Bobby Fischer

 
Bobby Fischer died yesterday in Reykjavik, Iceland, where he had been living for the past several years [Bobby Fischer, 64: Former chess champion].

Back in 1972, Fischer beat Boris Spassky of the USSR to become world chess champion. The event has been glorified as part of the cold war competition between the USA and the USSR but this was only part of the story. Some of us were just interested in it as a major sporting event featuring a radical new hero who didn't always play by the rules.

I remember following the games live on television—yes, that's right, the moves in each game were broadcast live on a large chessborad, with plenty of color commentary. As an amateur chess player, it was a real insight into the world of high level play.

Go to World Chess Championship 1972 for a brief summary of this extraordinary event. We'll never see anything like it again.

Here's the position at adjournment in the final (21st) game [Spassky vs Fischer Game #21]. Fischer (black) has just played h5. After thinking about the position all night Spassky phoned in the next morning to resign and concede the championship. Can you see why he gave up?

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Why I Like Richard Dawkins

 
Richard Dawkins doesn't pull punches and he doesn't beat around the bush. You always know where he stands on any given issue. This is what I admire about Richard Dawkins.

I don't agree with him on lots of things but whenever you engage him you know you've got a fight on your hands. It's the combination of intelligence and forthrightness that make him such a powerful voice in science. We need more scientists who are both smart, and willing to stand up for their ideas. We need more open controversy in science these days. Scientists need to speak up when they encounter silly ideas in the scientific literature. It is not a scientific virtue to be polite in such cases; in fact, it can be detrimental to science to clog up the scientific literature with scientific nonsense on the grounds that one shouldn't criticize fellow scientists in public. Richard Dawkins does not make that mistake.

Dawkins does not like group selection because it conflicts with his adaptationist, gene-centric, worldview. He's been very clear about this over the years. I admire him for sticking to his guns and standing by the original dismissal of group selection by George Williams.¹

David Sloan and E.O. Wilson have recently been pushing for a revival of group selection. They published a short summary of their new book in the Nov. 3 edition of New Scientist [Evolution: Survival of the selfless] where they said,

The concept of genes as "replicators" and "the fundamental unit of selection" averages the fitness of genes across all contexts to predict what evolves in the total population. The whole point of multilevel selection theory, however, is to ask whether genes can evolve on the strength of between-group selection, despite a selective disadvantage within each group. When this happens, the gene favoured by between-group selection is more fit overall than the gene favoured by within-group selection in the total population.

It is bizarre (in retrospect) to interpret this as an argument against group selection. Both Williams and Dawkins eventually acknowledged their error, but it is still common to find the "gene's-eye view" of evolution presented as a drop-dead argument against group selection.

The old arguments against group selection have all failed. It is theoretically plausible, it happens in reality, and the so-called alternatives actually include the logic of multilevel selection. Had this been known in the 1960s, sociobiology would have taken a very different direction. It is this branch point that must be revisited to put sociobiology back on a firm theoretical foundation.

Dawkins responds to this in a letter published in the Dec. 15 issue [Genes Still Central].

Genes still central

David Sloan Wilson's lifelong quest to redefine "group selection" in such a way as to sow maximum confusion - and even to confuse the normally wise and sensible Edward O. Wilson into joining him - is of no more scientific interest than semantic doubletalk ever is. What goes beyond semantics, however, is his statement (it is safe to assume that E. O. Wilson is blameless) that "Both Williams and Dawkins eventually acknowledged their error..." (3 November, p 42).

I cannot speak for George Williams but, as far as I am concerned, the statement is false: not a semantic confusion; not an exaggeration of a half-truth; not a distortion of a quarter-truth; but a total, unmitigated, barefaced lie. Like many scientists, I am delighted to acknowledge occasions when I have changed my mind, but this is not one of them.

D. S. Wilson should apologise. E. O. Wilson, being the gentleman he is, probably will.

* Richard Dawkins, Oxford UK

Does anyone have any doubts about where Dawkins stands on the issue of group selection?

David Sloan Wilson and E.O. Wilson responed to Dawkins' letter by claiming that they were only referring to one minor aspect of the argument against group selection but I don't think anyone is going to be fooled by that. In their article, they clearly imply that Dawkins has acknowledged his "error" in opposing group selection. This is a case where a simple apology would have worked better.

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1. Ironically, Dawkins is a huge fan of kin selection, which, in my opinion is just about as weak as group selection.

Gerty Cori Biochemist on USA Stamp

Biochemist Gerty Cori is going to be on a new USA stamp to be issued in March. Cori and her husband won the Nobel Prize in 1947 for their work on glycogen metabolism [Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori].

One of the key intermediates in this pathway is the Cori ester [Monday's Molecule #25]. That's the molecule pictured on the stamp. Unfortunately, there's a mistake in the structure. How many can spot it? Why didn't they ask a biochemist to check the design?

UPDATE: Here's the correct structure.

The error was first discovered by a reader of Chemical & Engineering News [Going postal over structural errors]. Here's how C&EN describes the mistake ...

It is a sad state of affairs, because it was precisely the isolation of glucose-1-phosphate, and discovery of the so-called Cori ester, that garnered Cori the Nobel Prize. "Long-dead carbohydrate chemists would roll over in their graves to see this structure after all the effort they made to get it right," one sugar chemist wrote in an e-mail to Newscripts.

The glitch made us rather glum, despondent even, as we considered the squandered opportunity to serve some first-class carbohydrates to the American public. For alas, the suboptimal stamps have already been printed and are still scheduled for release in early March, despite the error.

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[Hat Tip: Living the Scientific Life]

A Junk DNA Quiz

 
Take the junk DNA quiz in the left sidebar to let me know what you think of your genome. How much of it could be removed without affecting our species in any significant¹ way in terms of viability and reproduction? Or even in terms of significant ability to evolve in the future? In other words, how much is junk?

