How RNA Polymerase Binds to DNA

Most cells contain two forms of RNA polymerase. The "core" polymerase is the part that carries out transcription of a gene where the DNA sequence is copied to produce a single-stranded RNA molecule. The core polymerase binds DNA non-specifically as you might expect for a DNA binding protein that has to travel down a large number of different genes.

When transcription is terminated the core RNA polymerase is released. In order to start a new round of transcription, the core RNA polymerase has to be directed to bind at a promoter, defined as the specific DNA sequence where transcription is initiated. There are specific DNA binding factors that bind to promoters and to RNA polymerase. That's how they direct RNA polymerase to the place where transcription has to start. These factors bind first to core polymerase forming the second form of RNA polymerase called the holoenzyme.

The binding parameters of the E. coli core polymerase and the holoenzyme have been studied in detail. In E. coli cells there are several different versions of holoenzyme. Each one contains a different initiation factor that binds to a different series of promoters. The most common initiation factor is called σ⁷⁰ (sigma-70) and it binds to most of the promoters in the cell.

The steps in transcription initiation are shown in the figure. First, holoenzyme consisting of core polymerase + σ⁷⁰, binds non-specifically to any stretch of DNA. It then moves along the DNA in a one-dimensional search until it finds a promoter sequence. This is followed by a local unwinding of the DNA and synthesis of a short piece of DNA.

Subsequent steps (not shown) require the dissociation of the initiation factor (σ⁷⁰) and the formation of an elongation complex. RNA polymerase is then free to leave the promoter region and move down the gene making RNA.

THEME:
Transcription
The same kinds of parameters that we discussed yesterday are used to describe RNA polymerase binding [see DNA Binding Proteins and Repression of the lac Operon]. The core RNA polymerase by itself binds DNA non-specifically with an association, or binding, constant (K_a) of 10¹⁰ M^-1. This is very tight binding for a DNA binding protein. Once bound to DNA the core RNA polymerase dissociates very slowly (t_1/2 = 60 minutes).

The holoenzyme can also bind non-specifically. In this case the association constant is 5 × 10⁶ M^-1 and the complex dissociates rapidly (t_1/2 = 3 seconds). The holoenzyme binds specifically to promoter sequences with an association constant of 2 × 10¹¹ M^-1 and t_1/2 = 2 to 3 hours. Thus, the interaction of the initiation factor with core RNA polymerase has two effects: it decreases the affinity for random stretches of DNA and increases the affinity for the promoter sequence.

A typical E. coli cell contains about 5000 molecules of RNA polymerase. When the cells are growing rapidly, 2500 molecules will be bound to genes in transcription complexes. Another 1250 will be in initiation complexes of various sorts and most of the remaining RNA polymerase molecules (1200) will be bound to DNA non-specifically. Only a small number (~50) will be free in the cytoplasm.

Since the holoenzyme molecules are capable of initiating transcription on their own, a small number of the non-specifically bound molecules will accidentally transcribe short stretches of DNA. These spurious transcripts don't usually cause a problem since they are quite rare. Nevertheless, their presence means that much of the intergenic DNA in the E. coli genome is transcribed at one time or another.

Eukaryotic cells contain three different kinds of RNA polymerases [Eukaryotic RNA Polymerases]. Each one is much more complex that the bacterial enzymes but the principles of transcription initiation are the same.

In eukaryotes there are about a dozen general initiation factors for each of the different RNA polymerases. The ones for RNA polymerase II—the enzyme that transcribes protein-encoding genes—are called transcription factor IID (TFIID) etc. All of the factors are required for specific RNA polymerase binding at a promoter site and all of them associate with the core RNA polymerase to form a large holoenzyme complex. The eukaryotic general initiation factors do the same thing for eukaryotic core polymerase as the bacterial ones do for the bacterial RNA polymerase; they convert the complex to a specific DNA binding protein and lower its affinity for binding non-specifically.

As is the case in bacteria, a substantial number of holoenzyme complexes will be bound non-specifically to DNA at any one time. The proportion is much, much higher in mammalian cells because of the presence of so much junk DNA in the genome. This has the effect of soaking up a lot of holoenzyme complexes.

