and chicken vitellogenin (VTG) genes. (Synteny refers to the alignment of sequences in order and identity between stretches of DNA from two species.) This evidence came from the Brawand paper. I had been meaning to address the opossum data, but events (Torley's post) got in the way. So rather than debate, I'll make it simple. The evidence for synteny in opossums and chickens is good. Surprised? I had already planned on saying this before the latest information about human alignments came up.
Now, is this synteny between chicken, opossum, and human evidence for common descent? Could be. Remember, some intelligent design proponents accept common descent based on evidence like this. They may think that this particular scenario happened by purely naturalistic processes. But they also acknowledge that at least some processes could not happen in an unguided fashion. These people may accept common descent but also affirm the necessity and detectability of design. Anyone who affirms the detectability of design is by definition a friend of intelligent design, even if not publicly so.
Others think for various reasons that a designer guided the process, but in such a way that the design is undetectable. They think that the designer has hidden the evidence of design, and may even go so far as to question why he would do such a thing, since everything looks like a purely natural process. This viewpoint might as well be full-blown materialistic neo-Darwinism.
Then there are people who reject common descent to one degree or another. They may proffer different explanations for sequence similarity. Synteny, for example, can be the result of a need for a particular chromosomal organization or structure. Thus, gene expression regulatory blocks can lead to the appearance of conserved synteny. It is also possible that the apparent remains of vitellogenin genes may be being used for other purposes. The vitellogenin protein itself is multi-purpose -- it and its derived proteins are involved in the innate immune response in fish. Has anyone looked into this in higher vertebrates? Probably not. There is evidence of long non-coding RNA (lncRNAs) in the region of similarity, plus other possibly functional elements. In response to a comment from Professor Josh Swamidass, I note that lncRNAs can act in cis (on their own region, rather than a distant location) making their location on the chromosome important. It is not therefore beyond the realm of possibility that any similarities we see among opossums, chickens, and humans are there for functional reasons. The signal we see could be the result of essential sequence-dependent function in the region, with different sequences shared between species. I agree with Swamidass that all these proposals are possibilities only and would need to be demonstrated as real and functional.
But even if it's the case that this region shares the remnants of egg yolk genes and ancient synteny, common descent from an egg-laying ancestor is not the only possible reason there could be old genetic code lying around. It depends on your model for how the designer acts. Consider an analogy with how human programmers work. A programmer I know says that coders routinely use old code in new programs. It's hard to write new code, but easy to use code that has already been designed, and to plug it into the new program. It takes time to get rid of the unused code that comes along for the ride so to speak. It's easier to just leave it alone. (My pardon to my friend if I did not express properly what he said.) In fact, in our case, the designer might have plans for that unused code further down the road. I should also say, there is no intent by the programmer to deceive anyone who later comes along to deconstruct the code as to its origin. It looks like ancient code shared between organisms, but it's not due to common descent. It's simply the way the designer works.
In all these cases, it could be that once the old code has been created it is subject to the same process of neutral or near-neutral evolution as for standard neo-Darwinian evolution. Mutations happen all the time -- most are largely neutral, with little or no effect, so they tend to accumulate. Unless there is some reason to maintain a particular sequence without change (because it has a necessary function), its sequence will tend to drift and degrade, like the vitellogenin genes in opossum, dog, and human are proposed to have done. This will tend to mimic the signal of synteny and pseudogenization in the vitellogenin gene.
This analogy will probably irritate the materialists among us. So let me propose another possibility. The signal we see could result if there is essential sequence-dependent function in the region, with different sequences shared between species.
I acknowledge that common descent is an appealing explanation for this synteny. I know the strength of the common descent argument. I am also aware of its weaknesses, which I will address in my next post. The evidence for common descent is mixed, as we shall see. The reason I doubt common descent is not because of the ways that it succeeds, but rather because of the ways that it fails. And I am still inclined to accept the design explanation because I expect to see function rather than junk in our genomes.
Finally, let me give an answer to one very specific question posed by Vincent Torley, as put to him by Josh Swamidass, as an example of the difference in approach to the data.

