SCIENCE Questions: What Is the Biological Basis of Consciousness?

 
"What Is the Biological Basis of Consciousness?" is one of the top 25 questions from the 125th anniversary issue of Science magazine [Science, July 1, 2005]. The complete reference is ...

Miller, Greg (2005) What Is the Biological Basis of Consciousness? Science 309: 79.
[Text] [PDF]

Greg Miller is a news writer for Science. He begins by describing the classic mind/body problem in philosophy. Rene Descartes claimed that mind and body were two separate things.

Recent scientifically oriented accounts of consciousness generally reject Descartes's solution; most prefer to treat body and mind as different aspects of the same thing. In this view, consciousness emerges from the properties and organization of neurons in the brain. But how? And how can scientists, with their devotion to objective observation and measurement, gain access to the inherently private and subjective realm of consciousness?

This is a slippery slope. The real question is "Does Consciousness Exist?" There's no point in asking about the biological basis of something until you establish that the "something" actually exists. As Miller hints in his introduction, consciousness could be just an epiphenomenon—a kind of illusion that's produced when a brain operates.

If that's true then the right question would be something like "How Are Memories Stored and Retrieved?" As it turns out, that is one of the top 25 questions, but it's not this one.

The article ends by pointing to promising lines of research that might arise from asking the "right" question.

Ultimately, scientists would like to understand not just the biological basis of consciousness but also why it exists. What selection pressure led to its development, and how many of our fellow creatures share it? Some researchers suspect that consciousness is not unique to humans, but of course much depends on how the term is defined. Biological markers for consciousness might help settle the matter and shed light on how consciousness develops early in life. Such markers could also inform medical decisions about loved ones who are in an unresponsive state.

This is begging the question (in the old-fashioned sense of the phrase). The question we should be answering is not "why does consciousness exist?" but "does consciousness exist?" I don't think it does exist, so naturally this ranks as a very silly question as far as I'm concerned.

The statement that "some researchers suspect that consciousness is not unique to humans" is very disturbing. It implies that most workers think otherwise, as does Greg Miller. Personally, I'm not aware of any serious research scientist who thinks that "consciousness" (if it exists) is something that only a human possesses and not a chimpanzee or even (gasp!) an octopus. (Readers are invited to post the names of anyone who thinks otherwise.)

And the idea that there might be "biological markers for consciousness" seems to portray sloppy thinking at best and profound misunderstanding at worst.

Questions about how the brain works rank right at the top of my list of important questions. This question is not one of those. It is badly formulated and the explanation in the article makes it even worse.

SCIENCE Questions: Why Do Humans Have So Few Genes?

"Why Do Humans Have So Few Genes?" is one of the top 25 questions from the 125th anniversary issue of Science magazine [Science, July 1, 2005]. The complete reference is ...

Pennisi, Elizabeth (2005) Why Do Humans Have So Few Genes? Science 309: 80. [Text] [PDF]

Elizabeth Pennisi is a news writer for Science magazine. She has been publishing articles there for at least ten years. She had previously written about genes and genomes, including earlier articles about the number of genes in the human genome.

Pennisi begins with the usual mythology about how surprised scientist were to discover that humans had fewer than 30,000 genes [see Facts and Myths Concerning the Historical Estimates of the Number of Genes in the Human Genome]. She continues by using most of the standard excuses for the Deflated Ego Problem [The Deflated Ego Problem].

That big surprise reinforced a growing realization among geneticists: Our genomes and those of other mammals are far more flexible and complicated than they once seemed. The old notion of one gene/one protein has gone by the board: It is now clear that many genes can make more than one protein. Regulatory proteins, RNA, noncoding bits of DNA, even chemical and structural alterations of the genome itself control how, where, and when genes are expressed. Figuring out how all these elements work together to choreograph gene expression is one of the central challenges facing biologists. [Numbers 1,2,5,6,7]

It's downhill from then on. Pennisi goes on to briefly describe the leading contenders for solving the imaginary problem. Not once does she mention that these have all been challenged in the scientific literature and not once does she mention that they are not specific to humans even though they must be if they're going to get you out of the pickle.