Since the holenzyme complexes, like those in bacteria, are capable of initiating basal levels of transcription, we should not be surprised to find spurious transciption in all parts of the genome. These transcript will be rare but they will come from any site where RNA polymerase holoenzme can bind.

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Bibliography

Bustamante,C., Guthold,M., Zhu,X., and Yang,G. (1999) Facilitated target location on DNA by individual Escherichia coli RNA polymerase molecules observed with the scanning force microscope operating in liquid. J. Biol. Chem. 274, 16665-16668.
Goodrich,J.A., Cutler,G., and Tjian,R. (1996) Contacts in context: promoter specificity and macromolecular interactions in transcription. Cell 84, 825-830.
Koleske,A.J. and Young,R.A. (1995) The RNA polymerase II holoenzyme and its implications for gene regulation. Trends Biochem. Sci. 20, 113-116.
Myer,V.E. and Young,R.A. (1998) RNA polymerase II holoenzymes and subcomplexes. J. Biol. Chem. 273, 27757-27760.
Ossipow,V., Tassan,J.P., Nigg,E.A., and Schibler,U. (1995) A mammalian RNA polymerase II holoenzyme containing all components required for promoter-specific transcription initiation. Cell 83, 137-146.
Pan,G., Aso,T., and Greenblatt,J. (1997) Interaction of elongation factors TFIIS and elongin A with a human RNA polymerase II holoenzyme capable of promoter-specific initiation and responsive to transcriptional activators. J. Biol. Chem. 272, 24563-24571.
Ricchetti,M., Metzger,W., and Heumann,H. (1988) One-Dimensional Diffusion of Escherichia-Coli Dna-Dependent Rna-Polymerase - A Mechanism to Facilitate Promoter Location. Proceedings of the National Academy of Sciences of the United States of America 85, 4610-4614.
Shimamoto,N. (1999) One-dimensional diffusion of proteins along DNA. Its biological and chemical significance revealed by single-molecule measurements. J. Biol. Chem. 274, 15293-15296.
Singer,P. and Wu,C.W. (1987) Promoter search by Escherichia coli RNA polymerase on a circular DNA template. J. Biol. Chem. 262, 14178-14189.
Singer,P.T. and Wu,C.W. (1988) Kinetics of promoter search by Escherichia coli RNA polymerase. Effects of monovalent and divalent cations and temperature. J. Biol. Chem. 263, 4208-4214.
von Hippel,P.H. (2007) From "simple" DNA-protein interactions to the macromolecular machines of gene expression. Annual Review of Biophysics and Biomolecular Structure 36, 79-105.
von Hippel,P.H. and Berg,O.G. (1989) Facilitated target location in biological systems. J. Biol. Chem. 264, 675-678.

Genetics and Race

 
John Hawks has some interesting things to say about genetics and race based on a New York Times article about David Goldstein. The article can be found at: A Dissenting Voice as the Genome Is Sifted to Fight Disease, and the Hawks' posting is at: David Goldstein profile.

Scientists are discovering more and more genetic differences between human races and this is starting to cause some problems as described in the New York Times article ...

Another pursuit that interests him, one of high promise for reconstructing human evolutionary history, is that of discovering which genes bear the mark of recent natural selection. When a new version of a gene becomes more common, it leaves a pattern of changes that geneticists can detect with various statistical tests. Many of these selected genes reflect new diets or defenses against disease or adaptations to new climates. But they tend to differ from one race to another because each human population, after the dispersal from Africa some 50,000 years ago, has had to adapt to different circumstances.

This newish finding has raised fears that other, more significant differences might emerge among races, spurring a resurrection of racist doctrines. “There is a part of the scientific community which is trying to make this work off limits, and that I think is hugely counterproductive,” Dr. Goldstein said.

John Hawks is an expert in these kinds of studies so it's interesting to read his comments. Note that there's no disagreement over the facts; races are genetically different. I disagree with Hawks and Goldstein on the cause of some of this variation. In my opinion they are placing too much emphasis on selection as the cause of variation between species and not enough emphasis on chance. Differences in ABO blood type frequencies, for example, are probably not due to selection.

At the end of his posting Hawks mentions a quotation from Theodosius Dobzhansky. This is a quotation that everyone should keep in mind as they enter the debate. You can find out more by reading a 2006 posting about Dobzhansky on continuing human evolution. Here's the actual Dobzhansky quotation from that posting ...

