Does Disbelieving Evolution Reflect a Lack of Understanding of It?

 
Bill Dembski is troubled by the latest report in Science that shows a correlation between acceptance of evolution and education. [See PZ Myers' summary on Pharyngula.] The data suggests that the more educated you become the more likely you are to accept evolution. In other words, the data suggests that IDiots are, well, idiots.

You can see why Dembski is upset [Does understanding coerce belief?]. The truth hurts. Dembski then goes on to give us a good demonstration of the negative correlation between intelligence and belief in intelligent design.

But why should disbelieving evolution reflect a lack of understanding of it? Alternatively, does understanding evolution automatically force one to believe it? I remember speaking at the University of Toronto in 2002 when a biologist challenged me about how holding to ID renders one a nonscientist. I asked him if that disqualified Isaac Newton from being a scientist. His instant response was, “but he didn’t know about evolution.”

I don't know if Dembki is referring to me or to one of my colleagues who was at the meeting. I recall accusing Dembski of stupidity and of not being a good scientist, but there were so many of us making the same point that I don't know which one Dembski remembers. (Dembski has mentioned this meeting many times. It must have been very traumatic for him.)

At the risk of boring anyone with an IQ over 80, let me make the point that Dembski is deliberately missing. In 2002, if you rejected evolution you were an idiot. That's because the evidence for evolution is overwhelming. The same correlation holds today, only more so.

To answer the question posed in the title; yes, disbelieving in evolution reflects a lack of understanding of evolution. That's an empirical observation. There are very, very few IDiots who understand evolution. (Don't believe me? Read Uncommon Descent and Evolution News & Views.) Dembski sure aint' one of them. He didn't understand the basic principles of evolutionary theory in 2002 and he's given no indication of having learned anything since then.

Newton didn't know about evolution so he couldn't have rejected it. He wasn't stupid and he wasn't a bad scientist. He also didn't know about general relativity and plate tectonics but that didn't mean he was stupid either. If Newton were alive today you can be sure he would accept evolution, continental drift and general relativity. In the 21st century, anyone who rejects these fundamental concepts in science doesn't deserve to be called a scientist.

Barack Obama Is a Closet Muslim

 
Friday's Urban Legend: FALSE

There's an email circulating that Barack Obama was educated as a Muslim in a Wahabbi school in Indonesia. According to the email message ("The Enemy Within"), his step-father, Lolo Soetoro, was a Muslim who brought up Obama in the Muslim tradition. (The truth is that Obama's mother was an atheist and so was his biological father. His step-father was a non-practicing Muslim.)

Later on as an adult, Obama joined the United Church of Christ in order to convince voters that he was a Christian but he's still an ideological Muslim, according to the email message.

The take-home message is FALSE according to snopes.com [The Enemy Within] but there are elements of truth in the email message. It's worth reading the entire snopes article in order to understand Obama's religious views. This is the sort of thing that's going to come out during the Presidential campaign and if the snopes article is accurate, there's trouble brewing.

Stem Cell Debate in the USA

 
Furriners like me sometimes have a hard time following American politics. Take the debate over funding stem cell research, for example. America doesn't do it. Bush is very much against changing the law to permit development of new lines of stem cells. It's against his religion.

Mathew Nesbit has written an excellent summary of the situation over at Skeptical Inquirer [Political Communication in the 2007 Stem Cell Debate]. He follows up with a report on his blog [STEM CELL BILL PASSES THIRTY-SEVEN VOTES SHORT OF VETO OVERRIDE]. Apparently this is another fight over which "power" (President or Congress) is supposed to make laws. You'd think the Constitution would be clear about those things.

Now, if only someone could explain who's supposed to be in charge of making war ..... people seem to be confused about that as well.

Human Races Populations

 
I get pretty sick of hearing that there's no such thing as "races" in the species Homo sapiens. RPM has revived the controversy in More About Human Populations. Read the comments as well.

Apparently, it's more politically correct to refer to human "populations" and avoid the r-word.

We Really Are Quite Small

 

Olfactory Receptor Genes

 
The human genome contains 388 different olfactory receptor (OR) genes. These genes encode olfactory receptors, the molecules that detect odors [A Sense of Smell: Olfactory Receptors]. Our genome also has 414 olfactory receptor pseudogenes. These are stretches of DNA that resemble functional genes but they have accumulated mutations rendering them non-functional. In some cases, a single mutation has disrupted the open reading frame—these pseudogenes have recently evolved from functional genes. In most cases the olfactory receptor pseudogenes have multiple mutations, including extensive insertions and deletions, indicating that these pseudogene lost functionality millions of years ago.

None of the olfactory receptor genes have introns. This is a huge advantage because it is much easier to recognize functional genes and pseudogenes by scanning the genome.