Is this one of the "right" questions that I talked about earlier? [SCIENCE Questions: Asking the Right Question] Nope. Not even close. In fact, it's a very "wrong" question that reflects an ignorance of the scientific literature and a profound misunderstanding of evolution, developmental biology, and gene expression. Humans have exactly the number of genes that we expect. They don't need to have many more genes than fruit flies or worms because a small number of unique genes are all that's required to make significant differences in development. They don't need to have special complexity mechanisms to "explain" anything because there's nothing that needs explaining. Human genes are fundamantally the same as those in Drosophila melanogaster (fruit fly), Caenorhabditis elegans (nematode worm), and Arabidopsis thaliana (a small flowering plant).

This "top 25 question" illustrates exactly the problem that I alluded to earlier. You don't recognize the important questions in science by polling science writers and editors. The "right" questions are the ones being asked on the frontiers by the creative experts who are thinking outside the box. This is an "inside the box" question and very few of those ever turn out to be important.

The right question would have been "Why Were You Surprised?"

SCIENCE Questions: Asking the Right Question

 
In July 2005 Science magazine published a list of the top questions in science [Science, July 1, 2005]. I was reminded of this list when I attended a meeting last month because the publishers of Science were handing out a special isue devoted to those questions. There are two categories; the top 25 questions, and 100 other questions. (It was the 125th aniversary of the magazine, hence 125 questions.)

I'd like to spend some time discussing those questions because not only are they interesting from a scientific point of view but they also reveal a great deal about science journalism and the public perception of science.

The issue began with an essay titled "In Praise of Hard Questions." The author, science writer Tom Siegfried, notes that hard questions stimulate science. He says,

The pressures of the great, hard questions bend and even break well-established principles, which is what makes science forever self-renewing—and which is what demolishes the nonsensical notion that science's job will ever be done.

Everyone agrees with the sentiment behind this statement. We all know that asking the right questions is the essence of good science. We all know that hard questions challenge prevailing models. On the other hand, we also know that there is such a thing as a stupid question in spite of what your Professors might have told you. Stupid questions can mislead scientists and stiffle creativity.

The opening article quotes David Gross, the 2004 Nobel Laureate in Physics who says,

One of the most creative qualities a research scientist can have is the ability to ask the right questions.

So, what are the "right" questions to ask? In my experience, the "right" questions are not immediately obvious. As stated above, they often challenge the prevailing dogma and this means that in the beginning they are dismissed as silly questions. Over time, the idea that this is a good question becomes more and more acceptable until finally it starts to stimulate active research.

What this means is that at any given point in time the "right" questions are only known to a few scientists on the cutting edge. These are ones who have begun to understand that the old questions aren't working any more. The vast majority of scientists will be sticking with the paradigm that's about to be overthrown. If you were to take a vote they would overwhelmingly dismiss the very questions that need to be asked.

Now, don't get me wrong. This is the way science is supposed to work. We all know that 99.9% of all attacks on orthodoxy deserve to be dismissed. The wonderful thing about science is that the 0.1% of "right" questions will almost certainly bubble to the surface. The real tricky part is picking out that 0.1% in advance.

So, if you were the editors of Science magazine how would you identify the important questions in science without falling into the trap of reinforcing orthodoxy and missing those very questions that a small group of experts are beginning to pay attention to? One way would be to seek out those experts and ask their opinion. This seems to be what is being advocated in the lead article where Tom Siegfried says,

Science's greatest advances occur on the frontiers, at the interface between ignorance and knowledge, where the most profound questions are posed. There's no better way to assess the current condition of science than listing the questions that science cannot answer.

But, Science magazine did not ask the experts at the frontiers. The actual procedure is explained in the editorial accompanying the July 1, 2005 issue. According to editors Donald Kennedy and Colin Norman, here's what they did.

We began by asking Science’s Senior Editorial Board, our Board of Reviewing Editors, and our own editors and writers to suggest questions that point to critical knowledge gaps. The ground rules: Scientists should have a good shot at answering the questions over the next 25 years, or they should at least know how to go about answering them. We intended simply to choose 25 of these suggestions and turn them into a survey of the big questions facing science. But when a group of editors and writers sat down to select those big questions, we quickly realized that 25 simply wouldn’t convey the grand sweep of cutting-edge research that lies behind the responses we received. So we have ended up with 125 questions, a fitting number for Science’s 125th anniversary.

The "right" questions were selected by editors and science journalists. I'm going to examine some of these questions in the next few days, concentrating exclusively on biology questions. Let's see how well they did when asked to identify the top "hard" questions in science.