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1. I did not choose the word "significant" in order to be obtuse. I picked it in order to eliminate some trivial possibilities that really don't make any difference. For example, no matter how little DNA you delete you would be able to detect some change, even if it's just a reduction in the time to replicate the genome of the amount of energy used. If you think that such changes are "significant" then you should answer "none" to the question in the quiz.

The Plausibility of Life

The Plausibility of Life is an evo-devo book by Mark Kirschner and John Gerhart. I read it a long time ago and had pretty much put it out of my mind except for the occasional potshot [Evo-Devo: Innovation and Robustness in Evolution] [Animal Chauvinism].

A couple of days ago I was shocked into taking another look at the book. The shocker was Alex Palazzo of The Daily Transcript who wrote [Today's rant - the biggest story never covered].

The most insightful book on biology written in the past decade was Gerhart & Kirschner's book, The Plausibility of Life.

That's so far out of line with my opinion that I began to wonder if I had missed something important. Alex is a smart guy and he's not likely to be way off base.

Alas, in this case Alex got it wrong. This is certainly not one of the most insightful books on biology in this decade, or any other decade. It's pretty much adaptationist, animal chauvinistic, evo-devo-centric gobbledygook from a pair of scientists who don't understand evolution.

The central question of the book is, "... how can small, random genetic changes be converted into complex and useful innovations?" (p. ix). Apparently this is a puzzlement to evolutionary developmental biologists. One that has eluded them until the last decade of the twentieth century.

Kirschner and Gerhart's effort is a valuable update of some of these ideas, but it hardly constitutes "a new theory" to complement the Modern Synthesis.

Massimo Pigliucci
Have We Solved Darwin's Dilemma?Kirschner and Gerhart have the solution.

In this book we propose a major new scientific theory: facilitated variation that deals with the means of producing useful variation.

Since the essence of their theory is "facilitated variation" you would think that this concept would be clearly explained in the book. It isn't. There's a lot of beating around the bush and hand waving about a fundamental new process of evolution but little in the way of concrete facts and evidence.

When I read the book for the very first time I was astonished to realize that by the end of the book I still didn't know what the authors meant by "facilitated variation." So, I looked it up in the glossary ....

Facilitated Variation: An explanation of the organism's generation of complex phenotypic change from a small number of random changes of the genotype. We posit that the conserved components greatly facilitate evolutionary change by reducing the amount of genetic change required to generate phenotypic novelty, principally through their reuse in new combinations and in different parts of their adaptive ranges of performance.

Is that clear? Of course it isn't. You have to go back and read very carefully to even begin to understand what they're talking about.

... Kirschner and Gerhart do not present any detailed examples of how the properties of developmental systems have actually contributed to the evolution of a major evolutionary novelty. Nor have they shown that alternative properties would have prevented such evolution. Although The Plausibility of Life contains many interesting facts and arguments, its major thesis is only weakly supported by the evidence.

Brian Charlesworth
On the Origins of Novelty and VariationHere's how I see it. Animals have a number of conserved core processes like transcription, membrane trafficking, formation of eyes, compartments, etc. that contribute to the success of the organism. You can't mess with these core processes because that would be lethal. However, new phenotypes can arise when existing core processes are expressed in new combinations or at different times during development. The core processes have been selected for adaptability. In particular, they have evolved in a way that facilitates phenotypic variation by encouraging the evolution of new combinations and new timing while, at the same time discouraging evolution of the core processes themselves.

Over time, animal species have been selected for the ability to evolve by taking advantage of facilitated variation without threatening the core processes. This one of the definitions of evolvability.

In summary, we believe that evolvability—the capacity for organisms to evolve—is a real phenomenon. We believe that facilitated variation explains the variation side of evolvability, through the reuse of a limited set of conserved processes in new combinations and in different parts of their adaptive ranges due to genetic modifications of nonconserved regulatory components ....

Facilitated variation has arisen and increased by selection, we say. Since it facilitates the generation of innumerable complex, selectable heritable traits with only a small investment of random genetic variation, it is indeed the greatest adaptation of all, at least for animals since the Cambrian.

I'm not buying any of this. I'd like to see real evidence that the process of evolution in animals is different than evolution in prokaryotes. Whether you're dealing with the genetic switch in bacteriophage λ, sporulation in Bacillus subtilis, or the formation of heterocysts in cyanobacteria, it is always the case that the processes are controlled by a cascade of regulatory factors and drastic changes in the timing and extent of these regulatory genes can lead to significant phenotypic effects.

What's so special about animals that we have to develop a "major new scientific theory" to explain similar observations?

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Nobel Laureate: Sidney Altman

 

The Nobel Prize in Chemistry 1989.

"for their discovery of catalytic properties of RNA"



In 1989, Sidney Altman (1939 - ) was awarded the Nobel Prize in Chemistry for discovering that the RNA component of RNase P was the catalytic component of the enzyme [Transfer RNA Processing: RNase P]. He shared the prize with Thomas Cech who worked on self-splicing ribosomal RNA precursors.

The presentation speech was delivered by Professor Bertil Andersson of the Royal Swedish Academy of Sciences.
THEME:

Nobel Laureates

Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,

The cells making up such living organisms as bacteria, plants, animals and human beings can be looked upon as chemical miracles. Simultaneously occurring in each and every one of these units of life, invisible to the naked eye, are thousands of different chemical reactions, necessary to the maintenance of biological processes. Among the large number of components responsible for cell functions, two groups of molecules are outstandingly important. They are the nucleic acids - carriers of genetic information - and the proteins, which catalyze the metabolism of cells through their ability to act as enzymes.

