Facts Supporting Intelligent Design Creationism?

 
We all know that the Intelligent Design Creationist movement consists almost exclusively of attacks on science. The idea seems to be that if you can cast doubt on evolution then this is evidence in favor of God.

Some unnamed Professor has challenged students to come up with facts that support Intelligent Design Creationism. The only criterion is; "fact can be any observation in biology that is substantiated by publication in a scientific journal,"

Casey Luskin attempts to meet the challenge over on the Discovery Institute propaganda site, Evolution News & Views: Helping Students Answer a Professor's Challenge to "Find a Fact" That Supports Intelligent Design (Part 2).

Here's a list of "scientific" publications submitted by Luskin. I haven't read all of them but, of the ones I've read, there isn't a single one containing a fact that supports the existence of God, let alone evidence that he/she designed anything at all. Furthermore, many of them aren't from a scientific journal. It looks like Casey Luskin has goofed, once again.

Let me know if any of these publications contain evidence of Intelligent Design Creationism. Is this the best they can do? (I've put asterisks in front of the ones I've read.)

*Douglas D. Axe, "Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors," Journal of Molecular Biology, Vol. 301:585-595 (2000)

*Douglas D. Axe, "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds," Journal of Molecular Biology, 1-21 (2004)

*Michael Behe, Darwin's Black Box: The Biochemical Challenge to Evolution (Free Press, 1996)

*Michael J. Behe & David W. Snoke, "Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues," Protein Science, Vol 13:2651-2664 (2004)

Geoff Brumfiel, “Outrageous Fortune,” Nature, Vol. 439: 10-12 (Jan. 5, 2006)

Bract, "Inventions, Algorithms, and Biological Design," in Progress in Complexity, Information, and Design (Vol. 1.1, 2002)

*William A. Dembski, The Design Inference: Eliminating Chance Through Small Probabilities (Cambridge University Press, 1998)

a. William A. Dembski and Robert J. Marks II, “Conservation of Information in Search: Measuring the Cost of Success” (In publication, 2009)

b. William A. Dembski and Robert J. Marks II, “The Search for a Search: Measuring the Information Cost of Higher Level Search” (In publication, 2009)

*William Dembski and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Living Systems, (FTE, 2008) (see www.thedesignoflife.net)

*Wayt T. Gibbs, “The Unseen Genome: Gems among the Junk,” Scientific American (November, 2003)

Guillermo Gonzalez and Jay Wesley Richards, The Privileged Planet: How our Place in the Cosmos is Designed for Discovery, (Regnery, 2004)

*Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009)

Hiroaki Kitano, ”Systems Biology: A Brief Overview,” Science, Vol. 295: 1662-1664 (March 1, 2002)

Wolf-Ekkehard Lönnig, "Dynamic genomes, morphological stasis, and the origin of irreducible complexity," in Dynamical Genetics pp. 101-119 (Valerio Parisi, Valeria De Fonzo, and Filippo Aluffi-Pentini eds., 2004)

Casey Luskin, “Human Origins and Intelligent Design,” Progress in Complexity and Design, (Vol 4.1, November, 2005)

Casey Luskin, "Intelligent Design Has Scientific Merit in Paleontology," part of the "Does Intelligent Design Have Merit?" debate at OpposingViews.com (September, 2008)

*Wojciech Makalowski, “Not Junk After All,” Science, Vol. 300(5623) (May 23, 2003)

Stephen C. Meyer, Marcus Ross, Paul Nelson & Paul Chien, "The Cambrian Explosion: Biology's Big Bang," in Darwinism, Design, and Public Education (John A. Campbell and Stephen C. Meyer eds., Michigan State University Press, 2003)

*a. Stephen C. Meyer, “The Cambrian Information Explosion,” in Debating Design (edited by Michael Ruse and William Dembski; Cambridge University Press 2004)

b. Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings of the Biological Society of Washington, Vol. 117(2):213-239 (2004)

Scott A. Minnich & Stephen C. Meyer, “Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria,” in Proceedings of the Second International Conference on Design & Nature, Rhodes Greece (M.W. Collins & C.A. Brebbia eds., 2004)