The Deflated Ego Problem

"How humans get away with having a small genome"

Believe it or not, that's actually the subtitle of a short article in this month's issue of SEED (June, 2007). Who knew that humans have a small genome?

The author, Yohannes Edemariam, is a frequent contributor to SEED. He lives here in Toronto. Edemariam begins with the usual mythology designed to make you think there's a problem with the human genome [see Facts and Myths Concerning the Historical Estimates of the Number of Genes in the Human Genome]. This "problem" cries out for an explanation ...

Given our complexity—our capabilities for abstract thought, language, the building of civilizations—biologists were surprised at the relatively small number of genes we possess when they first began studying the human genome. It has since been become clear that our 20,000 to 25,000 genes can be manipulated by processes that statistically enhance the variety of ways in which each gene becomes manifest in our physical makeup.

This is typical of the rhetoric that pervades the popular science literature and, more importantly, the real scientific literature. The scientific evidence shows that our genome has about 25,000 genes and that's not much more than nematode worms or fruit flies. What this tells us is the same message that developmental biologists have been shouting for 35 years—small changes can have big effects. Clearly, some people haven't been listening.

The human chauvinists are disappointed that our genome isn't as complex as our brains and behavior suggest (to them). They expected to see tangible evidence that humans were at the top of the heap. I call this "The Deflated Ego Problem." The question before us is whether this is a real scientific problem or whether it stems from an incorrect understanding of evolution and development.

Having barely survived a major blow to their ego when the human genome turned out to have fewer than 30,000 genes, the deflated ones have fought back with various schemes to explain the "paradox." What they look for is some special mechanism that we humans possess in order to get a bigger bang for our buck. In other words, they're looking for their missing complexity in other places.

Ironically, the chauvinists don't realize that their "problem" can only be solved by discovering hithertofore unknown mechanisms that are confined to humans, or possibly mammals. The reason is obvious. If the mechanism is universal then fruit flies and worms have it as well and we can't use the new-found genome complexity to rationalize why we have so few genes compared to them. After all, the goal here is to explain why we only have a few thousand genes more than those "simple," "primitive," species and the explanation won't work if we all have the same complexity-generating mechanisms. I say "ironically" because many of the special mechanisms being proposed were first discovered in these "primitive" species. Now they're being used to solve the Deflated Ego Problem.

So, what are these magical complexity-generators that "statistically enhance the variety of ways in which each gene becomes manifest ...?" Are they going to solve the Deflated Ego Problem?

I'm not going to tell you which one is being promoted in the SEED article. You'll have to buy the magazine—which I highly recommend in spite of its flaws—to find out the answer. Here's the latest list of the sorts of things that may salvage your ego if it has been deflated.

1. Alternative Splicing: We may not have many more genes than a fruit fly but our genes can be rearranged in many different ways and this accounts for why we are much more complex. We have only 25,000 genes but through the magic of alternative splicing we can make 100,000 different proteins. That makes us almost ten times more complex than a fruit fly. (Assuming they don't do alternative splicing.)

2. Small RNAs: Scientists have miscalculated the number of genes by focusing only on protein encoding genes. Our genome actually contains tens of thousands of genes for small regulatory RNAs. These small RNA molecules combine in very complex ways to control the expression of the more traditional genes. This extra layer of complexity, not found in simple organisms, is what explains the Deflated Ego Problem.

3. Pseudogenes: The human genome contains thousands of apparently inactive genes called pseudogenes. Many of these genes are not extinct genes, as is commonly believed. Instead, they are genes-in-waiting. The complexity of humans is explained by invoking ways of tapping into this reserve to create new genes very quickly.

4. Transposons: The human genome is full of transposons but most scientists ignore them and don't count them in the number of genes. However, transposons are constantly jumping around in the genome and when they land next to a gene they can change it or cause it to be expressed differently. This vast pool of transposons makes our genome much more complicated than that of the simple species. This genome complexity is what's responsible for making humans more complex.

5. Regulatory Sequences: The human genome is huge compared to those of the simple species. All this extra DNA is due to increases in the number of regulatory sequences that control gene expression. We don't have many more protein-encoding regions but we have a much more complex system of regulating the expression of proteins. Thus, the fact that we are more complex than a fruit fly is not due to more genes but to more complex systems of regulation.