Genetic information is programmed like a chemical code in deoxyribonucleic acid, better known by its abbreviated name of DNA. The cell, however, cannot decipher the genetic code of the DNA molecule directly. Only when the code has been transferred, with the aid of enzymes, to another type of nucleic acid, ribonucleic acid or RNA, can it be interpreted by the cell and used as a template for producing protein. Genetic information, in other words, flows from the genetic code of DNA to RNA and finally to the proteins, which in turn build up cells and organisms having various functions. This is the molecular reason for a frog looking different from a chaffinch and a hare being able to run faster than a hedgehog.

Life would be impossible without enzymes, the task of which is to catalyze the diversity of chemical reactions which take place in biological cells. What is a catalyst and what makes catalysis such a pivotal concept in chemistry? The actual concept is not new. It was minted as early as 1835 by the famous Swedish scientist Jöns Jacob Berzelius, who described a catalyst as a molecule capable of putting life into dormant chemical reactions. Berzelius had observed that chemical processes, in addition to the reagents, often needed an auxiliary substance - a catalyst - to occur. Let us consider ordinary water, which consists of oxygen and hydrogen. These two substances do not react very easily with one another. Instead, small quantities of the metal platinum are needed to accelerate or catalyze the formation of water. Today, perhaps, the term catalyst is most often heard in connection with purification of vehicle exhausts, a process in which the metals platinum and rhodium catalyze the degradation of the contaminant nitrous oxides.

As I said earlier, living cells also require catalysis. A certain enzyme, for example, is needed to catalyze the breakdown of starch into glucose and then other enzymes are needed to burn the glucose and supply the cell with necessary energy. In green plants, enzymes are needed which can convert atmospheric carbon dioxide into complicated carbon compounds such as starch and cellulose.

As recently as the early 1980s, the generally accepted view among scientists was that enzymes were proteins. The idea of proteins having a monopole of biocatalytic capacity has been deeply rooted, and created a fundamental dogma of biochemistry. This is the very basic perspective in which we have to regard the discovery today being rewarded with the Nobel Prize for Chemistry. When Sidney Altman showed that the enzyme denoted RNaseP only needed RNA in order to function, and when Thomas Cech discovered self-catalytic splicing of a nucleic acid fragment from an immature RNA molecule, this dogma was well and truly holed below the waterline. They had shown that RNA can have catalytic capacity and can function as an enzyme. The discovery of catalytic RNA came as a great surprise and was indeed met with a certain amount of scepticism. Who could ever have suspected that scientists, as recently as in our own decade, were missing such a fundamental component in their understanding of the molecular prerequisites of life? Altman's and Cech's discoveries not only mean that the introductory chapters of our chemistry and biology textbooks will have to be rewritten, they also herald a new way of thinking and are a call to new biochemical research.

The discovery of catalytic properties in RNA also gives us a new insight into the way in which biological processes once began on this earth, billions of years ago. Researchers have wondered which were the first biological molecules. How could life begin if the DNA molecules of the genetic code can only be reproduced and deciphered with the aid of protein enzymes, and proteins can only be produced by means of genetic information from DNA? Which came first, the chicken or the egg? Altman and Cech have now found the missing link. Probably it was the RNA molecule that came first. This molecule has the properties needed by an original biomolecule, because it is capable of being both genetic code and enzyme at one and the same time.

Professor Altman, Professor Cech, you have made the unexpected discovery that RNA is not only a molecule of heredity in living cells, but also can serve as a biocatalyst. This finding, which went against the most basic dogma in biochemistry, was initially met with scepticism by the scientific community. However, your personal determination and experimental skills have overcome all resistance, and today your discovery of catalytic RNA opens up new and exciting possibilities for future basic and applied chemical research.

In recognition of your important contributions to chemistry, the Royal Swedish Academy of Sciences has decided to confer upon you this year's Nobel Prize for Chemistry. It is a privilege and pleasure for me to convey to you the warmest congratulations of the Academy and to ask you to receive your prizes from the hands of His Majesty the King.

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Transfer RNA Processing: RNase P

 

RNase P is one of the key enzymes in the processing of tRNA primary transcripts [Transfer RNA: Synthesis].

RNase P is a ribozyme. Most of the enzyme consists of an RNA molecule called RNA P and the rest is composed of small proteins. In bacteria there is a single protein subunit while in eukaryotes there are up to eight small proteins bound to the RNA component.

RNA P, by itself, can catalyze the cleavage reaction [Monday's Molecule #58]. The role of the protein is simply to facilitate the reaction.¹

The structure of the RNA component from two different species has recently been published. The one shown here is RNA P from Thermophilus maritima (reviewed in Baird et al. 2007). This catalytic RNA is found in all species and it's the classic example of an RNA that can catalyze a reaction in the absence of protein. Sidney Altman received the Nobel Prize in 1989 for demonstrating that the activity was confined to the RNA part of the holoenzyme.

The exact structure of the complete holoenzyme (RNA + protein) is not known but the evidence suggest a model such as the one shown on the left (Smith et al. 2007). The RNA is blue, the protein subunit is red, and the bound tRNA precursor is brown. Note that the protein subunit is positioned at the site of the cleavage near the 5′ end of the mature tRNA.

Part of the RNA ribozome is interacting with the TΨC loop of the tRNA molecule. This loop is present in all tRNAs which explains why the RNase P enzyme can cleave all tRNA precusors no matter which particular tRNA going to be produced.

There are two different types of RNase P depending on the species. Although both of them have similar catalytic RNAs they differ in size of the RNA and in the proteins that are bound to it.

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1 When the reaction is carried out under in vivo concentrations of ionic strength, temperature etc., the protein component is absolutely required in order to get significant activity.