Why is the genetic signal stronger in the opossum (a marsupial mammal) than in human beings, who are placentals? The common descent model has an answer to this question: the various lines of mammals made the transition away from eggs at different times, so they inactivated their yolk genes at different times. How does the design model answer this question?

First of all, marsupials are placentals also, but of a different kind. Second, my response to the question is that I hope Torley and Swamidass are not making the mistake of thinking of marsupials as partway up the evolutionary ladder, therefore closer to their egg-laying roots than are eutherian mammals. If common descent is true, the theory says that eutherian mammals and marsupials share a common egg-laying ancestor that diverged from the chicken lineage a long time ago, so present day marsupials and mammals are equidistant from chickens in evolutionary time. There can be no a priori prediction about which should have a vitellogenin pseudogene with closer resemblance to an egg-laying chicken's gene, without prior, independent knowledge of when egg laying was lost in either lineage.
The Brawand paper is the only paper I could find that assigns a date to when egg yolk proteins were lost in each lineage. It was the reason for their study. They based their estimate on the genetic signal of the degree of degeneracy between the sequences. It is faulty reasoning to say the reason for the greater degeneracy is because of earlier loss of egg-laying, when the reason for the dating of the egg-laying loss is based on said degeneracy.
Common descent cannot explain why egg-laying genes were lost earlier in one lineage than another, since it could have happened either way. Or not at all. See above.
From a design perspective, I would say the reason for the difference in apparent inactivation times is because each animal has a different design. How the DNA is used may differ.
So now on to the next and final explosive post. Stay tuned. It's my riposte to the "explain and predict" test for common descent versus common design offered by Torley. And I am done with talking about egg yolk proteins.
Editor's note: For previous replies by Dr. Gauger to Dr. Torley, see here and here.
 

 

Trying to fool all of the people all of the time?

Public Opinion Is the Ultimate Peer Review

Douglas Axe

 

In his recent Caltech commencement address, surgeon and New Yorker staff writer Atul Gawande offered advice on how to rebuild the public's confidence in the scientific community. He ends with the right idea, but only after showing that even he needs to take that idea more seriously.

What does truth-seeking look like? Gawande concludes by saying that "it is the effort not of a single person but of a group of people -- the bigger the better -- pursuing ideas with curiosity, inquisitiveness, openness, and discipline." I agree... more wholeheartedly now than I would have back in 1990, when I was wearing the Caltech mortarboard.

Back then I considered scientists to be a breed apart -- a privileged class of gifted people trained to think in a different way. That this different way of thinking was better than other ways of thinking didn't have to be proclaimed aloud. We all knew it with quiet confidence. Had Gawande been the commencement speaker in 1990, I would have interpreted his call for inclusivity and openness as a call for members of this elite community to conduct themselves in a way that would sustain our elevated status.

The "we" versus "they" stance that characterizes Gawande's speech would have resonated with me then, I think. When he said, "People are prone to resist scientific claims when they clash with intuitive beliefs," I would have understood the coded language. "People" here means mere people -- those who haven't been inducted into the superior scientific "way of being." So, what are we scientists to do when those unenlightened outsiders don't follow us? Using smaller words and speaking more slowly only goes so far, because "once an idea has got embedded and become widespread, it becomes very difficult to dig it out of people's brains -- especially when they do not trust scientific authorities."

Yes, indeed. People tend to be wary of that kind of brain surgery.

Maybe the better way to restore public confidence is to abandon the condescending mindset and embrace a much more radically inclusive view of science. Maybe the moms Gawande referred to -- the ones who jumped to the conclusion that vaccines were dangerous -- aren't all that different from professional scientists who jump to the conclusion that public dissent is dangerous. Gawande gave five handy tips for writing people off as pseudoscientists, but instead of alienating people by dismissing them in this way, what if we were to view public opinion as the ultimate form of peer review?