Paul Nelson and Jonathan Wells, “Homology in Biology,” in Darwinism, Design, and Public Education, (Michigan State University Press, 2003)

*Richard v. Sternberg, "On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic– Epigenetic System," Annals of the New York Academy of Sciences, Vol. 981: 154–188 (2002)

J.T. Trevors and D.L. Abel, "Chance and necessity do not explain the origin of life," Cell Biology International, Vol. 28: 729-739 (2004)

D. L. Abel & J. T. Trevors, “Self-organization vs. self-ordering events in life-origin models," Physics of Life Reviews, Vol. 3: 211–228 (2006)

Øyvind Albert Voie, "Biological function and the genetic code are interdependent," Chaos, Solitons and Fractals, Vol. 28:1000–1004 (2006)

Jonathan Wells, "Using Intelligent Design Theory to Guide Scientific Research" Progress in Complexity, Information, and Design (Vol. 3.1.2, November 2004)

Jonathan Wells, "Do Centrioles Generate a Polar Ejection Force?," Rivista di Biologia / Biology Forum, Vol. 98:71-96 (2005)

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The Trouble with NCSE

 
I am a member of National Center for Science Education (NCSE). That does not mean I agree with everything they do. My biggest bone of contention is over their accommodationist tactics [National Academies: Science, Evolution and Creationism, Appeasers, Spaghetti Monsters, and NCSE].

I don't like the fact that NCSE cozies up to theistic evolutionists like Ken Miller and Francis Collins while, at the same time, actively distancing itself from vocal atheist scientists like Richard Dawkins. I think NCSE shouldn't takes side and shouldn't promote the idea that science and religion are compatible.

Jerry Coyne agrees. He has published a lengthy essay on his blog where he takes NCSE to task [Truckling to the Faithful: A Spoonful of Jesus Helps Darwin Go Down]. I have warned many people at NCSE that they risk losing the support of non-theist scientists but, for the most part, they think the risk is worth it.

I wonder if they still think that way?

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How to Evaluate Genome Level Transcription Papers

It's often very difficult to evaluate the results of large-scale genome studies. Part of the problem is that the technology is complicated and the controls are not obvious. Part of the problem is that the results depend a great deal on the software used to analyze the data and the limitations of the software are often not described.

But those aren't the only problems. We also have to take into consideration the biases of the people who write the papers. Some of those biases are the same ones we see in other situations except that they are less obvious in the case of large-scale genome studies.

Laurence Hurst has written up a nice summary of the problem and I'd like to quote from his recent paper (Hurst, 2009).

In the 1970s and 80s there was a large school of evolutionary biology, much of it focused on understanding animal behavior, that to a first approximation assumed that whatever trait was being looked at was the product of selection. Richard Dawkins is probably the most widely known advocate for this school of thought, John Maynard Smith and Bill (WD) Hamilton its main proponents. The game played in this field was one in which ever more ingenious selectionist hypotheses would be put forward and tested. The possibility that selection might not be the answer was given short shrift.

By contrast, during the same period non-selectionist theories were gaining ground as the explanatory principle for details seen at the molecular level. According to these models, chance plays an important part in determining the fate of a new mutation – whether it is lost or spreads through a population. Just as a neutrally buoyant particle of gas has an equal probability of diffusing up or down, so too in Motoo Kimura's neutral theory of molecular evolution an allele with no selective consequences can go up or down in frequency, and sometimes replace all other versions in the population (that is, it reaches fixation). An important extension of the neutral theory (the nearly-neutral theory) considers alleles that can be weakly deleterious or weakly advantageous. The important difference between the two theories is that in a very large population a very weakly deleterious allele is unlikely to reach fixation, as selection is given enough opportunity to weed out alleles of very small deleterious effects. By contrast, in a very small population a few chance events increasing the frequency of an allele can be enough for fixation. More generally then, in large populations the odds are stacked against weakly deleterious mutations and so selection should be more efficient in large populations.