Baird, N.J., Fang, X.W., Srividya, N., Pan, T. and Sosnick, T.R. (2007) Folding of a universal ribozyme: the ribonuclease P RNA. Quarterly Rev. Biophys. 40:113-161. [doi:10.1017/S0033583507004623] [PubMed]

Smith, J.K., Hsieh, J. and Fierke, C.A. (2007) Importance of RNA-protein interactions in bacterial ribonuclease P structure and catalysis. Biopolymers 87:329-38. [PubMed]

Transfer RNA: Synthesis

 
Transfer RNA's are produced by transcribing a tRNA gene to produce a single-stranded tRNA precursor molecule. tRNA genes are just one of the many examples of genes that don't encode proteins. It's worth keeping this in mind when you read discussions about how genes are defined and the role of "noncoding" DNA in the genome.

tRNA genes can be individual isolated genes or they can be linked to other genes in a larger transcriptional unit. A common example of the latter situation occurs in ribosomal RNA operons where tRNA genes are located in the regions between the large and small ribosomal RNA genes. In bacteria, the tRNA genes can be part of a co-transcribed operon containing protein-encoding genes. In eukaryotes the tRNA genes are transcribed by RNA polymerase III [Eukaryotic RNA Polymerases].

No matter how the tRNA genes are arranged, the primary transcriptional product is larger than the functional tRNA and it contains no modified bases. This primary transcript has to be processed to: (a) reduce it to the proper length, (b) remove any introns and (c) convert the standard nulceotides into modified nucleotides like dihydrouridylate (D) or pseudouridylate (Ψ) [Transfer RNA: Structure].

The trimming steps involve a number of specific RNA cleavage enzymes. RNase P specifically cuts the precursor at the 5′ end of the mature tRNA. Other endonucleases cut the precursor near the 3′ end of the mature molecule.

The 3′ end must then be trimmed back to the proper position. This step is carried out by an exonuclease called RNase D in bacteria. Finally, the nucleotides CCA are added to the 3′ end by tRNA nucleotidyl transferase. (All tRNA's have the same 3′ nulceotides—this is where the amino acid is attached later on.) Some tRNA genes have already have the sequence CCA at the 3′ end of the mature molecular so the last step isn't always required.

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Transfer RNA: Structure

 
Transfer RNA (tRNA) is an essential component of the protein synthesis reaction. There are at least twenty different kinds of tRNA in the cell¹ and each one serves as the carrier of a specific amino acid to the site of translation.

tRNA's are L-shaped molecules. The amino acid is attached to one end and the other end consists of three anticodon nucleotides. The anticodon pairs with a codon in messenger RNA (mRNA) ensuring that the correct amino acid is incorporated into the growing polypeptide chain.

The L-shaped tRNA is formed from a small single-stranded RNA molecule that folds into the proper conformation. Four different regions of double-stranded RNA are formed during the folding process.

The two ends of the molecule form the acceptor stem region where the amino acid is attached. The anticodon is an exposed single-stranded region in a loop at the end of the anticodon arm.

The two other stem/loop structures are named after the modified nucleotides that are found in those parts of the molecule. The D arm contains dihydrouridylate residues while the TΨC arm contains a ribothymidylate residue (T), a pseudouridylate residue (Ψ) and a cytidylate (C) residue in that order. All tRNA's have a similar TΨC sequence. The variable arm is variable, just as you would expect. In some tRNA's it is barely noticable while in others it is the largest arm.

tRNA's are usually drawn in the "cloverleaf" form (below) to emphasize the base-pairs in the secondary structure.

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1. Most genomes contain 40-80 different tRNA genes. While there are only 20 common amino acids, there are 61 different codons. Many codons are recognized by more than one different tRNA—the classic example is the codon AUG that can be recognized by methionyl-tRNA and initiator tRNA.

First Rule of Holes

 
Greg Laden has responded to criticism of his views on junk DNA [Moran, Gregory, Give me a Break!].

In the comments to Greg's post, Steve LaBonne brings up the First Rule of Holes. This is an excellent example. In case there are some people who are not familiar with the First Rule of Holes, here it is ....

FIRST RULE OF HOLES

If you're in one, stop digging.

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Greg Laden Gets Suckered by John Mattick

 
Oh dear. Greg Laden reviews a paper from John Mattick's group and he falls for the hype, hook line and sinker. Here's what Greg says [Genes are only part of the story: ncRNA does stuff].

The "Junk DNA" story is largely a myth, as you probably already know. DNA does not have to code for one of the few tens of thousands of proteins or enzymes known for any given animal, for example, to have a function. We know that. But we actually don't know a lot more than that, or more exactly, there is not a widely accepted dogma for the role of "non-coding DNA." It does really seem that scientists assumed for too long that there was no function in the DNA.

I hate to break it to you Greg, but junk DNA is not a myth. It really is true that a huge amount of our genome is junk. It's mostly defective transposons like SINES and LINES [Junk in your Genome: LINEs]. It's a lie that we don't know what most non-coding DNA is doing. We do know. It's not doing anything because it's mostly screwed up transposons and pseudogenes like Alu's.

Mattick may have found a few bits of DNA that encode regulatory RNAs but that's only a small part of the total genome. He, and you, have fallen for excuse #5 of The Deflated Ego Problem.

Ryan Gregory has already tried to teach Greg some real science about junk DNA so I won't pile on any more than I have [Signs of function in non-coding RNAs in mouse brain.].

UPDATE: RPM chimes in to expose the flawed thinking of Greg Laden [How Easy is it to Write About Junk DNA?]

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Humans Have Only 20,500 Protein-Encoding Genes

The first drafts of the human genome indicated about 30,000 genes, a number that was very much in line with many predictions that had been made over the years by scientists who were studying the topic. (Other scientists, and most science writers, thought there were about 100,000 genes [Facts and Myths Concerning the Historical Estimates of the Number of Genes in the Human Genome]).

Since the publication of the first draft, the number of genes has been dropping as annotators eliminate sequences that were falsely attributed to protein-encoding genes. Current estimates suggest there are about 28,000 different genes all together with about 4,000 of them encoding RNA products such as ribosomal RNA, tRNA, and the small RNAs involved in a numer of metabolic processes [Ensembl: Homo sapiens].

