The Emperor's New Clothes and the Courtier's Reply

I recently referred to the "Courtier's Reply", a term invented by PZ Myers to rebut the claims of believers who insist that their superstitious beliefs are ever so much more sophisticated than the simple version that Dawkins attacks.

PZ's response deserves much more publicity because it goes to the heart of the debate between rationalism and supersition. I'm going to post his original Courtier's Reply below (without permission, but I'm sure he'll understand) but before doing so I need to remind everyone about the original fairy tale [The Emperor's New Clothes].

THE EMPEROR'S NEW CLOTHESby Hans Christian Anderson

Once upon a time there lived a vain Emperor whose only worry in life was to dress in elegant clothes. He changed clothes almost every hour and loved to show them off to his people.

Word of the Emperor's refined habits spread over his kingdom and beyond. Two scoundrels who had heard of the Emperor's vanity decided to take advantage of it. They introduced themselves at the gates of the palace with a scheme in mind.

"We are two very good tailors and after many years of research we have invented an extraordinary method to weave a cloth so light and fine that it looks invisible. As a matter of fact it is invisible to anyone who is too stupid and incompetent to appreciate its quality."

The chief of the guards heard the scoundrel's strange story and sent for the court chamberlain. The chamberlain notified the prime minister, who ran to the Emperor and disclosed the incredible news. The Emperor's curiosity got the better of him and he decided to see the two scoundrels.

"Besides being invisible, your Highness, this cloth will be woven in colors and patterns created especially for you." The emperor gave the two men a bag of gold coins in exchange for their promise to begin working on the fabric immediately.

"Just tell us what you need to get started and we'll give it to you." The two scoundrels asked for a loom, silk, gold thread and then pretended to begin working. The Emperor thought he had spent his money quite well: in addition to getting a new extraordinary suit, he would discover which of his subjects were ignorant and incompetent. A few days later, he called the old and wise prime minister, who was considered by everyone as a man with common sense.

"Go and see how the work is proceeding," the Emperor told him, "and come back to let me know."

The prime minister was welcomed by the two scoundrels.

"We're almost finished, but we need a lot more gold thread. Here, Excellency! Admire the colors, feel the softness!" The old man bent over the loom and tried to see the fabric that was not there. He felt cold sweat on his forehead.

"I can't see anything," he thought. "If I see nothing, that means I'm stupid! Or, worse, incompetent!" If the prime minister admitted that he didn't see anything, he would be discharged from his office.

"What a marvelous fabric, he said then. "I'll certainly tell the Emperor." The two scoundrels rubbed their hands gleefully. They had almost made it. More thread was requested to finish the work.

Finally, the Emperor received the announcement that the two tailors had come to take all the measurements needed to sew his new suit.

"Come in," the Emperor ordered. Even as they bowed, the two scoundrels pretended to be holding large roll of fabric.

"Here it is your Highness, the result of our labour," the scoundrels said. "We have worked night and day but, at last, the most beautiful fabric in the world is ready for you. Look at the colors and feel how fine it is." Of course the Emperor did not see any colors and could not feel any cloth between his fingers. He panicked and felt like fainting. But luckily the throne was right behind him and he sat down. But when he realized that no one could know that he did not see the fabric, he felt better. Nobody could find out he was stupid and incompetent. And the Emperor didn't know that everybody else around him thought and did the very same thing.

The farce continued as the two scoundrels had foreseen it. Once they had taken the measurements, the two began cutting the air with scissors while sewing with their needles an invisible cloth.

"Your Highness, you'll have to take off your clothes to try on your new ones." The two scoundrels draped the new clothes on him and then held up a mirror. The Emperor was embarrassed but since none of his bystanders were, he felt relieved.

"Yes, this is a beautiful suit and it looks very good on me," the Emperor said trying to look comfortable. "You've done a fine job."

"Your Majesty," the prime minister said, "we have a request for you. The people have found out about this extraordinary fabric and they are anxious to see you in your new suit." The Emperor was doubtful showing himself naked to the people, but then he abandoned his fears. After all, no one would know about it except the ignorant and the incompetent.

"All right," he said. "I will grant the people this privilege." He summoned his carriage and the ceremonial parade was formed. A group of dignitaries walked at the very front of the procession and anxiously scrutinized the faces of the people in the street. All the people had gathered in the main square, pushing and shoving to get a better look. An applause welcomed the regal procession. Everyone wanted to know how stupid or incompetent his or her neighbor was but, as the Emperor passed, a strange murmur rose from the crowd.

Everyone said, loud enough for the others to hear: "Look at the Emperor's new clothes. They're beautiful!"

"What a marvellous train!"

"And the colors! The colors of that beautiful fabric! I have never seen anything like it in my life!" They all tried to conceal their disappointment at not being able to see the clothes, and since nobody was willing to admit his own stupidity and incompetence, they all behaved as the two scoundrels had predicted.

A child, however, who had no important job and could only see things as his eyes showed them to him, went up to the carriage.