The human genes and pseudogenes are clustered. Some clusters contain dozens of genes while others have only a few. There are 95 different clusters spread over all chromosomes except chromosome 20 and the Y chromosome. The first figure (below) is from a review by Niimura and Nei (2006). It shows the locations of the OR gene clusters. The vertical lines above the chromosome indicate the number of functional genes at that position—the taller the line the more genes. Lines below the chromosome indicate pseudogenes at that position.


A phylogenetic tree of the 388 functional OR genes reveals two main classes. All 57 class I genes are clustered together on chromosome 11. The class II genes can be subdivided into several subgroups labelled A to S in the figure below (Fig. 2 from Niimura and Nei (2006)). Several clusters are shown in order to illustrate the fact that genes of the same subclass tend to cluster together. Large letters indicate functional genes and small letters indicate related pseudogenes. Genes below the line are transcribed in the opposite direction from those above the line. (X identifies unclassified genes.)

Adjacent, closely related genes that are transcribed in the same direction are said to be tandemly duplicated, indicating that they probably arose by gene duplication. For example, most of the subclass A genes in cluster 11.11 probably resulted from repeated duplication of single A-type gene at that site.

The mouse genome contains 1037 functional genes and 354 pseudogenes in 69 clusters. Almost all of the clusters map to related clusters in the human genome. If we look at the relationship between the clusters on human chromosome 11 (Hs11) and mouse chromosome 2 Mm2), we see that the mouse cluster is larger and parts of it have been split up into four different clusters in humans. Nevertheless, the general order of genes is similar in mice and humans. There are more mouse OR genes, as expected. It has long been known that genes on human chromosome 11 are related to genes on mouse chromosome 2. (The figure is from Niimura and Nei (2006)).

How did this large gene family evolve? It seems clear that the common ancestor of mice and humans must have had many OR genes. It appears that the number of genes has probably changed considerably in one, or both, lineages. Why, and how, do some genes become inactivated? Is evolution of gene families due to natural selection or someting else? See "The Evolution of the Olfactory Receptor Gene Family" in tomorrow's posting.)

Niimura Y. and Nei M. (2006) Evolutionary dynamics of olfactory and other chemosensory receptor genes in vertebrates. J. Hum. Genet. 51:505-17

Cut and Run

 
"Cut and run" is straight talk for a military strategy otherwise known as "strategic redeployment" or "tactical victory." In some circles it's called "defeat" but that's a little too close to the truth to be acceptable.

The cut and run strategy means withdrawing all troops from Iraq and Afghanistan immediately. Not next year, and not next month. Tomorrow would be good. I'd vote for that.

Why should our troops stay in the Middle East? The most common argument in favor of continued occupation is that we broke Afghanistan and Iraq and it's now up to us to stay there and fix them (The Pottery Barn Rule).

This is a strange argument if you think about it for more than a second—a length of time that seems to just about cover the average attention span of neocon war hawks. What we've done in Afghanistan and Iraq is to destabilize those countries by removing a strong central government that provided peace and security to the majority of their citizens—albeit, at the expense of freedom and, in many cases, lives. Not perfect but better than what they've got today. That's why 80% of Iraqis preferred the life they had before the invasion (Iraqis say they were better off under rule of Saddam Hussein).

By staying there and propping up a Quisling "democracy" that's incapable of maintaining law and order, we are encouraging and protecting the local warlords and private militia. We are creating an environment that promotes a low-level civil war that will never produce a victory for either side. In other words, our troops might be contributing to the problem, not the solution. Furthermore, the Pottery Barn Rule runs counter to the stated goal of the invasions, which were supposed to allow the citizens to choose their own form of government. They own it; they should fix it.

The proper strategy is to withdraw. Cut your loses and get out as fast as possible. That's the only honorable way out of a losing strategy. Just like Vietnam. If we don't leave now, we'll be having this debate a year from now, only the countries will be even more broken. (I said the same thing a year ago, and I expect to be saying it in 2008 and 2009 and ....)

Thousands of allied soldiers died during the invasions and the subsequent occupations of Afghanistan and Iraq. Many people are opposed to the idea to admitting we made a mistake because of the extreme sacrifices that these soldiers have made. They ask the tough question, "Does this mean that all those men and women died in vain?"

Yes. That's one of the unfortunate consequences of making a bad decision. While there was some justification for invading Afghanistan in 2001, we have overstayed our welcome and it's time for the Afghanis to settle their own internal squabbles.

But there was never any rational justification for invading Iraq. Most of us know that by now. Everyone who has died there has died in vain—including tens of thousands of innocent Iraqi citizens. It's sad to have to admit this, especially when talking to the friends and loved ones of fallen soldiers, but pretending it ain't so isn't going to help. You can't use the fact that soldiers died unnecessarily as an excuse to send more troops into battle.