6. The Unspecified Anti-Junk Argument: We don't know exactly how to explain the Deflated Ego Problem but it must have something to do with so-called "junk" DNA. There's more and more evidence that junk DNA has a function. It's almost certain that there's something hidden in the extra-genic DNA that will explain our complexity. We'll find it eventually.

7. Post-translational Modification: Proteins can be extensively modified in various ways after they are synthesized. The modifications, such as phosphorylation, glycosylation, editing, etc., give rise to variants with different functions. In this way, the 25,000 primary protein products can actually be modified to make a set of enzymes with several hundred thousand different functions. That explains why we are so much more complicated than worms even though we have similar numbers of genes.

I don't think any of these explanations are valid because I don't think there's a problem that need explaining in the first place. I wish scientists and science writers would stop pretending that the Deflated Ego Problem is a real scientific problem and I wish they'd stop promoting their favorite, logically flawed, arguments to defend it.

Since that ain't going to happen, I'd like to offer a bit of advice designed to spare us from rhetorical overload. Here's a little template that all science writers can use next time they're tempted to write about this "problem."

(I/we/the authors) believe that the Deflated Ego Problem is a real scientific problem. (I/we/the authors) propose that explanation number (1/2/3/4/5/6/7) will account for the fact that we have too few genes.

What kind of atheist are you?

 

You scored as Scientific Atheist, These guys rule. I'm not one of them myself, although I play one online. They know the rules of debate, the Laws of Thermodynamics, and can explain evolution in fifty words or less. More concerned with how things ARE than how they should be, these are the people who will bring us into the future. Scientific Atheist 92% Militant Atheist 50% Agnostic 42% Theist 33% Angry Atheist 25% Spiritual Atheist 17% Apathetic Atheist 8% What kind of atheist are you? created with QuizFarm.com

I scored 42% agnostic. This is accurate in spite of what John Wilkins thinks. There's nothing wrong with being an agnostic atheist. I'm in good company with Richard Dawkins and PZ Myers. Please, let's drop this silly idea that you have to be either an atheist or an agnostic.

I'm also agnostic about Santa Claus and the tooth fairy because I know I can't prove their non-existence. But I don't believe in them so I'm an asantaclausist and an athoothfairyist.

Bloggers in Toronto

 
A gaggle of science bloggers got together for dinner last night. From left to right they are: Jonathan Badger of T. TAXUS, Mona (back) of Science Notes, Eva Amsen (front) of easternblot, Andrew Staroscik (back) of Mixotrophy, Tara Smith (front) of Aetiology, John Logsdon (back) of Sex, Genes & Evolution and Chris Condayan from the American Society of Microbiology—the man behind Microbe WORLD.

Chris showed up with several bags of camera equipment and proceeded to interview everyone for his video podcasts on Microbe WORLD. It was a bit embarrassing to be asked about the most outstanding discovery in microbiology within the last ten years! There are so many.

Presumably Tara had a much better answer. That's her on the left being filmed in front of the Medical Sciences Building on the University of Toronto campus.

The group met in my office where they were introduced to Darwin, the talk.origins server. Everyone was suitably impressed (not). After some preliminary chit-chat we went outside to the front of the building where Chris set up his camera.

Then it was off to Baldwin street for Asian food and more conversation. We talked about all kinds of things ranging from Intelligent Design Creationism to science blogging and real science.

After three hours or so, we managed to solve most of the problems in the world so we decided to go home. Problem is, I can't remember the solutions. Hopefully someone took notes.

I had a wonderful time. Thanks to everyone who came to visit me.


Other versions of the event:
Dinner with science bloggers!
Mini-Blogger convention at ASM 2007
Science Bloggers Storm Toronto

Intelligent Design Creationism Is Anti-Science

 
I'm not saying that everyone who subscribes to Intelligent Design Creationism (IDC) is anti-science. There are some, like Michael Behe, Michael Denton, and Scott Minnich who are clearly not anti-science in any meaningful sense of the word. They're not personally guilty of the crime but they're intellectual cowards for not speaking out against the worst offenders.

There is a hard core of IDiots who are against everything that real science stands for. They attack evolution, for example, at every opportunity. They claim that "Darwinism," as they call it, is just plain wrong.

You can find this hard core of creationists in the usual places such as Post-Darwinist, Evolution News & Views, and Uncommon Descent. Most of the people who blog at those sites are supporters of Bill Dembski and Jonathan Wells and all the other kooks at The Discovery Institute.