A gene encoding a protein will have an open reading frame (ORF) consisting of multiple codons— usually more than 100. Some of these potential protein-encoding genes appear to be unique to humans. They weren't found in the other mammalian genomes that had been sequenced (e.g., mouse, dog). Quite a few scientists took this as evidence for genes that distinguish humans from other mammals. According to them, these unique genes arose during the recent evolution of Homo sapiens and that's why there are no homologues in the other mammalian genomes.

Other scientists looked at the data in a different light. They suspected that these "unique" or "orphan" genes were more likely to be artifacts because they were not conserved. In other words, they reached exactly the opposite conclusion based on their understanding of evolution. Their prediction was that these orphan genes resulted from spurious ORF's and not real genes.

This problem has been examined by Eric Lander's group in Boston, MA (USA) and the results were published in PNAS (Clamp et al., 2007). Their careful analysis has eliminated most of the orphan genes and the new gene count for protein-encoding genes is now 20,488.

Here's how the authors describe the purpose of their study,

The purpose of this article is to test whether the nonconserved human ORFs represent bona fide human protein-coding genes or whether they are simply spurious occurrences in cDNAs. Although it is broadly accepted that ORFs with strong cross-species conservation to mouse or dog are valid protein-coding genes (7), no work has addressed the crucial issue of whether nonconserved human ORFs are invalid. Specifically, one must reject the alternative hypothesis that the nonconserved ORFs represent (i) ancestral genes that are present in our common mammalian ancestor but were lost in mouse and dog or (ii) novel genes that arose in the human lineage after divergence from mouse and dog.

To begin the study they choose to analyze the 21,895 protein-encoding genes in the Ensembl database. They looked for genes that were related to similar sequences in the mouse and dog genomes. (These are the only two well-characterized non-human, mammalian genomes.) After visual inspection of low scoring sequences they were able to eliminate about 1600 potential genes because they were pseudogenes, transposons, or artifacts of various sorts.

They were left with 19,108 verified genes and 1177 orphan "genes"—human ORF's that were not similar to any gene in the mouse and dog genomes. These genes could be newly evolved genes in the human/primate lineage or ancient genes that had been lost in mice and dogs.

The next step was to categorize the orphan "genes" to see if they looked like real protein-encoding genes. The results indicated that in terms of sequence similarity to the same regions in the mouse and dog genomes, the orphan ORF's were indistinguishable from random sequences. Similarly, the characteristics of the presumed codons of these genes were very different from conserved genes and very similar to random sequences with short accidental reading frames. Thus, the orphan sequences look like artifacts.

To confirm this conclusion, the authors compared the sequences to the macaque and chimpanzee genomes. They were not found in those genomes either.

If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes.

This analysis was extended to the other gene catalogs (Vega, and RefSeq) as well as an updated version of the Ensembl catalog (v38). This resulted identification of an additional 1271 valid genes. Adding in the genes in the mitochondrial genome (13) and the Y chromosome (78) gives a total of 20,470 genes.

Finally, reanalysis of the transposons and pseudogenes revealed 18 cases where a real gene had evolved from an inactive pseudogene. This gives a grand total of 20,488 protein-encoding genes in the human genome.

There are several conclusions that can be drawn from this excellent study.

We show that the vast majority of ORFs without cross-species counterparts are simply random occurrences. The exceptions appear to represent a sufficiently small fraction that the best course is would be consider such ORFs as noncoding in the absence of direct experimental evidence.

This is going to be a major challenge for many workers who prefer to see evolution in a different manner. There are a number of papers that view these orphans sequences as direct evidence that human specific genes had arisen in the recent past. Clamp et al. (2007) are saying that if the sequences aren't present in the macaque and chimpanzee then one should conclude that they are artifacts.

Remember, many of the artifactual genes are supported by EST/cDNA data suggesting that they are transcribed. This study calls that evidence into question—correctly in my opinion—indicating that we should be skeptical of the EST data.

One important biological implication of our results is that truly novel protein-coding genes (encoding at least 100 amino acids) arise only rarely in mammalian lineages. With the current gene catalogs, there are only 168 "human-specific" genes (<1% of the total; only 11 are manually reviewed entries in RefSeq; see SI Table 4). These genes lack clear orthologs or paralogs in mouse and dog, but are recognizable because they belong to small paralogous families within the human genome (2 to 9 members) or contain Pfam domains homologous to other proteins. These paralogous families shows a range of nucleotide identities, consistent with their having arisen over the course of ~75 million years since the divergence from the mouse lineage.

This is an important conclusion and I think it is accurate. There are very few "new" genes in the human genome, and, by implication, in other mammalian genomes. This conclusion is consistent with what we know about evolution but it contradicts studies that purport to show rapid evolution of novel genes and novel regulatory mechanisms in humans.

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[Image Credit: The human karyotype is from the Ensembl website.]

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]

Digital Object Identifier (DOI)

 
The digital object identifier, or DOI, is a unique identifier that's given to electronic documents. The idea is that it serves as a permalink to the item. An item can be moved to a different webpage but the DOI will always point to it as long as the DOI is undated when the item is moved.

We often encounter these DOI identifiers in online journal articles. For example, a recently published PNAS article has the following DOI 10.1073/pnas.0709013104. I usually forget how to resolve those DOI's. In case I'm not the only one, I thought I'd post the information.

The resolver is locatad at http://dx.doi.org/. So if you want to see the PNAS article you type in the following URL: http://dx.doi.org/10.1073/pnas.0709013104. Try it.

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Best Canadian Sci/Tech Blog 2007

 
Nominations have closed and the voting has begun for the best Sci/Tech blog in Canada. Here's the ballot.

The nominees are ....

• The World's Fair
• Eastern Blot
• Climate Audit
• XSAMPLEX
• Clangmann
• A Few Things Illconsidered
• jules.ca
• WinExtra
• Weighty Matters
• cyberbuzz
• Mark Evans
• Dark Matter
• Internet Duct Tape

The only blogs that I've read before today are Eastern Blot and The World's Fair. Should I be reading the others? Please let me know if you think any of these are science blogs worth reading. Several of the Canadian science blogs that I read every day are not on the list.