In this framework, mutations in protein-coding genes that are synonymous – that is, that replace one codon with another specifying the same amino acid and, therefore, do not affect the protein – or mutations in the DNA between genes (intergene spacers) are assumed to be unaffected by selection. Until recently, a neutralist position has dominated thinking at the genomic/molecular level. This is indeed reflected in the use of the term 'junk DNA' to describe intergene spacer DNA.

These two schools of thought then could not be more antithetical. And this is where genome evolution comes in. The big question for me is just what is the reach of selection. There is little argument about selection as the best explanation for gross features of organismic anatomy. But what about more subtle changes in genomes? Population genetics theory can tell you that, in principle, selection will be limited when the population comprises few individuals and when the strength of selection against a deleterious mutation is small. But none of this actually tells you what the reach of selection is, as a priori we do not know what the likely selective impact of any given mutation will be, not least because we cannot always know the consequences of apparently innocuous changes. The issue then becomes empirical, and genome evolution provides a plethora of possible test cases. In examining these cases we can hope to uncover not just what mutations selection is interested in, but also to discover why, and in turn to understand how genomes work. Central to the issue is whether our genome is an exquisite adaption or a noisy error-prone mess.

Sandwalk readers will be familiar with this problem. In the context of genome studies, the adaptationist approach is most often reflected as a bias in favor of treating all observations as evidence of functionality. It you detect it, then it must have been selected. If it was selected, it must be important.

As Hurst points out, the real question in evaluating genome studies boils down to a choice between an exquisitely adapted genome or one that is messy and full of mistakes. The battlefields are studies on the frequency of alternative splicing, transcription, the importance of small RNAs, and binding sites for regulatory proteins.

Let's take transcription studies as an example.

Consider, for example, the problem of transcription. Although maybe only 5% of the human genome comprises genes encoding proteins, the great majority of the DNA in our genome is transcribed into RNA [1]. In this the human genome is not unusual. But is all this transcription functionally important? The selectionist model would propose that the transcription is physiologically relevant. Maybe the transcripts specify previously unrecognized proteins. If not, perhaps the transcripts are involved in RNA-level regulation of other genes. Or the process of transcription may be important in keeping the DNA in a configuration that enables or suppresses transcription from closely linked sites.

The alternative model suggests that all this excess transcription is unavoidable noise resulting from promiscuity of transcription-factor binding. A solid defense can be given for this. If you take 100 random base pairs of DNA and ask what proportion of the sequence matches some transcription factor binding site in the human genome, you find that upwards of 50% of the random sequence is potentially bound by transcription factors and that there are, on average, 15 such binding sites per 100 nucleotides. This may just reflect our poor understanding of transcription factor binding sites, but it could also mean that our genome is mostly transcription factor binding site. If so, transcription everywhere in the genome is just so much noise that the genome must cope with.

There is no definitive solution to this conflict. Both sides have passionate advocates and right now you can't choose one over the other. My own bias is that most of the transcription is just noise—it is not biologically relevant.

That's not the point, however. The point is that as a reader of the scientific literature you have to make up your mind whether the data and the interpretation are believable.

Here's two criteria that I use to evaluate a paper on genome level transcription.

1. I look to see whether the authors are aware of the adaptation vs noise controversy. If they completely ignore the possibility that what they are looking at could be transcriptional noise, then I tend to dismiss the paper. It is not good science to ignore alternative hypotheses. Furthermore, such papers will hardly ever have controls or experiments that attempt to falsify the adaptationist interpretation. That's because they are unaware of the fact that a controversy exists.¹
2. Does the paper have details about the abundance of individual transcripts? If the paper is making the case for functional significance then one of the important bits of evidence is reporting on the abundance of the rare transcripts. If the authors omit this bit of information, or skim over it quickly, then you should be suspicious. Many of these rare transcripts are present in less that one or two copies per cell and that's perfectly consistent with transcriptional noise—even if it's only one cell type that's expressing the RNA. There aren't many functional roles for an RNA whose concentration is in the nanomole range. Critical thinkers will have thought about the problem and be prepared to address it head-on.