The chief reasons why so many people are loath to admit the genetic variability of socially and culturally significant traits are two. First, human equality is stubbornly confused with identity, and diversity with inequality, as though to be entitled to an equality of opportunity, people would have to be identical twins. Human diversity is not incompatible with equality. Secondly, it is futile to look for one-to-one correspondence between cultural forms and genetic traits. Cultural forms are not determined by genes, but their emergence and maintenance are made possible by the genetically conditioned human diversity

Let me sound a note of caution to those who wish to comment. The fact that humans races might be genetically different says absolutely nothing at all about equality and racism. For this thread only, I will delete any comments where the author is confused about this distinction. This is a discussion about science and whether some scientific investigations should be censored because they might be misinterpreted.

Hawks doesn't allow comments on his blog. This is such an interesting topic that I thought I'd mention it here to get some feedback.

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[Image Credit: The image is obviously the cover of Scientific American from December 2003. This is one of the most blatant examples of political correctness ever published in a prestigious journal and it's one more example of the decline of Scientific American. It doesn't take much to recognize that the faces on the cover are identical except for skin color. As if that's all there is to human populations.]

DNA Binding Proteins

Proteins that bind to DNA can be divided into two groups: those that bind to a specific DNA sequence and those that bind non-specifically. Proteins in the latter category include those required for DNA replication, repair, and recombination, as well as packaging proteins like the histones.

Proteins that bind to specific DNA sequences are often activators or repressors involved in regulating gene expression. These are proteins that interact with a short, well-defined, nucleotide sequence found near the start site for transcription. The purpose of this posting is to review some of the basic characteristics of such proteins using lac repressor as a well studied example.

The figure below shows the structure of a lac repressor dimer bound to DNA.


The rate and strength of binding of lac repressor to DNA has been the subject of many papers over the course of several decades. Lac repressor binds tightly to a specific DNA sequence at the beginning of the lac operon. When it is bound to DNA it prevents, or represses, transcription of the operon.

Now, here's the important point: all specific DNA binding proteins also bind DNA non-specifically. In many cases it's part of the search mechanism for the specific binding site. In the case of lac repressor, for example, the protein binds to any old place on the DNA molecule and slides along the DNA searching for a specific binding sequence. After sliding for a second or so it falls off and re-binds to another part of the DNA molecule.

Once the repressor finds its specific binding site it remains bound for about twenty minutes. In biochemical terms we say that it's bound half-life is 20 minutes. The strength of binding is described by an equilibrium binding constant (K_B) that reflects the ratio of free repressor to bound repressor. For lac repressor the binding constant is one of the highest measured for any DNA binding protein (= 10¹³ M^-1). What this means is that lac repressor binds very tightly to its specific binding site.

The equilibrium binding constant for non-specific binding is only 4 × 10⁴ M^-1. Thus, repressor binds nearly one billion (10⁹) times more strongly to its specific binding site than to any old stretch of DNA. That's very impressive. In fact, it's one of the largest differences known for any DNA binding protein. When bound non-specifically the half-life is measured in seconds. It falls off (dissociates) rapidly.

These measurements have interesting consequences. There are about ten repressor molecules in each cell (E. coli). At any given time one of them will almost certainly be at its binding site near the lac operon but the other nine will be bound to DNA somewhere else. There are millions of places where the repressor can bind non-specifically but only one where it can bind specifically.¹

Some of these non-specific binding sites will, by chance, resemble the sequence of the specific binding site so lac repressor will linger longer at those sites than at sites that are completely unrelated to the specific binding sites. The point is that even for a highly specific DNA binding protein like lac repressor, most of the protein is bound to other sites most of the time.

For lac repressor, this fundamental property doesn't have serious consequences but for activators it's a different story. An activator is a protein that binds near a gene and recruits RNA polymerase to the site where it can begin transcription. Since most activators will be bound to random DNA sequences most of the time, the chances of accidentally recruiting RNA polymerase to begin a spurious transcript are quite high. From what we know about basic biochemistry, we expect that random spurious transcription should be quite common.

Tomorrow we'll look at RNA polymerase binding in the presence and absence of a specific DNA binding activator.

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1. The specific binding sites are called operators. There are actually three different operator sequences to which lac repressor can bind but that doesn't make much different for the point I trying to make.