Is there an easy way of finding out how popular those blogs are? There must be some tool out there that will tell me the average number of visits per day/week/month for each of the nominees.

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What Is this Dog Thinking?

 
If you think you know what's going on in the mind of this dog, get over to Friendly Atheist and enter the contest [Friendly Atheist Contest #14: Dog Prays to God].

Remember the rules. According to Hemant Mehta, "Funny and creative answers will have a shot at winning."

You can enter as often as you like.

Here's what the boy is thinking, "This is so embarrassing. I'm soon gonna have to break it to him that I'm an atheist."

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Insurance Against Alien Abductions

 
According to some studies, up to four million Americans may have been abducted by aliens [Abduction by Aliens or Sleep Paralysis?]. I often use this information when questioning religious people about the rationality of their inner convictions. As it turns out, most theists reject the silly beliefs of alien abductees without seeing any connection between this and their own proof of God by religious experience.

A group of people have banded together to exploit help those who fear being abducted by aliens. They have prepared special dog tags [www.earthbounddog.com].

Picture yourself lost in the galaxy...UFO sightings and Alien Abductions are on the rise...Will you return to tell the story?

In case of alien abduction these dog tags may save your life. The crucial data an alien will need to get you back to Earth is die stamped into these dog tags.

The design is based on NASA research for the Pioneer 10 Space Mission that used a gold plaque attached to the craft to inform any Extraterrestrials of it's Earthly origin.

You can buy them for only $12.99 (US). I suggest you buy several sets of dog tags for all your close friends. Do not buy them for other people.

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[Hat Tip: Bad Astronomy]

Convocation 2007

 
A few months ago I told you about my first convocation as a Professor [Bruce Alberts in Toronto]. Here's the formal photograph of the main participants. Don't we look pretty?

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Monday's Molecule #58

 
This is one example of a very common molecule found in every cell. You have to give us the common name of this molecule and identify the species. You'll be pleased to know that I don't need the systematic IUPAC name for this one.

There's a direct connection between this molecule and Wednesday's Nobel Laureate. Your task is to figure out the significance of today's molecule and identify the Nobel Laureate who studied its function. (Hint: The Nobel Laureate is a Canadian—there aren't very many Canadian Nobel Laureates so this is a very big hint.)

The reward goes to the person who correctly identifies the molecule and the Nobel Laureate. Previous winners are ineligible for one month from the time they first collected the prize. There is one ineligible candidates for this week's reward because Sandwalk readers were not very successful in December. The prize is a free lunch at the Faculty Club.

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 the Nobel Laureate. Note that I'm not going to repeat Nobel Laureates so you might want to check the list of previous Sandwalk postings.

Correct responses will be posted tomorrow along with the time that the message was received on my server. I may 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! This one proved to be far more difficult than I imagined. Everyone got the Nobel Laureate (Sidney Altman) but very few people got the molecule correct. Some people failed to identify the species correctly even though I specifically asked for the species. Most people said that the molecule is RNase P but that isn't quite correct.

The molecule is the M1 RNA subunit of RNase P from E. coli. The other subunit is a small protein called the C5 protein cofactor. This RNA is sometimes called RNA P and that would have been an acceptable answer.

Only one person got everything right and that response just arrived a few minutes ago. Congratulations to PonderingFool for knowing that the molecule was the M1 RNA component of E, coli RNase P and the Nobel Laureate is Sidney Altman.

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Creation Science Papers

 
Phil Plait of Bad Astronomy must have had a great deal of free time on his hands now that the asteroids have missed us and the galaxy isn't going to be consumed by a hydrogen cloud for at least 40 million years. He was thinking of writing a paper for a new journal sponsored by Answers in Genesis [Creationists: publish and perish].

Phil was interested in the first two papers that were published in the Answers Research Journal. One was a geology paper and one was about microbiology. Phil wanted to know how good they were.

Being as relieved as him about the fact that the Earth survived the near miss, I decided I could spare a few minutes to read the microbiology article. It's by Alan L. Gillen from that famous center of research called Liberty University. Here's the abstract.

The world of germs and microbes has received much attention in recent years. But where do microbes fit into the creation account? Were they created along with the rest of the plants and animals in the first week of creation, or were they created later, after the Fall. These are some questions that creation microbiologists have been asking in recent years. Ongoing research, based on the creation paradigm, appears to provide some answers to these puzzling questions. The answers to these questions are not explicit in Scripture, so the answers cannot be dogmatic. However, a reasonable extrapolation from biological data and Scripture can be made about the nature of microbes in a fully mature creation. This article attempts to provide reasonable answers to when microbes were created and is meant to stimulate discussion and further research in this area.

Very little has been written in Bible commentaries or in creation literature on the subject of when microbes were created. Some have postulated that microbes were created on a single day of Creation, such as Day Three—when the plants were made. This is partially due to the “seed-like” characteristics that bacteria and fungi have—therefore classifying microbes as plants. In addition, we observe microbes (such as Escherichia coli) isolated in the lab and we tend to think of microbes as individual entities much like birds or fish or animals and, therefore, created on a single day. However, in nature, the vast majority of microbes live in biological partnerships, not in total isolation. The natural symbiosis of microbes with other creatures is the norm. Therefore, we postulate that microbes were created as “biological systems” with plants, animals, and humans on multiple days, as supporting systems in mature plants, animals, and humans. This idea is further supported by the work of Francis (2003). Francis calls microbial symbiotic systems a biomatrix, or organosubstrate. He proposes that microbes were created as a link between macroorganisms and a chemically rich but inert physical environment, providing a surface (i.e., substrate) upon which multicellular creatures can thrive and persist in intricately designed ecosystems. From the beginning, God made His creation fully mature, and complex forms fully formed. This would insure continuity and stability for the times to come. Although we cannot be certain as to specifically when the Creator made microbes, it is within His character to make entire interwoven, “packaged” systems to sustain and maintain life.