You need only read their books to see how much Wells and Dembski hate science and how far they will go to discredit evolution. Anyone who stands under the big tent with those people will be assumed to condone their opinions of science.

The IDC crowd is now all a twitter over the Gonzalez case. Guillermo Gonzalez was recently denied tenure in the Physics Department at Iowa State University. His case is under appeal. Gonzalez is an Intelligent Design Creationist sympathizer and a Senior fellow at the Discovery Institute [Guillermo Gonzalez, Senior Fellow - CSC]. One suspects that Gonzales is anti-science. Either that or he is an intellectual coward for not speaking out against those who are anti-science.

The creationists are hoping to influence the outcome of the appeal by writing letters of support to the President of the University. They have also recruited right wing religious conservative politicians to speak out on behalf of Gonzalez.

At least they're being consistent. Their attack on the scientists at Iowa State is no different than their attack on all other scientists.

But, don't they get it? As a group who are known to be anti-science do the IDC's really think they're helping Gonzalez by confirming the worst fears of the tenure committee? Their stupid meddling has made it almost certain that Gonzales will be denied tenure. Or maybe it wasn't stupid at all. Maybe that's what they really want—a martyr.

I almost feel sorry for Gonzales. With friends like that ...

Tangled Bank #80

 
Read the 80th version of Tangled Bank at geek counterpoint.

Nobel Laureates: Alfred G. Gilman and Martin Rodbell

 
 
The Nobel Prize in Physiology or Medicine 1994.

"for their discovery of G-proteins and the role of these proteins in signal transduction in cells"



Alfred Gilman (1941- ) and Martin Rodbell (1925-1998) shared the Nobel Prize in 1994 for discovering G proteins [G Proteins Are Signal Transducers]. Here's the complete presentation speech.

Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,

It is not very strange that a car, a television set or some other complex device sometimes stops working. No, the extraordinary thing is that these devices usually work faultlessly. When it comes to the most complicated machine we know - the human body - it is less surprising that it sometimes breaks down and we become ill, than that it works at all. After all, our body consists of thousands of billions of individual units, which must cooperate perfectly. The cooperation between the individual building blocks in our body, our cells, runs so smoothly in every possible situation that we seldom have cause to reflect on what a tremendously sophisticated communication system is required. The cells communicate with each other using chemical signals, such as hormones; we know these quite well. But efficient communication requires not only that the right signals are sent: it also requires that those signals are received in a proper way and lead to the right type of action.

The cell is enveloped in a thin membrane, which effectively separates the cell's inside from its surroundings. Nonetheless, a chemical signal that reaches the outside of the cell can evoke changes in its inner machinery, changes suited to the needs of the cell and of the entire organism. Alfred G. Gilman and Martin Rodbell have studied this particular aspect of the communication problem.

About 25 years ago, Martin Rodbell and his colleagues decided to investigate how a chemical signal - a hormone - that came in contact with the outer surface of the cell membrane could bring about changes on the inside of the same membrane. They discovered that the transduction of signals across the cell membrane could be described as a three-step process. First the cell must recognize what kind of chemical signal is reaching it from other parts of the body - this requires what Rodbell called the discriminator. The last step in the signaling pathway is an amplifier, which ensures that the signal created inside the cell is strong enough to make something happen. The major breakthrough was Martin Rodbell's realization that there was a switch between these two steps, and that this switch, which he called the transducer, could be turned on by a high-energy compound, guanosine triphosphate. The letter G in G protein stands for guanosine triphosphate.

At this point, Alfred Gilman and his colleagues took over. Using a combination of genetic and biochemical techniques they managed, after a heroic effort, to isolate the G protein from all the other parts of the cell membrane. The workings of the protein could then be studied. Among other things, Gilman showed that the G protein works like a timed switch that allows the signal to go through just long enough. G proteins might perhaps be compared to those little gadgets that can be plugged into a telephone and that make it possible - with a phone call - to turn lamps on and off, start electric heaters, or draw curtains, depending entirely on what the gadget is connected to.

Today we know that every one of the components in the signaling pathway - discriminator, switch and amplifier - exists in several varieties. Each individual cell has its own specific array of components in the signaling pathway and thus has an almost unique way of reacting to the incoming signals. In other words, each cell differs as to which of the body's myriad signals it will recognize, how and for how long the signal will be passed on, and which of the cell's own internal machines will start (or stop) working.