"The Emperor is naked," he said.

"Fool!" his father reprimanded, running after him. "Don't talk nonsense!" He grabbed his child and took him away. But the boy's remark, which had been heard by the bystanders, was repeated over and over again until everyone cried:

"The boy is right! The Emperor is naked! It's true!"

The Emperor realized that the people were right but could not admit to that. He though it better to continue the procession under the illusion that anyone who couldn't see his clothes was either stupid or incompetent. And he stood stiffly on his carriage, while behind him a page held his imaginary mantle.

Here's how PZ Myers describes those people who claim to have a much more intellectual version of religion; one that can not be as easily dismissed as the "simple" version that Richard Dawkins addresses. These people seem to think that by dressing up their superstitious beliefs in fancy language with philosophical references they can escape the simple fact the the Emperor has no clothes.

The Courtier's Replyby PZ Myers

I have considered the impudent accusations of Mr Dawkins with exasperation at his lack of serious scholarship. He has apparently not read the detailed discourses of Count Roderigo of Seville on the exquisite and exotic leathers of the Emperor's boots, nor does he give a moment's consideration to Bellini's masterwork, On the Luminescence of the Emperor's Feathered Hat. We have entire schools dedicated to writing learned treatises on the beauty of the Emperor's raiment, and every major newspaper runs a section dedicated to imperial fashion; Dawkins cavalierly dismisses them all. He even laughs at the highly popular and most persuasive arguments of his fellow countryman, Lord D. T. Mawkscribbler, who famously pointed out that the Emperor would not wear common cotton, nor uncomfortable polyester, but must, I say must, wear undergarments of the finest silk.

Dawkins arrogantly ignores all these deep philosophical ponderings to crudely accuse the Emperor of nudity.

Personally, I suspect that perhaps the Emperor might not be fully clothed — how else to explain the apparent sloth of the staff at the palace laundry — but, well, everyone else does seem to go on about his clothes, and this Dawkins fellow is such a rude upstart who lacks the wit of my elegant circumlocutions, that, while unable to deal with the substance of his accusations, I should at least chide him for his very bad form.

Until Dawkins has trained in the shops of Paris and Milan, until he has learned to tell the difference between a ruffled flounce and a puffy pantaloon, we should all pretend he has not spoken out against the Emperor's taste. His training in biology may give him the ability to recognize dangling genitalia when he sees it, but it has not taught him the proper appreciation of Imaginary Fabrics.

Richard Dawkins on the Agenda

 
The Agenda with Steve Paikin is an interview show on TVO (TV Ontario). I watch it quite often.

Lately I've been more and more annoyed at Steve Paikin for his naive, simplistic views of religion and it's importance in the modern world. A few weeks ago he had an entire week of shows about the "resurgence" of religion in Canada. A resurgence that apparently only he and his fellow believers can see.

The show on Thursday night was just about the last straw for me. His interview with Richard Dawkins and the panel discussion afterwards were so bad that I'm going to stop watching the show. You can see the entire hour of the May 10th episode at [Richard Dawkins | Can We Live by Reason Alone?].

Pay close attention to Jordan Peterson in the panel discussion at the end. He's a Professor of Psychology at the University of Toronto. He accuses Dawkins of being very simplistic and naive about religion—and by implication he (Jordan Peterson) has the correct, deeply intellectual, understanding of religion that would trump Dawkins in a debate. Trouble is, nothing coming out of the mouth of Peterson convinces me that his reasons for believing in superstition are any better than the reasons Dawkins criticizes in The God Delusion. Or, am I missing some incredibly sophisticated version of the Courtier's Reply that's way over my head?

I especially like the claim that all hell will break loose if religion is abolished. The interesting part about such claims is that they come from people who are completely ignorant of what's going on in Europe. We're about to find out what happens when a country abandons religion because Sweden and other European countries are very close to that point. If the true believers are correct then these countries will soon become dens of iniquity and depravity—in sharp contrast to very religious countries like the USA. I can't believe that one of my colleagues would make such a stupid statement in public.

UPDATE: Read the comments on Dawkins.net

Biochemist Gregor Mendel Studied Starch Synthesis

Starch is the plant equivalent of glycogen. It consist of long branched chains of glucose residues. Starch is often stored in roots and tubers but it is also deposited in seeds where it can be mobilized following germination.

Mendel didn't know it at the time but he was dealing with the genetics of starch synthesis while crossing peas in his garden.

One of the genetic traits that Gregor Mendel studied was round ( R) vs. wrinkled ( r) peas. The wrinkled pea phenotype is caused by a defect in the gene for starch branching enzyme. Starch synthesis is very similar to glycogen synthesis. The main polymerization enzyme is starch synthase and it works just like glycogen synthase [Glycogen Synthesis]. Both starch and glycogen synthesis require an additonal enzyme to create new branches. In plants this enzyme is starch branching enzyme.