Happy Sir John A. Macdonald Day!

 
Sir John A. Macdonald became the very first Prime Minister of Canada on July 1, 1867. He is one of the Fathers of Confederation. (There were no mothers back then.)

Sir John A. was a hard-working, hard-drinking immigrant. He was born in Glasgow, Scotland in 1815 and he celebrated his birthday on January 11th. There are many stories about his drinking. Here's what Wikipedia says,

Macdonald was well known for his wit and also for his alcoholism. He is known to have been drunk for many of his debates in parliament. Two apocryphal stories are commonly repeated; the first describing an election debate in which Macdonald was so drunk he began vomiting violently on stage while his opponent was speaking. Picking himself up Macdonald told the crowd, "see how my opponent's ideas disgust me." The second version has Macdonald responding to his opponent's query of his drunkenness with "It goes to show that I would rather have a drunk Conservative than a sober Liberal."

In typical Canadian fashion, we honour our most famous Canadian (he's on the $10 bill) by going off to work. There's no holiday for Canadians on January 11th. You celebrate by raising a glass of scotch when you get home in the evening, or maybe at lunch.

Now, don't get me wrong. I appreciate the fact that our government at least gives us a day off to celebrate the birthdays of two other famous people: Queen Victoria and Jesus. But they're not Canadians.

SBC - NC'07

 
I'm going to the 2007 North Carolina Science Blogging Conference. Are you?

Nobel Laureates: Richard Axel and Linda B. Buck

 
The Nobel Prize in Physiology or Medicine 2004.

"for their discoveries of odorant receptors and the organization of the olfactory system"

Richard Axel and Linda B. Buck won the Nobel Prize for discovering olfactory receptor genes. They showed that mice have about 1000 different olfactory receptor genes, each one encoding a different receptor.

You can watch a video recording of the acceptance speeches or read them as PDF documents [Axel Lecture][Buck Lecture].

Oh My God!

 
This is a photograph taken by Zarna, one of my students who just came back from a trip to India.

The Difference Between Rationalism and Superstition

 
Bill Dembski's Comments About Comments.

I don’t plan on policing or editing comments. If you post a comment that I don’t think is productive, I’ll probably not just eliminate your comment but you from this blog (which, given the way WordPress handles comments, means all your comments will be removed). So if you have any doubts about whether I’m going to react negatively to your comments, back them up — I won’t. Note also that I’ve had it happen where someone ingratiates himself with me and then turns. Bait and switch is a sure way to be banned from commenting here.

My policy on comments: anyone can post whatever they like, especially if they disagree. There will be no censorship of ideas on Sandwalk.

Darwin's Grave

 
Mike Dunford visited Westminster Abbey today and stood at the place where Charles Darwin is buried. He wonders what an agnostic should do under those conditions. See A Strange Moment.

Here's a photo of Darwin's final resting place in Westminster Abbey.

A Sense of Smell: Olfactory Receptors

 
The sense of smell in vertebrates is mediated by proteins called olfactory receptors (OR). In the case of mammals, these proteins are embedded in the membranes of sensory neurons in the nasal cavity. Each neuron is thought to contain a single type of olfactory receptor responding to a single type of odorant.

When an odorant binds to the outside of the olfactory receptor it transmits a signal to the interior of the cell. This signal triggers a response that excites the neuron and causes it to pass a message back along the axon to the brain. The brain then interprets the excitation as a specifc odor.

Olfactory receptors belong to a class of proteins called G-protein coupled receptors (GPCR). These proteins possess a characteristic bundle of seven membrane-spanning α-helices forming a tube within the membrane. The binding site for the specific odorant is located within the tube.

It has not been possible to crystallize any of the GPCR's that have been identified but the structures of some similar proteins are known. This enables workers to predict the structure of olfactory receptors using computer models. The models are then tested in various ways to confirm the predictions. We have a pretty good idea of what the olfactory receptors look like.

An example is shown in the figure on the left from a paper by Hall et al. (2004). This is the predicted structure of a mouse olfactory receptor that binds octanol. (Octanol is a sweet-smelling alcohol.) The bound molecule is shown as a red stick model in the side view (left) and the top view (right). The outside of the cell is at the top and that's where the odorant penetrates to the binding site.

The seven coils that you see in the structure are the seven α-helices that span the membrane. When the odorant binds, it changes the structure of the protein a little bit and this slight change includes the part of the receptor at the bottom, which is inside the cell. The change is enough to affect the binding of another protein, called a G-protein. This is what triggers the response.

Many different kinds of receptors activate a signalling pathway in the same manner as the olfactory receptors. A typical example is shown in the diagram below. In this case the signal is triggered by a hormone, but the same principle applies to signals triggered by odorants.