When our eyes perceive the procession of "Parfait glace Nobel" at the Nobel Banquet, various G proteins in the retina cooperate to transmit sensations of color, or of light and shadow. The aroma of the food activates other G proteins in our nostrils. When we taste the parfait, yet other G proteins on the tongue come into play. When, finally, all these sensory impressions are analyzed and interpreted in the brain, many different G proteins play vital roles.

Alfred Gilman's and Martin Rodbell's discoveries not only help us understand the immense diversity that is the hallmark and prerequisite of all life, but also why our bodies sometimes function less perfectly, and we become ill. For example, it has been found that changes in the function of G proteins in the intestine explain the severe diarrhoea associated with cholera. Alterations in G proteins can also be detected in connection with many other diseases. It is a reasonable hope that when we understand more about what causes diseases, it will become easier to treat them.

Drs. Alfred G. Gilman and Martin Rodbell,

I've tried to give some impression of the impact of your discoveries in the biomedical community. It is a privilege and a pleasure to convey to you the warm congratulations of the Nobel Assembly of the Karolinska Institute, and to ask you to receive the Nobel Prize from the hands of His Majesty the King.

G Proteins Are Signal Transducers

 
Many membrane receptors interact with a family of guanine nucleotide- binding proteins called G proteins. G proteins act as transducers, the agents that transmit external stimuli to effector enzymes. G proteins have GTPase activity; that is, they slowly catalyze hydrolysis of bound guanosine 5′-triphosphate (GTP, the guanine analog of ATP) to guanosine 5′-diphosphate (GDP). GDP was Monday's Molecule #27.

When GTP is bound to G protein it is active in signal transduction and when GDP is bound to G protein it is inactive. The cyclic activation and deactivation of G proteins is shown below. The G proteins involved in signaling by hormone receptors are peripheral membrane proteins located on the inner surface of the plasma membrane.

Each protein consists of an α, a β, and a γ subunit. The α and γ subunits are lipid-anchored membrane proteins; the α subunit is a fatty-acyl anchored protein, and the γ subunit is prenyl-anchored protein. The complex of G_αβγ and GDP is inactive.

When a hormone–receptor complex diffusing laterally in the membrane encounters and binds G_αβγ it induces the G protein to change to an active conformation. Bound GDP is rapidly exchanged for GTP, promoting the dissociation of G_α-GTP from G_βγ. Activated G_α-GTP then interacts with the effector enzyme. For example, it can stimulate adenylyl cyclase in regulating glycogen metabolism or in causing a sense of smell.

The GTPase activity of the G protein acts as a built-in timer since G proteins slowly catalyze the hydrolysis of GTP to GDP. When GTP is hydrolyzed the G_α-GDP complex reassociates with G_βγ and the G_αβγ-GDP complex is regenerated. G proteins have evolved into good switches but very poor catalysts, typically having a k_cat of only about 3 min^-1.

G proteins are found in dozens of signaling pathways, including the adenylyl cyclase and the inositol–phospholipid pathways. An effector enzyme can respond to stimulatory G proteins (G_s) or inhibitory G proteins (G_i). The α subunits of different G proteins are distinct, providing varying specificity, but the β and γ subunits are similar and often interchangeable. Humans have two dozen α proteins, five β proteins, and six γ proteins.

What Is an Aggregator?

 
There are probably some people who don't know what an aggregator is. It's a feed reader, or a program that reads the news feeds from your favorite web site. This is how you can keep up with the news on all the important blogs like Sandwalk!

I use the Goggle Reader that's featured in the following video by commoncraft. It will teach you all you need to know about Really Simple Syndication (RSS). There are other readers that are just as good but I like the web based readers 'cause I can access them from several different computers.

Click To Play

There are two types of Internet users, those that use RSS and those that don't. This video is for the people who could save time using RSS, but don't know where to start.

[Hat Tip: Shelley Batts who used to read blogs the old fashioned way.]

Darwin misconceptions in textbooks slammed in biology journal

 
"Darwin misconceptions in textbooks slammed in biology journal" is the title of an article posted by Denyse O'Leary on Post-Darwinist. Here's what she says,

British ID blog Truth in Science features a critique of Darwin hagiography and misconceptions promoted in textbooks, published by Brit prof Dr. Paul Rees in the Journal of Biological Education. The critique aims at inaccurate accounts of Charles Darwin "found in many A-Level textbooks", identifying seven common misconceptions in twelve popular textbooks published in 12 popular textboks over the last 35 years. The .pdf of the article is here. A suitable addition to examples of ridiculous hagiography in trade books and exhibitions.