I didn't read any further.

Phil, the bad news is that this is a pile of crap. The good news is that you won't have to waste very much time writing a paper for this journal. You can probably knock it off in an afternoon.

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[Image Credit: The Complete Idiot’s Guide to Just Doing It]

Scientific Illiteracy About Death Rates

 
Here's part of an article on ScienceDaily about death rates in New York City [New York City Death Rate Reaches Historic Low].

The death rate in New York City reached an all-time low in 2006, the Health Department reported today, as the number of deaths fell to 55,391 -- down from 57,068 in 2005 and 60,218 in 2001. Mortality declined in eight leading categories, including diabetes, HIV, chronic lung disease and kidney failure. The only leading killer that increased significantly was substance use (up 8%). Heart disease and cancer remained the city's biggest killers, claiming 21,844 lives and 13,116 lives, respectively. The figures come from the latest Annual Summary of Vital Statistics, the definitive registry of births and deaths in New York City.

The numbers of deaths are not death rates. This is one of my pet peeves. I get angry when newspaper reporters screw it up but this is much worse. It's from a website that's supposed to specialize in science ("Your Source for the Latest Research News").

The raw numbers are available at Summary of Vital Statistics 2006: The City of New York. They show that the death rate did, indeed, fall from 7.0 per 1000 citizens in 2004 to 6.7 per 1000 citizens in 2006. In 1916 it was 14.0 while in 1980, 1990, and 2000 it was 10.0, 10.1, and 7.6 respectively.

The absolute numbers of deaths tells you nothing about death rates. For all we know, the population of New York City could have fallen from 2004 to 2006 and the death rate could have gone up. (Incidentally, if you look at the raw data you'll see an interesting footnote. The rates in 2004-2006 were revised downwards when the 2007 census data for population was used. Previous estimates were based on the population according to the 2000 census.)

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[Image Credit: New York City in 1916 from The University of Texas at Austin]

Scientific Mistakes

 
During a recent discussion with undergraduates, they mentioned that it would be a good idea to discuss the more recent scientific papers in class. They seemed to be very impressed with a course that presented papers published within the past few months.

I pointed out that there's a problem with that kind of course. If the goal of a course is to teach fundamental principles and concepts then it's very unlikely that recent papers are going to advance that goal. Why is that? Because much of the scientific literature is either trivial or incorrect. You don't know that it's trivial or incorrect until some time has passed and other scientists react.¹

If the goal of a course is to teach how science is done on a day-to-day basis, then a key part of that course should be to drive home the concept of skepticism. Don't believe everything you read in the latest journals. An important part of that teaching goal is to pick examples of important mistakes in older literature.

John Dennehy has helped us out this week by posting a "citation classic" that turned out to be wrong [This Week's Citation Classic: Being Wrong]. In my opinion, it's far more important to look at examples like this than to expose undergraduates to several dozen hot new papers that are supposedly at the cutting edge.

The paper that John choose is by Paul Boyer who subsequently won the Nobel Prize in Chemistry [Nobel Laureates: Paul Boyer and John Walker] for his work on the mechanism of ATP synthase [How Cells Make ATP: ATP Synthase].

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1. Sometimes it takes a long time for scientists to react to mistakes in the literature. Wrong ideas can be perpetuated for decades after they've been refuted, especially if the original papers were widely referenced. I was reminded of this the other day when listening to a graduate student seminar—coincidently, on the structure of ATP synthase. The student posted an old-fashioned, out-of-date view of the citric acid cycle as an introduction to the function of ATP synthase. I have challenged my undergraduate biochemistry class to find a single example of a web site that gets the entire citric acid cycle correct. There's a prize. They can't use the IUBMB site, they can't use my sites, and they can't make one of their own. So far nobody has collected the prize.

How Much Junk in the Human Genome?

Ryan Gregory has another contribution to this question that's well worth a read [Is most of the human genome functional?].

Among other things, Ryan picks on the views of John Mattick who has got to be one of the worst scientists in the field. Whenever I read a paper by Mattick I revise my opinion of the value of peer-reviewed literature. It's bad enough that Mattick has silly ideas but it's even sadder that his "peer" reviewers don't recognize it.

Here's a quote from Mattick that I discussed in my article on the The Central Dogma of Molecular Biology. It's obvious that he doesn't understand the real meaning of the central dogma. Can you pick out the other conceptual flaws in this paragraph? [Hints: Worst Figure Ever and Dog Ass Plots.]

The central dogma of biology holds that genetic information normally flows from DNA to RNA to protein. As a consequence it has been generally assumed that genes generally code for proteins, and that proteins fulfil not only most structural and catalytic but also most regulatory functions, in all cells, from microbes to mammals. However, the latter may not be the case in complex organisms. A number of startling observations about the extent of non-protein coding RNA (ncRNA) transcription in the higher eukaryotes and the range of genetic and epigenetic phenomena that are RNA-directed suggests that the traditional view of genetic regulatory systems in animals and plants may be incorrect.

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

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Graduate Students Need to Publish Papers

 
In my field it takes five, or even six, years to complete a Ph.D. program. This time could be significantly reduced if there wasn't pressure on students to produce publishable work. The reduction in time is even more obvious at the M.Sc. level where it often take far more than two years to get a degree.

One could make a case for an M.Sc. degree that was not a "research" oriented degree. These programs would be useful for high school teachers, for example, or patent attorneys, or even physicians.

But those are exceptions. In most research departments the thesis is based on scientific research. Does that research have to produce results that can be published in the scientific literature? Yes it does.