If the safety of well-studied vaccines and the danger of forgoing them are observable facts, perhaps we should trust public peer review to affirm this. Indeed, it already has. Gawande mentioned the tragic human cost of a drop in vaccination rates in the US from 1989 to 1991. Ten years after that drop, Gallop results showed that "parents with the most information, both positive and negative, are most likely to get their children vaccinated." And this public verdict has held. According to a recent Pew Research Center report: "A vast majority of Americans view childhood vaccines as safe."

People aren't stupid. Science is a public enterprise, and public acceptance has always been its most significant seal of approval. Professional scientists should embrace this by doing more free sharing of information and less complaining about public opinion.

Editor's note: Dr. Axe is Director of Biologic Institute and author of the forthcoming book Undeniable -- How Biology Confirms Our Intuition That Life Is Designed (HarperOne). Undeniable will be published on July 12, 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.

 

On life's machine code.

Is Genome Grammar Just a Figure of Speech?

Evolution News & Views 

Without controversy, everyone knows texts written by human beings are intelligently designed, unless they are ramblings from a maniac. Human language is characterized by syntax (rules of word order) and grammar (rules of spelling, part of speech, case, person, number, voice, tense, mood, etc.). But that's not enough. One can follow the rules and make up nonsense sentences, such as "Banana voices improve inspirational aardvark submarines." For effective communication, language must also make sense. That's semantics: the communication of meaningful ideas.

Does DNA meet these conditions? How proper is it to discuss the DNA code as a language? We should point out that software meets the requirements of language. It, too, has rules of syntax, grammar, and semantics, even though humans do not speak it in conversation. The sender and receiver do not have to be sentient beings; software can drive actions on spacecraft, for example. We must also expand the range of languages beyond the English of this paragraph to include all languages, past and present, used by humans, plus all forms of coded information (including Morse code, sign language, mathematics, and even the rope-knot language of the Incas). Rules can vary widely between languages, but they all have in common the purposeful communication of meaningful information, regardless of the substrate or carrier of the symbols used.

Analogies can enlighten, but they can also mislead. We in intelligent design circles are prone to assume the comparison between DNA and language, but we must beware of drawing the analogy too tightly, even though most scientists unhesitatingly speak of the "genetic code" and the "language of life." Dubious comparisons have been made between brains and computers, as Dr. Michael Egnor has pointed out. Sometimes the differences are more significant than the similarities.

With these caveats in mind, we can examine the analogy between language and genomics. In a Commentary article in the Proceedings of the National Academy of Sciences, Scott Barolo from University of Michigan Medical School refers several times to the grammar and syntax of DNA. He's not trying to prove genes are analogous to language; the comparison just comes naturally as he discusses the roles of enhancers in gene expression.

Every cell's genome contains two main classes of functional DNA. The best understood type of DNA sequence, which was also the first to be discovered, is that which encodesRNA and protein products via the near-universal "genetic code". A more mysterious but equally important class of functional DNA is cis-regulatory sequence, which does not have a physical product but, instead,encodes the conditions under which a particular RNA will be produced.Cis-regulatory DNA sequences are the primary (although not the only) determinant of gene expression: Not only the rate of RNA production but also the timing, spatial patterning, and environmental control of every gene's activity are largely controlled by these DNA sequences, which are usually in the general vicinity of the gene they regulate. These DNA segments (often called enhancers) have no enzymatic activity on their own, but act as scaffolds for large complexes of proteins and RNAs that directly control the activity of a gene's promoter, sometimes over distances of 1 million base pairs or more. Transcription factors (TFs), key protein regulators of gene expression, bind DNA in a sequence-specific manner, which means that the nature of the complex assembled at a given enhancer at a given timedepends on its DNA sequence (cisinformation), in conjunction with the set of TFs present and active in the cell at that time (trans information). The chromatin state of regulatory DNA is also a very important factor, but local chromatin states are alsospecified, indirectly, by DNAsequence, because most chromatin-modifying enzymes are recruited to the genome by sequence-specific factors. [Emphasis added.]