In the absence of this enzyme, starch synthesis is partially blocked and the developing peas have a higher concentration of sucrose. (In plants, glucose is transported as the disacharide sucrose.) This causes the mutant peas to absorb more water than normal peas and they swell to a larger size. When the seeds begin to dry out the peas with the defective enzyme lose more water and their outer surface takes on a wrinkled appearance. One copy of the active gene for starch branching enzyme is sufficient so the presence of one defective allele has no observable phenotype. When two mutant alleles are present the wrinkled phenotype is expressed because there's no active starch branching enzyme. The mutant allele is recessive to the wild type allele.

For some strange reason Mendel is more famous for discovering this simple genetic rule than for his contributions to understanding starch metabolism.

Bhattacharyya, M. K., Smith, A. M., Ellis, T. H., Hedley, C., and Martin, C. (1990) The wrinkled-seed character of a pea described by Mendel is caused by a transposon-like insertion in a gene encoding starch-branching enzyme. Cell 60:115-122.

[©Laurence A. Moran. Some of the text is from Principles of Biochemistry 4th ed. ©Pearson/Prentice Hall]

Gosling Relocation

 
Eva is a Ph.D. student in our department. She has a really cool blog called easternblot (get it?). You have got to see what she posted today [Annual gosling relocation at York University].

I've only got one small problem. Do we really need more Canada geese?

Regulating Glycogen Metabolism

Mammalian glycogen stores glucose in times of plenty (after feeding, a time of high glucose levels) and supplies glucose in times of need (during fasting or in “fight-or-flight” situations). In muscle, glycogen provides fuel for muscle contraction. In contrast, liver glycogen is largely converted to glucose that exits liver cells and enters the bloodstream for transport to other tissues that require it [The Cori Cycle]. Both the mobilization and synthesis of glycogen are regulated by hormones.

The regulation of glycogen metabolism is a good way to introduce the idea of signal transduction. This is a very popular part of modern biochemistry. It's basically a way in which signals from outside the cell are transduced through a chain of molecules to affect a particular biochemical reaction. In this case, we'll examine how the hormones glucagon, epinephrine, and insulin regulate glycogen synthesis and glycogen degradation.

Let's look at glycogen synthesis. Glycogen synthase is the enzyme responsible for adding UDP-glucose to a growing chain of glycogen. There are two forms of this enzyme. The inactive form is called glycogen synthase b and it is phosphorylated (P). The active form is called glycogen synthase a and it does not carry a phosphate group. The activity of glycogen synthase is controlled by covalent modification just like pyruvate dehydrogenase [Regulating Pyruvate Dehydrogenase].

The phosphorlation of enzymes is performed by kinases. In this case it's a very common cellular kinase called protein kinase A (PKA). The complete name of the enzyme is cyclic AMP-dependent protein kinase A because its activity is regulated by a messenger molecule known as cyclic AMP (cAMP). Cyclic AMP is made from ATP by the enzyme adenylyl cyclase and it is degraded by the action of an enzyme called phosphodiesterase

When cAMP is present inside the cell it binds to protein kinase A and activates it so that it can phosphorylate glycogen synthase. This shuts down glycogen synthesis by deactivating the enzyme. The key to hormonal regulation is the effect of the hormones on the production of cAMP. This takes place on the cell surface when the hormone binds to a cell surface receptor molecule.

Insulin, glucagon, and epinephrine are the principal hormones that control glycogen metabolism in mammals. Insulin, a 51-residue protein is synthesized by the cells of the pancreas. It is secreted when the concentration of glucose in the blood increases. Thus, high levels of insulin are associated with the fed state of an animal. Insulin stimulates glycogen synthesis in the liver. This makes sense since high concentrations of glucose indicate that it's time to store it as glycogen.

Glucagon, a peptide hormone containing 29 amino acid residues, is secreted by the cells of the pancreas in response to a low blood glucose concentration. Glucagon restores the blood glucose concentration to a steady-state level by stimulating glycogen degradation. Only liver cells are rich in glucagon receptors, so glucagon is extremely selective in its target. The effect of glucagon is opposite that of insulin, and an elevated glucagon concentration is associated with the fasted state.

The adrenal glands release the catecholamine epinephrine (also known as adrenaline) in response to neural signals that trigger the fight-or-flight response. Epinephrine stimulates the breakdown of glycogen to glucose 1-phosphate, which is converted to glucose 6-phosphate. The increase in intracellular glucose 6-phosphate increases both the rate of glycolysis in muscle and the amount of glucose released into the bloodstream from the liver. Note that epinephrine triggers a response to a sudden energy requirement; glucagon and insulin act over longer periods to maintain a relatively constant concentration of glucose in the blood.

Epinephrine binds to β-adrenergic receptors of liver and muscle cells and to α1-adrenergic receptors of liver cells. The binding of epinephrine to β-adrenergic receptors or of glucagon to its receptors activates the adenylyl cyclase signaling pathway. The second messenger, cyclic AMP (cAMP), then activates protein kinase A.