Look at the stimulatory pathway on the left. This is how the olfactory receptors work. When an odorant binds, the conformational change is transmitted through the receptor (R_s) to the inside surface of the membrane. G-protein (green) normally binds to the bottom surface of the receptor but when the receptor is triggered, G-protein is released and moves over to bind to another membrane protein called adenylate cyclase. The release and movement of G-protein is coupled to exchange of GDP for GTP. (GTP is a nucleotide like ATP. The proteins are called G-proteins because they bind GDP/GTP.)

Adenlyate cyclase is an enzyme that catalyzes the conversion of ATP to cyclic AMP (cAMP). cAMP in turn activates an enzyme called protein kinase A. Kinases are enzymes that attach phosphate groups to proteins. In this case, protein kinase A phosphorylates a protein within the neurons converting it from an inactive to an active form. Eventually the signal is transmitted to membrane pumps that are stimulated to alter the flow of charged ions into and out of the cell. This results in an action potential that passes up the axon to the brain.

This is a classic signal transduction pathway. The example shown in the figure is a simplified version with only a single protein kinase phosphorylation. In most cases there is a cascade of phosphorylations (and dephosphrylations) involving a number of different proteins. The study of signal transduction cascades is a major focus of hundreds of biochemistry labs.

The net result of all this biochemistry is that the presence of an odorant in your nose will eventually cause your brain to recognize it, as long as you have a receptor for that odorant. We have 388 different olfactory receptors so we can detect lots of different smells, including cat urine. Mice have 1037 different olfactory receptors so they can probably smell things that we can't. Maybe they can smell cats directly.

The olfactory receptor genes were discovered by Linda Buck and Richard Axel in 1991. They got the Nobel Prize in 2004 (see tomorrow's "Nobel Laureates").

The evolution of these genes in vertebrates raises some interesting questions about mechanisms of evolution. We'll learn about birth-and-death evolution later on this week.

Hall, S., Floriano, W.B., Vaidehi, N. and Goddard III, W.A. (2004) Predicted 3-D Structure for Mouse 17 and Rat 17 Olfactory Receptors and Comparison of Predicted Odor Recognition Profiles with Experiment. Chem. Senses 28: 595-616.

The Smell of Cat Pee

 
Most mammals have a keen sense of smell. That's why urinary odorants and pheromones are used to attract mates and mark territory. In most cases we can't detect these odors but there's one major exception.

The urine of cats contains chemicals that are easily detectable by humans. The smell is not pleasant. Mature cats will spay almost anything to stake out their territory, especially males). This isn't a problem if it's outdoors but it can be a major problem for indoor cats because carpets and spraying are not a good mix.

The urine of mature cats contains a chemical known as felinine (2-amino-7 -hydrozxy-5, 5-dimethyl-4-thiaheptanoic avid). Felinine excretion is stimulated by the hormone testosterone, which isn't produced until the cat reaches maturity. Both male and female cats excrete felinine in their urine but males typically excrete twice as much.

Felinine is odorless, to us. A recent paper (October 2006) describes how it is made and how it is converted to more pungent compounds.

The biochemical pathway leading to felinine begins with 3-methylbutanol- glutathionine (3-MBG) (compound A in the figure below). 3-MBG is a normal precursor in the synthesis of cholesterol but in cats some of it is converted to 3-methylbutanol-cysteinylglycine (3-MBCG) (compound B) by a pepdidase activity that removes glutamate. This reaction takes place in the bloodstream and 3-MBCG is excreted in the urine in cats of from the time they are born.

Mature cat urine contains high levels of protein, 90% of which is a medium-sized protein (70kDa) called cauxin. Cauxin levels rise as the cats reach maturity because transcription of the gene is stimulated by sex hormones. Cauxin is produced only in kidney cells and is secreted directly into the urine. The novel finding is that cauxin is a peptidase that cleaves 3-MBCG producing felinine (compound C). What this means is that production of felinine from 3-MBCG takes place in urine, probably in the nephrons before urine is released into the bladder.

Felinine breaks down into a number of smaller compounds that give rise to the characteristic smell of cat urine. The main breakdown product is 3-mercapto-3-methy-1-butanol formed by splitting felinine at the sulfur atom. Other breakdown products are formed. The complex mixture of derivatives is probably produced by a combination of unknown enzymatic act ivies and spontaneous reactions. The characteristic odor of domestic cats differs from that of lynx and bobcats and the differences are due to the concentrations of the various breakdown products of felinine.

Miyazaki, M., Yamashita, T., Suzuki, T., Saito, Y., Soeta, S., Taira, H., and Suzuki, A. (2006) A Major Urinary Protein of the Domestic Cat Regulates the Production of Felinine, a Putative Pheromone Precursor. Chemistry & Biology 10: 1071-1079.