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1. Or, maybe they know there's a controversy but they don't want you to be thinking about it as you read their paper. Or, maybe they think the issue has been settled and the "messy" genome advocates have been routed. Either way, these are not authors you should trust.

Hurst, L.D. (2009) Evolutionary genomics and the reach of selection. Journal of Biology 8:12 [DOI:10.1186/jbiol113]

Monday's Molecule #118: Winners

 
UPDATE: The molecule is cyclin-dependent kinase 2 (CDK2), a protein involved in signaling [PDB 1b38]. The Nobel Laureate is Paul Nurse.

This week's winners are Mike Fraser of Toronto and Alex Ling of the University of Toronto.

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This is a very famous protein but most of you won't be able to identify it from the structure alone. You'll need a hint of some sort.

Letting you know that the ligands are Mg²⁺ and adenosine-5′-triphosphate might not be enough so I'll also tell you that one of the authors on the structure paper was M.E. Noble.

There is one Nobel Laureate who is most closely identified with the function of this particular molecule, although that scientist was NOT the first to identify it. You have to identify the Nobel Laureate who got the prize for working out the function of the protein.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, and Maria Altshuler of the University of Toronto.

I note that Canadians are trouncing the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

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 Prizes 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.

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

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Sequenced genomes contain thousands of "unknown" genes

 
The total number of genes in the human genome has dropped from the initial estimates of 30-35,000 to about 25,000. Of these, more than 4,000 encode functional RNAs, leaving about 20,500 protein-encoding genes in the human genome [Humans Have Only 20,500 Protein-Encoding Genes].

Up to 40% of these protein-encoding genes are "unknown" in the sense that no function has been assigned to their protein products. In the jargon of genomics, the genes are "unannotated," meaning that nobody has assigned a function to the gene in the human genome database (Reichardt, 2007).

That means 8,000 unknown genes. About 1000 of these genes are "orphan" genes—genes that have no homologues in other species, including chimpanzees (Clamp, 2007).

Humans aren't unique. All sequenced eukaryotic genomes have a high percentage (~30-40%) of "unknown" protein-encoding genes.

A new paper in PLoS One looks at the "unknown" genes in the filamentous fungus Neurospora crassa (pink bread mold) (Kasuga et al. 2009). The Neurospora genome has about 9,000 protein-encoding genes and more than half of them have not been annotated. They are the "unkown" genes.

The genomes of about 40 different species of fungus have been sequenced and many of these are filamentous fungi related to Neuropsora. What this means is that it's possible to compare the Neurospora genes to those in many different genomes from closely related species; those that are part of the same family (less closelyrelated); part of the same phylum; and distantly related. You can't do such an extensive study with human genomes because there aren't very many mammalian genomes that have been sequenced and carefullyannotated. A draft sequence of the chimpanzee genome, for example, has been published but it is neither complete nor reliable enough for genomic comparisons. The only other primate genome is from macaque (Rhesus monkey) and that's far from finished. (The human and mouse genomes are the only ones listed as "complete" on the NCBI/Entrez website.)

The question is: are the unknown genes confined to Neurospora and its close relatives? If so, it would suggest that new genes have evolved within the past several million years and that's why we don't know their function.

Kasuga et al. created six sets of genes ...

1. Genes with homologs in distantly related eukaryotes and possibly prokaryotes. These are ancient genes.
2. Genes that are only found in fungi and not in plants or animals or protists (Dikarya).
3. Genes found only in Ascomycetes.
4. Genes confined to the Pezizomycotina clade to which Neurospora belongs.
5. Genes found only in Neurospora.
6. Others: genes that are found in some of the first groupings but not in all the smaller grouping.

The classification depends on the similarity cutoff. If the lowest cutoff is 25% sequence identity, then there will be more homologs in the eukarote or prokaryote class than if the cutoff is raised to 35%. The distibution of the various classes at each of three minimum sequence identify cutoffs is shown in their second figure.


Taking the 30% threshold numbers (middle group), it looks like there are 2,358 highly conserved genes with homologs in distantly related eukaryotes and prokaryotes. In contrast, there are 2,219 genes that don't have homologs in any other species. These are the orphan genes in Neurospora.