Here's the link to the actual article by Raul A. Rees [The evolution of textbook misconceptions about Darwin]. Let's look at the seven misconceptions to see how they help Denyse and the Intelligent Design Creationists.

1. Darwin was the first to propound the theory of evolution by natural selection. Rees argues that natural selection was discovered by others before Darwin, and not just Wallace. This is rather silly, in my opinion. I don't take issue with textbooks that say Darwin discovered the theory of natural selction.
2. Darwin created the concept of "survival of the fittest". The term was coined by Herbert Spencer in 1864—five years after the first edition of Origin of Sepcies. If textbooks actually state flat out that Darwin made up the term then they need to be changed. Very few do this.
3. Darwin travelled around the world on HMS Beagle and published On the Origin of Species on his return to England. Rees doesn't actually give any examples of this misconception. Instead he laments the fact that most textbooks don't emphasize the long delay (23 years) between returning to England and publishing On the Origin of Species. It would be nice if the textbooks got this right.
4. Darwin was an observant naturalist and made careful collections of specimens during his voyage. Rees wants to make the point that Darwin didn't recognize the evidence for natural selection in the material he collected on the Beagle voyage. This isn't very important but it would be nice if the textbooks placed more emphasis on the theory and recognized that it didn't just fall out of the data.
5. Darwin recognized the evolutionary significance of the adaptations shown by the Galapagos finches. It's not true that the Galapagos finches played an important role in developing the theory of natural selection. In fact, Darwin didn't appreciate the signficance until Gould pointed it out in 1837 and even then it took a while for Darwin to start using the finches as evidence for selection.
6. Darwin first heard that Alfred Russel Wallace had independently formulated a theory of evolution when he received a letter from him in 1858. This is essentiall correct. Rees wants textbooks to point out that the two had corresponded for several years.
7. Darwin and Wallace jointly presented papers on their ideas at a meeting of the Linnean Society in London in 1858. Wallace was in the Far East and Darwin was at home burying his son. It would be wrong for textbooks to state that they were both present at the meeting where their papers were read. Rees quotes from two textbooks published in 1984 and 1987 that imply otherwise. Tempest in a teapot.

How do these "misconceptions" affect evolution? Not at all. The IDiots would like to think that all criticism of Charles Darwin and his ideas represent evidence against evolutionary biology. They are fixated on Darwinism and events that happened 148 years ago when On the Origin of Species was first published.

Denyse O'Leary and her creationist friends seem incapable of understanding that modern evolutionary biology has moved far beyond anything that Darwin could have imagined. He is rightly credited with founding modern evolutionary biology but the scientific facts of evolution do not depend on any of the seven "misconceptions" that Paul A. Rees raises.

---

Rees, P.A. (2007) The evolution of textbook misconceptions about Darwin. J. Biol. Education 41: 53-55 [PDF]

American Society for Microbiology in Toronto

 
The American Society for Microbiology is meeting in Toronto this week. There are several bloggers and blog readers in town and we'll be getting together over the next few days. Email me at "sandwalk at "bioinfo dot med dot utoronto dot ca" if you'd like to join us.

Tara Smith did not have a great first day. Hopefully today will be better. Jonathan Badger had a much better first day. He even met a scientifically literate Canadian customs agent. (Let's not tell him that many custom agents are university students employed for the summer.) John Logsdon is landing right now but he hasn't announced it on his blog (yet).

Monday's Molecule #27

 
Today's molecule is an easy one. The trivial name will do since it's very well known but if you can supply the correct chemical name that would be good.

As usual, there's a connection between Monday's molecule and this Wednesday's Nobel Laureate(s). This one is very straightforward. The reward (free lunch) goes to the person who correctly identifies both the molecule and the Nobel Laureate(s). Previous free lunch winners are ineligible for one month from the time they first collected the prize. There are no ineligible candidates for this Wednesday's reward.

Comments will be blocked for 24 hours. Comments are now open.

Queen Victoria Day

 

Today is Victoria Day in Ontario. It's the day we celebrate Queen Victoria's birthday (she was actually born on May 24, 1819). In 2007 it's just a good excuse for a holiday.