Random Genetic Drift Simulator

 
Here's a nice Java applet from Kent Holsinger at the University of Connecticut [Genetic Drift]. Thanks to Pascal for the link.

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It's the Leader, Stupid

 
Canada is in the middle of a federal election and the Liberal Party under Stéphane Dion is going to lose a lot of seats. The losses may even be enough to give our current Prime Minister, Stephen Harper of the Conservative Party, a majority.

This is not an election about the economy. It's not about Canada's foreign policy. It's not about the environment and the carbon tax of the Liberal party. It's not about health care and it's not about education.

It's about leadership. Stéphane Dion does not inspire confidence and a lot of Liberal supporters, including me, can't bring themselves to vote for him. We want him to resign as soon as possible and we're willing to vote for someone else in order to make sure that Dion gets the message.

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Monday's Molecule #88

 
For this week's quiz you need to identify the top molecule. The bottom one is a hint so you can get the correct molecule.

There's a connection between today's molecule and a Nobel Prize but the connection is indirect. I'm looking for the person who discovered the molecule. This person won the Nobel Prize for the discovery and for identifying the function but, as it turns out, the function was incorrect.

The first one to correctly identify the molecule and name the Nobel Laureate, wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first collected the prize. There are three ineligible candidates for this week's reward. You know who you are.

THEME:

Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Laureate(s) so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.

Correct responses will be posted tomorrow. I reserve the right to select multiple winners if several people get it right.

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

UPDATE: We have a winner! Dima Klenchin from the University of Wisconsin figured out that the molecule was cytochrome c from some organism. (It was tuna, Thunnus alalungo, PDB 5CYT.) The Nobel Laureate was difficult but Dima uses scientific reasoning to get the correct answer: Otto Warburg (1931). Congratulations Dima!

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The Michael Reiss Issue

 
I agree with Michael Reiss that we should challenge creationists head-on by debunking their claims in science class. When students bring up bogus objections to evolution we should make sure they understand why they are wrong. It's all part and parcel of teaching critical thinking—the main objective in education [see The Royal Society and Teaching Creationism].

Some people disagree. They think that even mentioning these bogus objections in class lends credence to creationism. This is what I call the Ostrich Approach to teaching.

The New Humanist has an article on the controversy [Creationism in schools row rumbles on]. Here's the issue as they see it.

The issue of creationism in class is a difficult one. Critics such as Kroto, Roberts and Dawkins are understandably wary of religious ideas being allowed anywhere near school science labs, especially at a time when creationist organisations and proponents of Intelligent Design are stepping up efforts to shoehorn their ideas into science curricula. But if we take Reiss at his word (and if you read the blog posted on the Guardian last week, it's clear he wasn't suggesting creationism should be taught), then wasn't he just pointing out that the classroom should be a forum for free and open debate, and teachers must be ready to enter discussion with their pupils, and put them right when the views they bring from home clearly contradict the overwhelming evidence for evolution? Isn't this part of the aim of education?

PZ Myers has weighed in against Reiss [Michael Reiss's big mistake]. According to PZ ...

Michael Reiss, the director of education, is pushing this idea with a noble and reasonable intent: he thinks it is the only way to reach some students who will shut off learning if their religious biases are challenged. Unfortunately, he's also suggesting that non-science/anti-science concepts should be specified as a course objective in science classes, he's buying into common creationist propaganda ploy, and he's asking for unwarranted deference for wrong ideas held for unscientific reasons by students. He argues for respecting misplaced concerns.

I don't agree with PZ. I think he misunderstands what Michael Reiss is advocating and, furthermore, I think he's projecting an American perspective on to teaching in the UK.

The New Humanist website is running a poll on the question. The poll asks for your views on Michael Reiss' opinion. The choices are:

• Outrageous – creationism has no place in schools and he should be removed from his post


• Irresponsible – no one wants to stifle debate, but his comments risk encouraging the encroachment of creationism into schools


• Misunderstood – his sensible comments on free debate were misrepresented by hysterical media


• Brave – In a scientific community hostile to religion, he has made a stand for open debate

So far 54% are calling for Reiss' dismissal and 41% say he is irresponsible. I voted for the third option on the assumption that "hysterical media" includes "hysterical bloggers."