You might expect that most of the unknown/unannotated genes would be confined to Neurospora and closely related species. You might expect that highly conserved genes would be more likely to have been identified. That's partly true. Here are the numbers.


Only 16.5% of the highly conserved genes are mystery genes of unknown function. While this is much lower that the total (56%), it's still surprising that so many of the core genes remain unidentified. Presumably they are doing something very important. There are dozens of thesis projects available for talented graduate students who want to make a valuable contribution to biology.

It's not a surprise that 94% of the orphans are unannotated. These genes are likely to be new genes that have evolved recently in Neurospora and they would be expected to carry out unusual reactions that aren't found in other species. These "genes" are also the ones most likely to be artifacts (false positives) of the gene searching software. They may not be genes at all.

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[Image Credit: Neurospora-National Institute of General Medical Sciences]

Clamp, M., Fry, B., Kamal, M., Xie, X., Cuff, J., Lin, M.F., Kellis, M., Lindblad-Toh, K. and Lander, E.S. (2007) Distinguishing protein-coding and noncoding genes in the human genome. Proc. Natl. Acad. Sci. (USA) 104:19428-19433. [DOI 10.1073/pnas.0709013104]

Kasuga, T., Mannhaupt, G., and Glass, N.L. (2009) Relationship between Phylogenetic Distribution and Genomic Features in Neurospora crassa. PLoS ONE 4(4):e5286. [DOI:10.1371/journal.pone.0005286]

Reichardt, J.K.V. (2007) Quo vadis, genoma? A call to pipettes for biochemists. Trends in Biochemical Sciences (TIBS) 32:529-530. [DOI:10.1016/j.tibs.2007.10.001]

Conservative Spin

 

Canadian Cynic has built a career out of keeping an eye on The Blogging Tories. Every now and then CC comes up with something that makes you scratch your head and ask, "Can The Blogging Tories really be that stupid?"

Here's a posting from ErwinGerrits.com that will answer the question.

Funny how the current deficit budget is now universally referred to as “The Conservative Deficit”, even after this current budget was forced upon us by the Liberals, NDPers and the bloc-heads after a mid-winter stand-off on the Governour General’s front stoop. As I recall, the Conservative’s Economic Update, brought forward in December, did not make us go into a deficit at all. It was after the three stooges reared their ugly heads and blackmailed the country, that the current deficit budget was tabled.

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International team cracks mammalian gene control code

International team cracks mammalian gene control code

Stop the presses! Revise the textbooks! John Mattick and his collaborators have discovered how genes are controlled in mammals.

Anyone who knows Mattick's past history will know what's coming—Mattick overthrew the Central Dogma of Molecular Biology over six years ago (Mattick, 2003; Mattick, 2004).^1,2

An international consortium of scientists, including researchers from The University of Queensland (UQ), have probed further into the human genome than ever before.

They have discovered how genes are controlled in mammals, as well as the tiniest genetic element ever found.

Their discoveries will be published in three milestone papers in leading journal Nature Genetics.

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1. See Basic Concepts: The Central Dogma of Molecular Biology for the truth about the Central Dogma.

2. See Greg Laden Gets Suckered by John Mattick for an example of how easy it is to get fooled by John Mattick.

Mattick, J.S. (2003) Challenging the dogma: the hidden layer of non-protein-coding RNAs in complex organisms. BioEssays 25:930-939.

Mattick, J.S. (2004) The hidden genetic program of complex organisms. Sci. Am. 291:60-67.

Idiot America?

 
Oh dear, my accommodationist friends aren't gonna like this.

From the amazon.com site ....

The Culture Wars Are Over and the Idiots Have Won

A veteran journalist's acidically funny, righteously angry lament about the glorification of ignorance in the United States.

In the midst of a career-long quest to separate the smart from the pap, Charles Pierce had a defining moment at the Creation Museum in Kentucky, where he observed a dinosaur. Wearing a saddle.... But worse than this was when the proprietor exclaimed to a cheering crowd, “We are taking the dinosaurs back from the evolutionists!” He knew then and there it was time to try and salvage the Land of the Enlightened, buried somewhere in this new Home of the Uninformed.