So far, Barolo has only compared DNA to codes where the specific sequence matters. Next, he adds references to grammar and syntax:

In part, the DNA sequence of an enhancer encodes a pattern of gene expression through the combinations of sequence-specific regulators that bind to it (and the non-DNA-binding factors they recruit, in turn). However, cis-regulatory DNA sequences do more than merely determine which combinations of TFs will be recruited to an enhancer. The linear arrangement of binding sites (sometimes called "grammar" or "syntax") can play an important role in controlling enhancer output, especially by setting thresholds for gene activation.

By putting "grammar" and "syntax" in quotes, Barolo is acknowledging similarity but not necessarily identity.

In texts, we don't see alphabet letters swooping down and binding onto existing words or paragraphs to give them more "expression" or regulate what parts are readable. That's one important difference. In software, however, routines can be switched on or off depending on environmental factors. Also, in routing, tags can be attached to packets of information that permit or block their transmission, or determine their destinations. Those tags are very sequence-specific. One wrong character can disrupt function.

Barolo turns his attention to another paper inPNAS by Farley et al., who "investigate how the binding affinity and the spatial arrangement of TF binding sites within enhancers interact toencode precise patterns of gene expression in developing embryos." The scientists are basically trying to learn a foreign language by watching what certain words or paragraphs do. If they see one sequence (a binding site) activated by an enhancer, they might be able to predict other binding sites. The "spatial arrangement" refers to placement of binding sites within the sequence, analogous to word order in text, or to start-stop codes for switches in software routines. The analogy may not be exact, he suggests. We just don't know enough yet.

Taking the rules of syntax into account may provide an essentialsource of information for predicting enhancer outputs. However, theimportance of syntax/grammar for enhancer function is still debated; what has been needed is more experimental data.

While we still don't fully understand the rules of DNA, the assumption of syntax and grammar appears to be a fruitful heuristic. One only has to observe how accurate the DNA software runs!

In their new report, Farley et al. propose an interesting idea: Because current methods of enhancer prediction focus on high-affinity TF binding sites, perhaps they are best at identifying those enhancers that are the least subject to constraints on binding site syntax. If true, this approach would tend to paint a biased picture of the constraints that shape enhancer sequences. Now that a more complete view of the relationship between DNA sequenceand enhancer function is slowly emerging (Fig. 1), future predictive methods may be more effective at computing gene expression patterns from genomic DNA sequences. After all, that is a task that cells perform every day, with astonishing reliability and precision.

Let's take stock of the analogy between genomics and language.

• We know in human language and in software that "astonishing reliability and precision" depend strongly on sequence specificity. Unclear writing reduces information. Sloppy coding crashes or reduces functionality.
• The placement of binding sites, whether on cis (same) or trans (opposite) sides of the DNA double helix, matters. Similar constraints obtain for language and software code: word order matters in most languages.
• TFs must match their binding sites. In languages, subjects and verbs must agree. In codes, arguments for routines must follow the rules for length, character type, and order.
• Barolo's title, "How to tune an enhancer," refers to the ability of binding sites and transcription factors to affect "not only the rate of RNA expression but also the timing, spatial patterning, and environmental control of every gene's activity." One might compare this to keywords in internet searches, tags on social media messages, or prefixes and suffixes in certain languages that affect the meaning.
• DNA can be translated from the DNA code into the protein code. This resembles translators (whether human or machine) that can convert English into Chinese. Both have to share the same language convention.
• DNA uses molecules that symbolize or represent something else. Similarly, languages use symbols whose shapes do not necessarily represent what they mean.

An analogy is more useful the more factors it shares with its referent, and the fewer it doesn't share, especially when the shared factors are the most significant ones. Human language may lack the 3-D shape and activity of DNA "letters" but shares the most important characteristic: reliable communication of information for a functional result. It also shares requirements for specificity and rules of operation. If anything, the comparison is from the lesser to the greater: if human language is designed, how much more the "astonishing reliability and precision" of the genome?

Deconstructing a 'just so' story

Gegenbaur Revisited: Assessing the "Limbs from Gills" Scenario
Michael Denton 

Science Daily announces:

Sonic hedgehog gene provides evidence that our limbs may have evolved from sharks' gills

Latest analysis shows that human limbs share a genetic programme with the gills of cartilaginous fishes such as sharks and skates, providing evidence to support a century-old theory on the origin of limbs that had been widely discounted.