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GrrlScientist on the Sandwalk

 
If you send me a picture of you on the Sandwalk I'll post it here. GrrlScientist recently visited Down House and took some pictures of the Sandwalk [Visiting Darwin's Home, Part 4: The Sandwalk].

She is very shy so there are no pictures of her, or Prof. Steve Steve, on the Sandwalk. In spite of that oversight, I'm stealing her pictures so I can share them with Sandwalk readers.

PZ and I visited Down House two years ago on a trip to London. We were away for about eight days and we also visited the Natural History Museum, Wesminster Abby (Darwin's tomb), Oxford, and a few historic pubs. I think the total cost was about $1500 each. I wonder how many people would be interested in such a trip if I (we?) were to organize another?

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The God Gene and Evolutionary Psychology

 
Most of you have heard about the God gene by now. Strictly speaking, it isn't a God "gene" but a God allele. It's the variant that makes you believe in God. According to its proponents, most people are homozygous for this allele. That's why it's not their fault.

Evolutionary psychology has lots of similar examples of behavioral genes that put the blame on genetics. Here's a short video that explains the idea of genes controlling behavior.

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[Hat Tip: John Wilkins, who doesn't find it funny because he's a reductionist mechanist and an adaptationist. ]

Illustrating Random Genetic Drift

 
John Hawks has been generating some graphs for his class in order to illustrate random genetic drift. See how he does it at Some genetic drift graphs with Mathematica.


The important point, which most students don't get, is that eventually one allele will become fixed in the population and the other will be eliminated for ever.¹

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1. In a simple two allele situation in a sexual population.

Gene Genie #37

 
The 37th edition of Gene Genie has been posted at The Genetic Genealogist [Gene Genie 37: Human Genomes Are a Dime a Dozen].

Welcome to the September 14, 2008 edition of Gene Genie! Bloggers have begun to pick up posting with the end of summer, and it seems like everyday there’s a bunch of new interesting posts about the human genome.

The beautiful logo was created by Ricardo at My Biotech Life.

The purpose of this carnival is to highlight the genetics of one particular species, Homo sapiens.

Here are all the previous editions .....

1. Scienceroll
2. Sciencesque
3. Genetics and Health
4. Sandwalk
5. Neurophilosophy
6. Scienceroll
7. Gene Sherpa
8. Eye on DNA
9. DNA Direct Talk
10. Genomicron
11. Med Journal Watch
12. My Biotech Life
13. The Genetic Genealogist
14. MicrobiologyBytes
15. Cancer Genetics
16. Neurophilosophy
17. The Gene Sherpa
18. Eye on DNA
19. Scienceroll
20. Bitesize Bio
21. BabyLab
22. Sandwalk
23. Scienceroll
24. biomarker-driven mental health 2.0
25. The Gene Sherpa
26. Sciencebase
27. DNA Direct Talk
28. Greg Laden’s Blog
29. My Biotech Life
30. Gene Expression
31. Adaptive Complexity
32. Highlight Health
33. Neurophilosophy
34. ScienceRoll
35. Microbiology Bytes
36. Human Genetic Disordrs
37. The Genetic Genealogist

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The Royal Society and Teaching Creationism

 
Michael Reiss is a practicing priest in the Church of England. He is also director of education in The Royal Society. Reiss wrote an article about teaching creationism in schools. The complete article was posted on guardian.co.uk [Science lessons should tackle creationism and intelligent design].

This article is stirring up a lot of controversy because many people are interpreting it to be support for teaching creationism as a scientific viewpoint. That's not how I interpreted it. I thought Michael Reiss was saying the same thing I advocate. Here is the relevant part of the article so you can judge for yourself.

I feel that creationism is best seen by science teachers not as a misconception but as a world view. The implication of this is that the most a science teacher can normally hope to achieve is to ensure that students with creationist beliefs understand the scientific position. In the short term, this scientific world view is unlikely to supplant a creationist one.

So how might one teach evolution in science lessons, say to 14 to 16-year-olds? Many scientists, and some science educators, fear that consideration of creationism or intelligent design in a science classroom legitimises them.

For example, the excellent book Science, Evolution, and Creationism published by the US National Academy of Sciences and Institute of Medicine, asserts: "The ideas offered by intelligent design creationists are not the products of scientific reasoning. Discussing these ideas in science classes would not be appropriate given their lack of scientific support."