With his razor-sharp wit and erudite reasoning, Pierce delivers a gut-wrenching, side-splitting lament about the glorification of ignorance in the United States, and how a country founded on intellectual curiosity has somehow deteriorated into a nation of simpletons more apt to vote for an American Idol contestant than a presidential candidate.

With Idiot America, Pierce's thunderous denunciation is also a secret call to action, as he hopes that somehow, being intelligent will stop being a stigma, and that pinheads will once again be pitied, not celebrated.

I can't wait for the sequel—Idiot Canada.

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[Hat Tip: Canadian Cynic]

Bob McDonald Explains why Canadian Scientists Are Upset

 
Bob McDonald is the host of Quirks & Quarks on CBC radio. He has a blog and here's part of what he posted on Friday [Another Earth Day, Canadian scientists concerned].

While people around the globe celebrate the beauty of our planet on Earth Day, April 22nd, scientists in Canada are concerned that government funding is heading in the wrong direction to provide sensible solutions to environmental problems. More than 2000 scientists from across the country have signed an open letter to Prime Minister Harper and the Leader of the Opposition, expressing concerns over cuts to basic science research. It’s basic science that takes the pulse of the planet.

The scientists are concerned that government money is overlooking vital areas. For example, the current Conservative budget allocates $2 billion for university infrastructure - in other words, renovations to aging buildings. But those funds come with a catch. They must be matched with private funding, something everyone is having trouble finding during these tough economic times. Keeping roofs on buildings is important, but if there are no scientists to work in them, what’s the point?

The Canada Foundation for Innovation, a major source of science funding, did receive $740 million, but it also comes with that match-funding hook. The other funding agencies, the Natural Sciences and Engineering Research Council and the Canadian Institutes of Health Research, have had their budgets cut back, while Genome Canada was essentially ignored.

The rest of the government’s support for science is going towards the automotive industry, carbon sequestration, biofuels and scholarships for business students. In other words, applied science is taking precedent over basic science.

While we do need both, when it comes to the environment, the two types of science are often at loggerheads.

Politicians like to support applied science because it leads to jobs and products, such as more efficient cars or new wireless devices. Basic science, on the other hand, can’t promise an immediate economic return because it simply looks at nature to understand how things work - and more importantly these days, how things are changing. As we’ve seen with climate change, basic scientists have been out in the field watching ice caps disappear before their eyes, carbon dioxide levels rise and climate patterns shift. At the same time, those dealing with the technology at the heart of the problem resist the basic science to keep the current systems in place.

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[Hat Tip: T. Ryan Gregory]

Monday's Molecule #118

 
This is a very famous protein but most of you won't be able to identify it from the structure alone. You'll need a hint of some sort.

Letting you know that the ligands are Mg²⁺ and adenosine-5′-triphosphate might not be enough so I'll also tell you that one of the authors on the structure paper was M.E. Noble.

There is one Nobel Laureate who is most closely identified with the function of this particular molecule, although that scientist was NOT the first to identify it. You have to identify the Nobel Laureate who got the prize for working out the function of the protein.

The first person to identify the molecule and the Nobel Laureate wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.

There are six ineligible candidates for this week's reward: Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, Devin Trudeau from the University of Toronto, Shumona De of Dalhousie University, and Maria Altshuler of the University of Toronto.

I note that Canadians are trouncing the rest of the world. That's as it should be.

I still have one extra free lunch donated by a previous winner to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.

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 Prizes 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.

Comments will be blocked for 24 hours.

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Agnotology

 
A reader (David) posted a comment about my recent Denyse O'Leary quotation. He alerted me to a new word: agnotology [Comments].

The Wikipedia entry is informative [agnolology agnatology] but there's lots more to learn about this word. Everyone is agreed that the word was invented by Robert Proctor a Standford University Professor who studies the history of science. Everyone is agreed that it refers to the study of ignorance, or why we don't know certain things. But there's more to it than that ....