For now let's just take it as a given that glucagon and epinephrine trigger cAMP synthesis and this leads to shutting down of glycogen synthesis.


In addition to blocking glycogen synthesis, these hormones stimulate glycogen degradation. The glycogen degradation enzyme is called glycogen phosphorylase and it comes in two forms. Glycogen phosphorylase a is the active form and it's phosphorylated (it has an attached phosphate group). Glycogen phosphorylase b is the unphosphorylated form of the enzyme and it's inactive. Note the reciprocal relationship of the glycogen synthase and glycogen degradation enzymes. When both are phosphorylated, glycogen degradation is active and glycogen synthesis is not. When both are dephosphorylated, glycogen synthesis is active and glycogen degradation is blocked. This suggests a similar mechanism of regulation for the two enzymes.

The phosphorylation of glycogen phosphorulase is carried out by a kinase enzyme. In this case it's a specific kinase called phosphorylase kinase. Phosphorylase kinase is itself subject to activation by phosphorylation. The kinase that does this is our friend protein kinase A. Thus, epinephrine and glucagon will stimulate glycogen degradation in addition to stopping glycogen synthesis.



For every kinase there's a phosphatase that removes phosphate groups from proteins. Recall that insulin is released when glucose levels in the blood are high. The effect of insulin is the exact opposite of the effect of glucagon and epinephrine. Insulin binds to a cell surface receptor and triggers a pathway that leads to activation of protein phosphatase-1. This enzyme dephosphorylates the three enzymes shown above leading to activation of glycogen synthesis and deactivation of glycogen degradation. Insulin causes glucose to be stored as glycogen.



These kinds of kinase/phosphatase cascades are very common in eukaryotes. Believe it or not, this is one of the simpler examples.

Now, let's return to the effect of the hormone on cAMP synthesis. This is the key part of any signaling pathway and it's best illustrated by using a general model based on cAMP production. (There are other types of signaling pathways.)



The details aren't important unless you're seriously into signaling—like 50% of all biochemistry graduate students these days. Hormone binds to a cell surface receptor. The signal is transferred through the cell membrane to the inside part of the receptor molecule. This interacts with a G protein so that when hormone binds, the G protein is activated.

G protein then diffuses to the membrane bound adenylyl cyclase molecule and, when the two proteins connect, the activity of adenylyl cyclase is stimulated and cAMP is produced. This leads to activation of protein kinase A. The stimulatory effect of the signal transduction pathway is transient because cAMP is rapidly degraded by phosphodiesterase. Thus, hormone must usually be continuously present in order to get stimulation.

There are other hormones that inhibit cAMP production by activating different G proteins (G_i) that block adenylyl cyclase.

[©Laurence A. Moran. Some of the text is from Principles of Biochemistry 4th ed. ©Pearson/Prentice Hall]

Nicole Vienneau Has Gone Missing in Syria

 
Our friends are devastated because their niece, Nicole Vienneau, is missing in Syria. Her brother has a website with all the information [My Sister, Nicole Vienneau, Has Gone Missing in Syria].

My sister, Nicole Vienneau, has been missing in Syria since April 1st (40 days), near the town of Hama, while on a day-trip to see Qasr Ibn Wardan (a nearby castle) and the "Beehive Houses". We found her gear at the Cairo Hotel, but no sign of her after that.

If you have any details or contacts in the area, please contact me at mattv99@hotmail.com.

There's little chance that readers of Sandwalk can help but just in case please contact him immediately if you have any information.

Eye on DNA

 


Hsien-Hsien Lei, formerly of Genetics & Health, has a new blog called Eye on DNA. I've been reading it for a week or so and it looks really cool. Check it out.

Hsein-Hsein Lei (pronounced shen-shen lay) has a Ph.D. in epidemiology. She's ultimately interested in making everyone more healthy but she also wants everyone to know how your genes work. Right now she works out of London (UK) so North Americans can read her posting first thing in the morning!

City Lights Make Birds Sing at Night

 
Friday's Urban Legend: PROBABLY FALSE

BBC News reports that "Robins in urban areas are singing at night because it is too noisy during the day, researchers suggest" [City birds sing for silent nights].

Scientists from the University of Sheffield say there is a link between an area's daytime noise levels and the number of birds singing at night.

Until now, light pollution had been blamed because it was thought that street lights tricked the birds into thinking it was still daytime.

The findings are published in the Royal Society journal Biology Letters.

It turns out that it's not because of night lights that the birds are singing. It's because they can't make themselves heard over the din of city traffic so they wait 'till the dead of night to start singing. That way they get to annoy everyone around them.

I wonder if that's why people talk on cell phones when they're sitting on a quiet commuter train?

Lose Weight: Emigrate to Canada

 

Satellites solve mystery of low gravity over Canada

If it seems Canadians weigh less than their American neighbours, they do—but not for the reasons you might think. A large swath of Canada actually boasts lower gravity than its surroundings.