An idea first proposed 138 years ago that limbs evolved from gills, which has been widely discredited due to lack of supporting fossil evidence, may prove correct after all -- and the clue is in a gene named for everyone's favourite blue hedgehog.

Unlike other fishes, cartilaginous fishes such as sharks, skates and rays have a series of skin flaps that protect their gills. These flaps are supported by arches of cartilage, with finger-like appendages called branchial rays attached.

In 1878, influential German anatomist Karl Gegenbaur presented the theory that paired fins and eventually limbs evolved from a structure resembling the gill arch of cartilaginous fishes. However, nothing in the fossil record has ever been discovered to support this.

Now, researchers have reinvestigated Gegenbaur's ideas using the latest genetic techniques on embryos of the little skate -- a fish from the very group that first inspired the controversial theory over a century ago -- and found striking similarities between the genetic mechanism used in the development of its gill arches and those in human limbs.

Scientists say it comes down to a critical gene in limb development called 'Sonic hedgehog', named for the videogame character by a research team at Harvard Medical School.

The intriguing paper in the journal Development is here, and a very lucid description by one of the authors, J. Andrew Gillis, is here.

Gillis and his co-author Brian K. Hall provide evidence showing that in the development of the gill or branchial arches (a paired series of skeletal elements that support the gills and run down either side of the pharynx in fishes) and of the branchial rays (cartilaginous rods that articulate at their base with the gill arches in sharks and rays and protrude laterally from the gill arches), the common toolbox gene sonic hedgehog (Shh) establishes the anterior-posterior axis and the proliferative expansion of branchial endoskeletal progenitor cells. Those are the cells that give rise to the internal support system in vertebrates, composed of bone (in bony fishes and tetrapods) or cartilage (in sharks and rays).

What is the significance of their report? It is that precisely the same gene establishes the anterior-posterior axis in the tetrapod limb (in the human hand this is the axis from the thumb to the little finger) and promotes proliferation of the endosketal progenitor cells. This, as mentioned, supports a notion first proposed more than a century ago by the great German morphologist Carl Gegenbaur. As Gillis and Hall point out in a recent PNAS paper:

Gegenbaur drew parallels between the organization of the gill arch skeleton with that of the paired appendage skeletons of gnathostomes [jawed fishes], homologizing the appendage girdle with the proximal branchial arch, and the endoskeleton of paired fins proper with the distal branchial rays.

On this theory, the fin and limb girdles of vertebrates would be homologous to and derived from gill or branchial arch skeletal elements. Meanwhile the lateral appendages, the fins and limbs themselves, would be homologous to and derived from branchial rays.

In light of Gillis and Hall's research, Gegenbaur might turn out to have been right. However, as with so many other evolutionary transitions, one of the major problems in assessing his "arch to fin" scenario is, as Gillis and Hall confess, the absence of any known intermediates between branchial arches and fins. The gap between a branchial ray and a fish fin is certainly considerable (as is obvious in figure 1 in the Gillis and Hall paper). And the existence of developmental homologies throws no light on the question of how the evolutionary transformations might have come about.

Was it, as Darwin envisaged, via a long series of adaptive intermediates, i.e., imposed by external constraints? Or did it occur via a sudden, or series of relatively saltational events, driven by internal causal factors or constraints?

Intriguingly, there is a similar gap between fins and tetrapod limbs. And once more, although no one doubts that fins and limbs are homologous, how the fin-to-limb transition came about is not known. Again as with the considerable gap between branchial rays and fins, there is a considerable morphological gap between fins and limbs while no intermediate fossils are known that might throw light on the transition.


Thus the familiar question arises: Was the fin-to-limb transition gradual or sudden? And was the tetrapod limb imposed by the external pressure of natural selection or by internal causal factors? The same might be asked about the origin of many other novelties in nature even where, as would seem to be the case here, a novelty is clearly homologous to some preexisting structure.

Beyond the scroll.