I agree with the first sentence but disagree with the second. Just because something lacks scientific support doesn't seem to me a sufficient reason to omit it from a science lesson. When I was taught physics at school, and taught it extremely well in my view, what I remember finding so exciting was that we could discuss almost anything providing we were prepared to defend our thinking in a way that admitted objective evidence and logical argument.

So when teaching evolution, there is much to be said for allowing students to raise any doubts they have (hardly a revolutionary idea in science teaching) and doing one's best to have a genuine discussion. The word 'genuine' doesn't mean that creationism or intelligent design deserve equal time.

However, in certain classes, depending on the comfort of the teacher in dealing with such issues and the make-up of the student body, it can be appropriate to deal with the issue. If questions or issues about creationism and intelligent design arise during science lessons they can be used to illustrate a number of aspects of how science works.

The other approach is the one I call the "Ostrich" approach. It would ban all mention of creationism and refuse to even discuss any objections to evolution that students might have. This approach avoids the controversy altogether by claiming that creationism isn't science and therefore shouldn't be taught in science class.

That's just plain silly, in my opinion. We all know that creationist students have a lot of so-called "objections" to evolution and by ignoring them in evolution classes we are not doing our job. We need to face those "objections" and deal with them by explaining why they aren't scientific. If we don't do that, then we shouldn't be surprised when students accept the word of their pastor over that of their science teacher. You can be certain that their pastor doesn't limit his/her teaching to religion.

We agree that creationism isn't science. It's an attack on science and the best place to defend against such attacks is in a science class.

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[Hat Tip: RichardDawkins.net where you'll find plenty of discussion in the comments.]

How Should Scientific Societies Treat Religion?

 
The American Association for the Advancement of Science (AAAS) describes itself as ...

The American Association for the Advancement of Science,
"Triple A-S" (AAAS), is an international non-profit organization dedicated to advancing science around the world by serving as an educator, leader, spokesperson and professional association. In addition to organizing membership activities, AAAS publishes the journal Science, as well as many scientific newsletters, books and reports, and spearheads programs that raise the bar of understanding for science worldwide.

AAAS has taken a position on religion. It's position is that science and religion are compatible and it has no qualms about promoting religious scientists as spokepersons for their position. As far as I know, they do not have any publications representing the view of the majority of their members who are non-believers. The idea that science and religion may not be compatible isn't presented.

Should the AAAS, and other scientific societies take a stance on religion? And, if so, what position should they take? Should they try to raise the level of understanding of science by pointing out all those instances where religion attacks science or should they emphasize that, as science experts, they see no conflict with religion? I think that scientific societies should concentrate on those controversies where science is under attack and avoid taking a stance on the overall compatibility, or lack of compatibility, with religion [see Are Science and Religion Compatible? AAAS Says Yes].

The Royal Society is a similar organization in the UK and the Commonwealth.

The Royal Society, the national academy of science of the UK and the Commonwealth, is at the cutting edge of scientific progress.

We support many top young scientists, engineers and technologists, influence science policy, debate scientific issues with the public and much more. We are an independent, charitable body which derives our authoritative status from over 1400 Fellows and Foreign Members.

In Great Britain, unlike in America, there is at least debate on the issue of whether The Royal Society should take a position on religion. The latest round is an article posted on The Observer website, Our scientists must nail the creationists.

Robin McKie writes,

It is the duty of scientists to fight such onslaughts and be examples of rationality in a darkening world, it is argued. Hence the anger at the Royal Society for failing to firmly nail its colours to its mast. The organisation has a motto: 'Nullius in verba' (roughly, 'Take nobody's word for it'). In other words, verify everything by experiment and think for yourself. Both are noble aspirations. It is therefore baffling how an ordained minister - a man committed to believing the word of God without question - could have been asked to play a senior role in the society. Equally, the society's acceptance of money from the Templeton Foundation raises further concerns.

The Royal Society - which should set the fiercest of examples in its commitment to rationality - has shown worrying signs of spiritual sloppiness. (Its current president, Lord Rees, is a cosmologist who attends church 'as an unbelieving Anglican', it should be noted.) Those of a religious persuasion might welcome this softening. I would sound a note of caution, however. Britain is still a broadly secular society which guarantees freedoms not just to atheists but to all religions, no matter how few its adherents. If we follow the example of America then all are threatened by the rise of a powerful Christian right.