The Cori Cycle

Animals can synthesize glucose 6-phosphate via gluconeogenesis just like all other species. However, unlike most species, animals can convert glucose 6-phosphate to glucose, which is secreted into the circulatory system. Mammals, in particular, have a sophisticated cycle of secretion and uptake of glucose. It's called the Cori cycle after the Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori.


The glucose 6-phosphate molecules synthesized in the liver can either be converted to glycogen [Glycogen Synthesis] or converted to glucose and secreted into the blood stream. The glucose molecules are taken up by muscle cells where they can be stored as glucogen. During strenuous exercise the glycogen is broken down to glucose 6-phosphate [Glycogen Degradation] and oxdized via the glycolysis pathway. This pathway yields ATP that is used in muscle contraction.

If oxygen is limiting, the end product of glucose breakdown isn't CO₂ but lactate. Lactate is secreted into the blood stream where it is taken up by the liver and converted to pyruvate by the enzyme lactate dehydrogenase. Pyruvate is the substrate for gluconeogenesis. The synthesis of glucose in the liver requires energy in the form of ATP and this energy is supplied by a variety of sources. The breakdown of fatty acids is the source shown in the figure.

The Cori cycle preserves carbon atoms. The six carbon molecule, glucose, is split into two 3-carbon molecules (lactate) that are then converted to another 3-carbon molecule (pyruvate). Two pyruvates are joined to make glucose.

Adaptation and Accident in PNAS

 
This week's issue of the Proceedings of the National Academy of Sciences (USA) (PNAS) has a number of articles on evolution. The most interesting to me are the ones that debate the role of natural selection. I haven't had time to read them yet but here's a heads up.

Michael Lynch, The frailty of adaptive hypotheses for the origins of organismal complexity.

The vast majority of biologists engaged in evolutionary studies interpret virtually every aspect of biodiversity in adaptive terms. This narrow view of evolution has become untenable in light of recent observations from genomic sequencing and population-genetic theory. Numerous aspects of genomic architecture, gene structure, and developmental pathways are difficult to explain without invoking the nonadaptive forces of genetic drift and mutation. In addition, emergent biological features such as complexity, modularity, and evolvability, all of which are current targets of considerable speculation, may be nothing more than indirect by-products of processes operating at lower levels of organization. These issues are examined in the context of the view that the origins of many aspects of biological diversity, from gene-structural embellishments to novelties at the phenotypic level, have roots in nonadaptive processes, with the population-genetic environment imposing strong directionality on the paths that are open to evolutionary exploitation.

Francisco J. Ayala, Darwin's greatest discovery: Design without designer.

Darwin's greatest contribution to science is that he completed the Copernican Revolution by drawing out for biology the notion of nature as a system of matter in motion governed by natural laws. With Darwin's discovery of natural selection, the origin and adaptations of organisms were brought into the realm of science. The adaptive features of organisms could now be explained, like the phenomena of the inanimate world, as the result of natural processes, without recourse to an Intelligent Designer. The Copernican and the Darwinian Revolutions may be seen as the two stages of the one Scientific Revolution. They jointly ushered in the beginning of science in the modern sense of the word: explanation through natural laws. Darwin's theory of natural selection accounts for the "design" of organisms, and for their wondrous diversity, as the result of natural processes, the gradual accumulation of spontaneously arisen variations (mutations) sorted out by natural selection. Which characteristics will be selected depends on which variations happen to be present at a given time in a given place. This in turn depends on the random process of mutation as well as on the previous history of the organisms. Mutation and selection have jointly driven the marvelous process that, starting from microscopic organisms, has yielded orchids, birds, and humans. The theory of evolution conveys chance and necessity, randomness and determinism, jointly enmeshed in the stuff of life. This was Darwin's fundamental discovery, that there is a process that is creative, although not conscious.

Cynthia M. Beall, Two routes to functional adaptation: Tibetan and Andean high-altitude natives.

Populations native to the Tibetan and Andean Plateaus are descended from colonizers who arrived perhaps 25,000 and 11,000 years ago, respectively. Both have been exposed to the opportunity for natural selection for traits that offset the unavoidable environmental stress of severe lifelong high-altitude hypoxia. This paper presents evidence that Tibetan and Andean high-altitude natives have adapted differently, as indicated by large quantitative differences in numerous physiological traits comprising the oxygen delivery process. These findings suggest the hypothesis that evolutionary processes have tinkered differently on the two founding populations and their descendents, with the result that the two followed different routes to the same functional outcome of successful oxygen delivery, long-term persistence and high function. Assessed on the basis of basal and maximal oxygen consumption, both populations avail themselves of essentially the full range of oxygen-using metabolism as populations at sea level, in contrast with the curtailed range available to visitors at high altitudes. Efforts to identify the genetic bases of these traits have included quantitative genetics, genetic admixture, and candidate gene approaches. These reveal generally more genetic variance in the Tibetan population and more potential for natural selection. There is evidence that natural selection is ongoing in the Tibetan population, where women estimated to have genotypes for high oxygen saturation of hemoglobin (and less physiological stress) have higher offspring survival. Identifying the genetic bases of these traits is crucial to discovering the steps along the Tibetan and Andean routes to functional adaptation.