Here's an excerpt from an article by Clive Thompson in WIRED magazine [Clive Thompson on How More Info Leads to Less Knowledge].

Normally, we expect society to progress, amassing deeper scientific understanding and basic facts every year. Knowledge only increases, right?

Robert Proctor doesn't think so. A historian of science at Stanford, Proctor points out that when it comes to many contentious subjects, our usual relationship to information is reversed: Ignorance increases.

He has developed a word inspired by this trend: agnotology. Derived from the Greek root agnosis, it is "the study of culturally constructed ignorance."

As Proctor argues, when society doesn't know something, it's often because special interests work hard to create confusion. Anti-Obama groups likely spent millions insisting he's a Muslim; church groups have shelled out even more pushing creationism. The oil and auto industries carefully seed doubt about the causes of global warming. And when the dust settles, society knows less than it did before.

"People always assume that if someone doesn't know something, it's because they haven't paid attention or haven't yet figured it out," Proctor says. "But ignorance also comes from people literally suppressing truth—or drowning it out—or trying to make it so confusing that people stop caring about what's true and what's not."

This is an important insight. It's not something that we didn't know already but it's good to emphasize the concept and give it a name.

Creationism is an excellent example. It's not just that creationists fail to understand science, it's also that they are being actively lied to in an attempt to spread ignorance. In other words, there are people who deliberately spread misinformation in order to oppose knowledge.

If we are going to fight creationism we have to do more than just teach evolution in the schools. If we do that then we are just barely holding our own against the people who spread ignorance. At best, students will be aware of a conflict between what they learn in school and what they learn everywhere else.

In order to fight the spread of ignorance we have to take on the liars directly and show why they are lying. They need to be discredited and exposed. Unfortunately, many of the enemy are "Christians" and Christians get special protection in our society. You can criticize astrology and quackary but not religion.

That has to change. Perhaps we can lump them all under the term "agnotology" and treat them all the same?

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And Now for a Little Comic Relief

 
It's been a few weeks since my last humorous posting so at the start of a new week I thought I'd give you something to laugh about.

Here's a few words from Denyse O'Leary.

The reason so many of us have risen up against Darwinism is not that we think natural selection never occurs but that we have never accepted - without evidence - the idea that it produces a high level of information (and that was Darwin's argument) And - as Mike Behe shows in Edge of Evolution, it doesn't.

It is amazing what people who get tenure at prestigious universities are willing to support without evidence. Including "chance" as a key explanation of high levels of information, which we must all know is completely untrue.

If you doubt that, try throwing the bag of Scrabble letters around the room and reassembling them randomly, and see what happens.

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Modified Bases in DNA

 
Adenine: from the Greek adenas "gland": first isolated from pancreatic glands (1885)

Cytosine: derived from cyto- from the Greek word for "receptacle," refering to cells (1894)

Guanine: originally isolated from "guano" or bird excrement (1850)

Thymine: first isolated from thymus glands (1894)

(source Horton et al. 2006)Bacterial genomes contain a number of unusual bases in addition to the classic adenine (A), cytosine (C), guanine (G), and thymine (T). The most common of the unusual bases are 5-methylcytosine, N⁴-methylcytosine, and N⁶-methyladenine (Erlich et al. 1987).

Bacteriophage DNA, especially the DNA of bacteriophage T4 and its close relatives, can contain 5-hydroxymethylcytosine. The base is usually glycoslylated in normal phage. (A sugar group is attached to the hydroxymethyl group.)

Many of these modified bases serve to protect DNA from restriction endonucleases—enzymes that cleave foreign DNA at specific sites. The restriction endonucleases act on bacteriophage (virus) DNA preventing it from replicating inside the bacterial cell [see Restriction, Modification, and Epigenetics].

If bacteriophage modify their nucleotides at the site of cleavage, they will escape the defenses of the bacterial cell. Of course, bacteria that make restriction endonucleases have to protect their own DNA or else they will be committing suicide. That's why their genomes have modified nucleotides.