We badly need our premier scientific society to stand firm and present a clear vision of how our planet, our species, and the cosmos came into existence. It needs to be unequivocal about the wonders of nature as revealed through rational, scientific investigation. As Douglas Adams put it: 'Isn't enough to see that a garden is beautiful without having to believe there are fairies at the bottom of it too?'

Hear, hear.

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[Hat Tip: RichardDawkins.net]

Squirrel Smasher Ready to Go on Dec. 19, 2008

 
This just in from BBspot.

Dallas, TX – Scientists from the Evolutionary Acceleration Research Institute (EARI) announced that the first test of the Giant Animal Smasher (GAS) will begin on December 19, 2008, the 41st anniversary of the premiere of Dr. Dolittle.

Squirrel SmasherDr. Thomas Malwin, head of the research project, said, "The first test runs will only accelerate microscopic life-forms like bacteria and viruses to high speeds, but theoretically the GAS can handle animals as large as squirrels, hence the squirrel smasher moniker."

Biologists from around the globe hope the GAS will unlock the secrets of the so-called "Darwin particle" that could unlock the secrets to life.

"If we discover the Darwin particle we could possibly create new life-forms, or accelerate evolution to unimaginable levels," said Malwin.

Go to BBspot for more information.

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[Hat Tip: John Hawks]

Does Intelligent Design Have Merit?

 
Opposing Views has posted a debate on the question Does Intelligent Design Have Merit?. Here's the complete question ...

With about 70 billion stars and as many as 100 million life forms (at least here on Earth), the universe is a stunningly complex place. Did all of this matter evolve independently, or was it guided by a larger force – as proponents of intelligent design believe? With the debate raging in living rooms, classrooms and courtrooms, the stakes are high when it comes to determining intelligent design’s merit.

All the players are there so this is a good chance for everyone to see what the "debate" is all about. For the "yes" side we have the Discovery Institute (Casey Luskin), Michael Behe, and Jay Roberts. On the "no" side there's the National Center for Science Education, Americans United, and the Ayn Rand Center for Individual Rights.

Here's my take on some of the things that are being debated.

1. The question is whether intelligent design has merit and it presupposes that the formation of the universe was "guided by a larger force."¹ We all know that Intelligent Design Creationism is about religion and about God as a creator. That's not the question and any article that focus on whether IDC is religious and whether religious ideas should be taught in school are off topic. Same applies to whether IDC is unconstitutional in one country or another.


2. There are many definitions of "design" but it seems quite appropriate to use this word to describe at least some biological features. Richard Dawkins does it all the time. So the question isn't whether there is "design" in nature, it's how do you explain that design. Evolution is a perfectly reasonable explanation of "design" in nature. Any articles whose main point is that there is design in nature are completely useless. Let's stipulate that there is "design" in at least some parts of nature and get on with debating how best to explain that design.


3. In order for Intelligent Design Creationism to have merit it has to offer a reasonable explanation of design in nature. It's not sufficient to just say "God did it." We need to know when, where, and how God did it if it's going to count as an explanation for particular features. Any article that fails to do this isn't defending the proposition. Attacks on evolution do not count as Intelligent Design explanations for things like the bacterial flagella. If we don't see a single attempt on the "yes" side to offer a explanation, then IDC loses by default. It's just the same-old, same-old, cry-baby complaints about evolution that we've been hearing for decades.

I find it astonishing that after almost twenty years the Intelligent Design Creationists can't come up with any better arguments than what we see on this website. I find it mind-boggling that people like Casey Luskin are the best they can offer.

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1. The opening article from NCSE tries to deal with this in the first paragraph by saying, "The notion that the universe was created by God may have merit as a religious idea, but it has no merit as science. To some people, the phrase “intelligent design” evokes the belief that the universe, and especially human beings, were crafted by the guiding hand of a loving God. This is a belief shared by many people, including many scientists. NCSE takes no position on the merits of these religious beliefs, except to say that these are not scientific statements, and should not be presented as such." This is pretty dangerous territory. It essentially concedes that IDC has merit and that many scientists agree with it.