Adam S. Wilkins, Between "design" and "bricolage": Genetic networks, levels of selection, and adaptive evolution.

The extent to which "developmental constraints" in complex organisms restrict evolutionary directions remains contentious. Yet, other forms of internal constraint, which have received less attention, may also exist. It will be argued here that a set of partial constraints below the level of phenotypes, those involving genes and molecules, influences and channels the set of possible evolutionary trajectories. At the top-most organizational level there are the genetic network modules, whose operations directly underlie complex morphological traits. The properties of these network modules, however, have themselves been set by the evolutionary history of the component genes and their interactions. Characterization of the components, structures, and operational dynamics of specific genetic networks should lead to a better understanding not only of the morphological traits they underlie but of the biases that influence the directions of evolutionary change. Furthermore, such knowledge may permit assessment of the relative degrees of probability of short evolutionary trajectories, those on the microevolutionary scale. In effect, a "network perspective" may help transform evolutionary biology into a scientific enterprise with greater predictive capability than it has hitherto possessed.

John Gerhart and Marc Kirschner, The theory of facilitated variation

This theory concerns the means by which animals generate phenotypic variation from genetic change. Most anatomical and physiological traits that have evolved since the Cambrian are, we propose, the result of regulatory changes in the usage of various members of a large set of conserved core components that function in development and physiology. Genetic change of the DNA sequences for regulatory elements of DNA, RNAs, and proteins leads to heritable regulatory change, which specifies new combinations of core components, operating in new amounts and states at new times and places in the animal. These new configurations of components comprise new traits. The number and kinds of regulatory changes needed for viable phenotypic variation are determined by the properties of the developmental and physiological processes in which core components serve, in particular by the processes' modularity, robustness, adaptability, capacity to engage in weak regulatory linkage, and exploratory behavior. These properties reduce the number of regulatory changes needed to generate viable selectable phenotypic variation, increase the variety of regulatory targets, reduce the lethality of genetic change, and increase the amount of genetic variation retained by a population. By such reductions and increases, the conserved core processes facilitate the generation of phenotypic variation, which selection thereafter converts to evolutionary and genetic change in the population. Thus, we call it a theory of facilitated phenotypic variation.

Benjamin Prud'homme, Nicolas Gompel, and Sean B. Carroll, Emerging principles of regulatory evolution

Understanding the genetic and molecular mechanisms governing the evolution of morphology is a major challenge in biology. Because most animals share a conserved repertoire of body-building and -patterning genes, morphological diversity appears to evolve primarily through changes in the deployment of these genes during development. The complex expression patterns of developmentally regulated genes are typically controlled by numerous independent cis-regulatory elements (CREs). It has been proposed that morphological evolution relies predominantly on changes in the architecture of gene regulatory networks and in particular on functional changes within CREs. Here, we discuss recent experimental studies that support this hypothesis and reveal some unanticipated features of how regulatory evolution occurs. From this growing body of evidence, we identify three key operating principles underlying regulatory evolution, that is, how regulatory evolution: (i) uses available genetic components in the form of preexisting and active transcription factors and CREs to generate novelty; (ii) minimizes the penalty to overall fitness by introducing discrete changes in gene expression; and (iii) allows interactions to arise among any transcription factor and downstream CRE. These principles endow regulatory evolution with a vast creative potential that accounts for both relatively modest morphological differences among closely related species and more profound anatomical divergences among groups at higher taxonomical levels.

Nancy A. Moran, Symbiosis as an adaptive process and source of phenotypic complexity.

Genomics has revealed that inheritance systems of separate species are often not well segregated: genes and capabilities that evolve in one lineage are often stably acquired by another lineage. Although direct gene transfer between species has occurred at some level in all major groups, it appears to be far more frequent in prokaryotes than in multicellular eukaryotes. An alternative to incorporating novel genes into a recipient genome is acquiring a stable, possibly heritable, symbiotic association and thus enjoying benefits of complementary metabolic capabilities. These kinds of symbioses have arisen frequently in animals; for example, many insect groups have diversified on the basis of symbiotic associations acquired early in their evolutionary histories. The resulting associations are highly complex, often involving specialized cell types and organs, developmental mechanisms that ensure transfer of symbionts between generations, and mechanisms for controlling symbiont proliferation and location. The genomes of long-term obligate symbionts often undergo irreversible gene loss and deterioration even as hosts evolve dependence on them. In some cases, animal genomes may have acquired genes from symbionts, mirroring the gene uptake from mitochondrial and plastid genomes. Multiple symbionts often coexist in the same host, resulting in coadaptation among several phylogenetically distant genomes.

Giorgio Bernardi, The neoselectionist theory of genome evolution.