Many other modified bases have been found in DNA but they are quite rare. Examples are uracil, α-putrescinylthymine, and 5-dihydroxypentyluracil.


Eukaryotic DNA doesn't have as many modified bases. In fact, 5-methylcytosine is the only one that's common in all eukaryotes. N⁶-methyladenine is known to exist in protist and plant DNA and it is thought to exist at low levels in mammalian DNA as well (Ratel et al. 2006). The presence of hydroxymethycytosine has been reported in various animals as far back as 1972 (Penn et al. 1972).


Now Kriaucionis and Heintz (2009) have re-discovered hydroxymethylcytosine in mammalian DNA. Their paper appears in the latest issue of Science. Apparently the modified nucleotide is found in certain brain cells. Their result confirms the work done by Penn et al. (1972), a result that had not been confirmed in several other studies. This makes hydroxymethylcytosine the seventh modified base in eukaryotic DNA—unless there are some that I don't know about.

The problem with the press release is that it doesn't put the discovery in the proper context.

ScienceDaily (Apr. 17, 2009) — Anyone who studied a little genetics in high school has heard of adenine, thymine, guanine and cytosine – the A, T, G and C that make up the DNA code. But those are not the whole story. The rise of epigenetics in the past decade has drawn attention to a fifth nucleotide, 5-methylcytosine (5-mC), that sometimes replaces cytosine in the famous DNA double helix to regulate which genes are expressed. And now there's a sixth: 5-hydroxymethylcytosine.

In experiments to be published online April 16 by Science, researchers reveal an additional character in the mammalian DNA code, opening an entirely new front in epigenetic research.

We aren't told that the sixth nucleotide is actually N⁶-methhyladenine. We aren't told that many other modified bases have been discovered in bacteria, including hydroxylmethylcytosine. And we aren't told that the authors actually cite earlier work showing the presence of hydroxymethylcytosine in mammalian DNA.

That's a shame. The authors are quoted in the press release. They should have made more of an effort to ensure that it was scientifically accurate.

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Ehrlich, M., Wilson, G.G., Kuo, K.C., and Gehrke. C.W. (1987) N4-methylcytosine as a minor base in bacterial DNA. J Bacteriol. 169:939-943. [Journal of Bacteriology]

Kriaucionis, S. and Heintz, N. (2009) The Nuclear DNA Base 5-Hydroxymethylcytosine Is Present in Purkinje Neurons and the Brain. Science Published Online April 16, 2009 [DOI: 10.1126/science.1169786]

Penn, N.W., Suwalski, R., O'Riley, C., Bojanowski, K. and Yura, R. (1972) The presence of 5-hydroxymethylcytosine in animal deoxyribonucleic acid. Biochem J. :781–790. [Biochem. J.]

Ratel, D., Ravanat, J.L., Berger, F., and Wion, D. (2006) N6-methyladenine: the other methylated base of DNA. Bioessays :309-15. [PubMed

Dancing in Antwerp's Train Station

 
I have a confession to make. Ms. Sandwalk and I, along with four other couples we've known for many years, are learning how to do ballroom line dances. It's so much fun.

Perhaps that's why this video makes me smile. It's a promotion by a Belgian TV show that's looking for a "Maria" to play the lead in "The Sound of Music." I hope my daughter—who lives in Belgium— never hears about it 'cause she already knows all the words to every song in the musical.



UPDATE: Some people may not know about the T-Mobile add in the Liverpool Street Station in London [T-Mobile Dance].

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P.S. My dancing group is almost as good as these guys. Maybe we should do a performance in Union Station in downtown Toronto?

[Hat Tip: GrrlScientist]

Jerry Coyne's View of Evolutionary Psychology

 
You'll have to read Evolutionary psychology: the adaptive significance of semen flavor to find out what Coyne thinks of evolutionary psychology. I think he's captured the essence of the movement.

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P.S. I was looking for an appropriate illustration of the behavior that Coyne describes. Turns out that if you enter the appropriate term in your Google search box, you'll find quite a few photographs out there on the internet. I decided not to use any of them but the search was interesting.