The vertebrate genome is a mosaic of GC-poor and GC-rich isochores, megabase-sized DNA regions of fairly homogeneous base composition that differ in relative amount, gene density, gene expression, replication timing, and recombination frequency. At the emergence of warm-blooded vertebrates, the gene-rich, moderately GC-rich isochores of the cold-blooded ancestors underwent a GC increase. This increase was similar in mammals and birds and was maintained during the evolution of mammalian and avian orders. Neither the GC increase nor its conservation can be accounted for by the random fixation of neutral or nearly neutral single-nucleotide changes (i.e., the vast majority of nucleotide substitutions) or by a biased gene conversion process occurring at random genome locations. Both phenomena can be explained, however, by the neoselectionist theory of genome evolution that is presented here. This theory fully accepts Ohta's nearly neutral view of point mutations but proposes in addition (i) that the AT-biased mutational input present in vertebrates pushes some DNA regions below a certain GC threshold; (ii) that these lower GC levels cause regional changes in chromatin structure that lead to deleterious effects on replication and transcription; and (iii) that the carriers of these changes undergo negative (purifying) selection, the final result being a compositional conservation of the original isochore pattern in the surviving population. Negative selection may also largely explain the GC increase accompanying the emergence of warm-blooded vertebrates. In conclusion, the neoselectionist theory not only provides a solution to the neutralist/selectionist debate but also introduces an epigenomic component in genome evolution.

Eugenie C. Scott and Nicholas J. Matzke, Biological design in science classrooms.

Although evolutionary biology is replete with explanations for complex biological structures, scientists concerned about evolution education have been forced to confront "intelligent design" (ID), which rejects a natural origin for biological complexity. The content of ID is a subset of the claims made by the older "creation science" movement. Both creationist views contend that highly complex biological adaptations and even organisms categorically cannot result from natural causes but require a supernatural creative agent. Historically, ID arose from efforts to produce a form of creationism that would be less vulnerable to legal challenges and that would not overtly rely upon biblical literalism. Scientists do not use ID to explain nature, but because it has support from outside the scientific community, ID is nonetheless contributing substantially to a long-standing assault on the integrity of science education.

Science Journalism: A Bias in Favour of Truth

 
Peter McKnight is a science journalist who writes for The Vancouver Sun. Don't hold that against him, he's actually one of the most thoughtful science journalist around. Readers may recall that we had a discussion about his views concerning Marus Ross and his Ph.D. in geology [Peter McKnight of the Vancouver Sun Weighs in on the Marcus Ross Incident and Peter McKnight on the Marcus Ross Issue].

I disagreed with Peter back then but I agree with his latest column from last Saturday [what we need here is a bias in favour of truth]. McKnight argues that the tendency toward balance and fairness in journalism is hurting science journalism. When it comes to science there aren't always two legitimate sides to every story. For example, in the evolution vs. creationism controversy, journalists do not have an obligation to give equal time to creationist nonsense.

Similarly, when I write about evolution and creationism, I am invariably accused of bias -- a lack of balance -- for explaining that evolution is a scientific theory and creationism is not. To repair this problem, certain letter writers tell me that I should simply present both positions equally, without editorial comment, and let my readers decide the truth.

Doing that would amount to an abdication of my role as a columnist, since I have a responsibility to offer an opinion. It would also represent an affront to science, but I understand where my letter writers are coming from; journalism has long promoted the view that journalists ought to present both sides in a dispute and keep their opinions to themselves.

I agree. Science journalists should not be simple reporters of fact. They need to interpret those facts and put them in context. They need to contribute a certain added value to their reports, otherwise we might just as well read the original press releases or the abstract of the paper.

Despite this evidence from more than a century ago, false balance came to dominate journalism and still exists today. Many reasons for this have been identified: In our increasingly partisan era, journalists are ultra-sensitive to accusations of bias, so they ensure balance to ward off such allegations; some journalists don't have the time -- and some are too lazy -- to conduct a thorough investigation of an issue, so it's easier to just present competing opinions; and some journalists don't have the expertise to filter through various opinions and determine which ones are based on solid evidence.

This last reason is particularly common in science journalism, since few journalists outside of publications like Scientific American have backgrounds in science. Yet, remarkably, former New York University sociologist Dorothy Nelkin noted in her book Selling Science that some journalists are hostile to science reporters who have science backgrounds, because "journalists trained extensively in science may adopt the values of scientists and lose the ability to be critical."

I can understand why average journalists are afraid of real science journalists. It's because good science journalists can do something that the typical non-science journalist can't do. That goes against the fundamental credo of the profession; namely, that journalists can cover any story because they're trained to report the facts. (Are they also hostile to those journalists who are knowledgeable about the law, medicine, or business—or is it just science?)

I agree with Peter McKnight about the need for science journalists to inject their own (informed) opinion into their articles. But I want to take it one step further. From my perspective, the most annoying science articles are not the ones that give inappropriate "balance" to the ideas of kooks. The worst ones are those that show no informed skepticism at all but merely report whatever the scientific paper says. I want my science journalists to do some digging from time to time, which is why I criticized an article in the "TRUTH" issue of SEED last month [Silent Mutations and Neutral Theory].

It's complicated. I want science journalists to give us an informed opinion. I don't want them to go out of their way to present contrary opinions just for the sake of "balance" and "fairness." On the other hand, I do want them to present contrary points of view when the news they're covering is itself biased and unfair.

It's tough to be a science journalist these days. They don't get no respect from either their journalist colleagues, or their science colleagues!

[Hat Tip: Jason Spaceman on talk.origins]

John Wise on Science and the Supernatural

 
John Wise is a Professor of Biology at Southern Methodist University in Dallas, Texas (USA). He writes on the campus website [Intelligent Design is not science: why this matters].

Because science gives us methods to accurately understand and manipulate the world we live in. Few people would dispute that our present scientific understanding of the physical world has led to a tremendously long list of advances in medicine, technology, engineering, the structure of the universe and the atom, and on and on. The list is nearly endless, but it does not include everything. Science can tell us only what is governed by natural forces. Miracles are extra-ordinary events; gods are super-natural beings.

Are there reasonable philosophical arguments that can be made for the existence of God? Certainly. Are there reasonable philosophical arguments that can be made that God does not exist? Yes. Is there scientific evidence that answers either of these great questions one way or another? None that holds up to close scrutiny. Collins has no more scientific evidence that God exists than Dawkins has that God does not. Their evidence is philosophical, not scientific. Philosophy can encompass these issues, science cannot.

Okay, let's examine that argument. Science deals with the natural world, that's fair enough. Religion deals with the supernatural world so it's outside of science. That's also a fair statement. The question is, is there such a thing as a "supernatural world" and how can we learn anything about it?

We can deal with the natural world and we can at least imagine that there's a supernatural world beyond the reach of science. But there's a whole lot of middle ground that's being excluded here. Any religious claim that impinges on the natural world is subject to scientific analysis. That includes claims of miracles.

The only kind of religion that can be completely outside of science is one that believes in a God who never meddles in human affairs. Because as soon as that meddling occurs—answering prayers, for example—we scientists can legitimately ask whether the meddling is detectable or not.

Miracles either exist or they don't. If they do then we should have evidence for miracles. If there's no evidence then you should not believe in them. If you believe in miracles in the absence of evidence for their existence, then your belief is in conflict with science.

Professor Wise says that science can't prove the non-existence of God. That's true. In fact, we can't prove the non-existence of many things. We can't prove, for example, that astrology is completely false in every single case. What we can do is to limit its probability to such a small number that it makes no sense to believe in astrology. That's the power of science.

Professor Wise goes on to describe Professor Behe's testimony at the Dover trial in 2005.

Listen further to the transcripts of these hearings - they are astounding. Professor Behe, star witness for the ID proponents and Discovery Institute senior fellow, gave a Discovery Institute-approved definition of scientific theory in his testimony. Unfortunately for both Dr. Behe and the Discovery Institute, Eric Rothschild, the brilliant lawyer for the parents, asked Dr. Behe, "But you are clear, under your definition, the definition that sweeps in Intelligent Design, astrology is also a scientific theory, correct?" And Dr. Behe answered, "Yes, that's correct."

Is this what America wants and needs? A definition of science that is so weak and neutered that astrology qualifies?

Of course we don't want such a science. We want a science that rejects astrology because there's no evidence for it. We don't want astrologers to try and escape scientific scrutiny by claiming that astrology is outside of science, do we? We don't want astrologers to claim that their horoscopes are "miracles" and therefore just as legitimate as science.

Why is it that we feel very comfortable rejecting the ridiculous claims of astrology but we have to make special excuses to protect religion from close scientific scrutiny?

[Hat Tip: The Panda's Thumb]

Becoming Canadian

 
Jeffrey Shallit, a long time opponent of intelligent design creationism, is an American citizen living in Canada. Why doesn't he become a Canadian citizen?
[Towards a Canadian Republic]

My answer has always been the same: I'll seriously consider becoming a citizen when Canada removes one citizenship requirement: that I swear allegiance to "Her Majesty the Queen Elizabeth the Second, Queen of Canada, her Heirs and Successors".

As an American who is proud of the republican tradition (small "r" in "republican", please), the citizenship requirement that one swear allegiance to a person seems unappealingly feudal to me. Paul McCartney famously observed that the current Queen is a pretty nice girl, but that doesn't mean I want to swear allegiance to her.

It seems like an innocent enough anachronism to me.

But the more important question is how does Professor Shallit feel about pledging allegiance to a "thing" as in ....

I pledge allegiance to the flag of the United States of America, and to the Republic, for which it stands, one nation under God, indivisible, with liberty and justice for all.

Theme: ABO Blood Types

 
ABO Blood Types (Feb. 21, 2007)

Glycoproteins (Feb. 20, 2007)

Genetics of ABO Blood Types (Feb. 23, 2007)

Human ABO Gene (Feb. 22, 2007)