T. Ryan Gregory explains why [Why would advisors encourage students to publish?]. (This is a repost of an article that he published earlier on Genomicron but it's still relevant and topical, especially in our department where we are grappling with the issue of long times to completion.)

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[Photo Credit: Graduate students in the Department of Biochemistry 2007-2008.]

Test Your God Logic

 
Here's a quiz you can try to see if your positions on atheism and religion are consistent [Battleground God]. Be careful, this quiz has many pitfalls. I took three hits and a bullet but it's not because I'm illogical, in my opinion. It's because questions can be interpreted in several different ways.

Here's one of the questions that caused me trouble.

It is foolish to believe in God without certain, irrevocable proof that she exists.

I answered "true." What I mean by that is that you require evidence to believe in something. What the authors of the study mean is that "certain, irrevocable proof" is inconsistent with my answer about evolution! They say,

You stated earlier that evolutionary theory is essentially true. However, you have now claimed that it is foolish to believe in God without certain, irrevocable proof that she exists. The problem is that there is no certain proof that evolutionary theory is true - even though there is overwhelming evidence that it is true. So it seems that you require certain, irrevocable proof for God's existence, but accept evolutionary theory without certain proof. So you've got a choice:

Bite a bullet and claim that a higher standard of proof is required for belief in God than for belief in evolution.

Take a hit, conceding that there is a contradiction in your responses.

I did, indeed, reply "true" to the statement that evolutionary theory is essentially true. But that's only because I wasn't given the option of replying to the statement that evolution is a fact. I accept evolution because there is certain proof that it exists. I assumed, incorrectly as it turns out, that they were using "evolutionary theory" as a synonym for "evolution."

In order to be consistent I guess I should have replied that "evolutionary theory" is not essentially true.

Watch out for Question 15. It's also a trap.

Read the comments on FriendlyAtheist. Quite a few people got through the test with no hits. I wonder how they answered the question about evolution.

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Vegetarian Humor

 
Today after class we were having a wide-ranging discussion about all kinds of issues when one of my students announced that she was a vegan. She claimed that all us meat-eaters were ignoring the slaughter of animals required to justify our habit.

I retorted with the standard reply that she was conveniently ignoring all the plants that had to die for her. Her response caught me off-guard—it was new to me but may be old hat to you. Anyway, she said, "I'm not vegan because I love animals, I'm a vegan because I hate plants!"

The original quote is ...

I am not a vegetarian because I love animals; I am a vegetarian because I hate plants.

                                             A. Whitney Brown

I like it. From now on I'll say that I'm an omnivore because I hate all living things!

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The photo honors National Meatloaf Appreciation Day. At least one animal, and several plants, were seriously injured during the making of this photo.

Electoral Compass

 
I'm a sucker for these things but take them with a huge grain of salt because I'm not an American. Some of the questions were very difficult to answer and I ended up having to guess what they wanted a socialist like me to say.

Why isn't Kucinich on the chart? How accurate are the positions of the candidates?

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Stop the Presses! Denyse O'Leary Says Something Thruthful!

 
You'd better sit down before I tell you this. Over on Uncommon Descent Denyse O'Leary has just posted an article complaining about evolution, as Intelligent Design Creationists tend to do¹ [Today at Design of Life: The Avalon explosion: Another intricate, Darwin-busting puzzle].

But she really blows it in the first sentence when she accidentally gets something right, suggesting that she is finally beginning to understand what we've been telling her for years.

Contrary to popular misconceptions, the history of life shows no steady Darwinian march of progress ...

Congratulations, Denyse. You finally understand that there's no progress in evolution. There's no purpose either.

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1. They think that criticism of evolution is the same as promoting Intelligent Design Creationism—but then, that's why we call them IDiots.

What's Going On Here ?

 


Go to easternblot to find out. The photos were taken in the 2nd year introductory Cell and Molecular Biology course at the University of Toronto.

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Drinking Cold Water Causes Cancer

 

Friday's Urban Legend: FALSE

This one was sent to me a few days ago.

This is a very good article. Not only about the warm water after your meal, but about heart attacks. The Chinese and Japanese drink hot tea with their meals, not cold water, maybe it is time we adopt their drinking habit while eating.

For those who like to drink cold water, this article is applicable to you. It is nice to have a cup of cold drink after a meal. However, the cold water will solidify the oily stuff that you have just consumed. It will slow down the digestion. Once this "sludge" reacts with the acid, it will break down and be absorbed by the intestine faster than the solid food. It will line the intestine. Very soon, this will turn into fats and lead to cancer. It is best to drink hot soup or warm water after a meal.

A serious note about heart attacks - You should know that not every heart attack symptom is going to be the left arm hurting. Be aware of intense pain in the jaw line.

You may never have the first chest pain during the course of a heart attack. Nausea and intense sweating are also common symptoms. 60% of people who have a heart attack while they are asleep do not wake up. Pain in the jaw can wake you from a sound sleep. Let's be careful and be aware. The more we know, the better chance we could survive.

A cardiologist says if everyone who reads this message sends it to 10 people, you can be sure that we'll save at least one life. Read this & Send to a friend. It could save a life.

So, please be a true friend and send this article to all your friends you care about.

Snopes.com checked it out and guess what? It's not true [Cold Comfort].

The email message originated only two years ago (February, 2006) so it's a relatively recent urban legend.

One of the tests I recommend when you receive free medical advice on the internet is to ask yourself whether your doctor gives out the same advice. If so, then it may be true. But you would already suspect that since your doctor told you.

If your doctor never told you about the email warning then there are three possibilities ...

1. Your doctor doesn't know about this important problem that could cause cancer but all your friends and neighbours do know about it.


2. Your doctor has heard the story but knows that it's false.


3. Your doctor knows that cold liquids cause cancer (or whatever) but for some reason doesn't want you to know this so she won't tell you.

Ask yourself which possibility is most likely?

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[Photo Credit: [FreeFoto.com]

Student Evaluations

Yesterday we had a departmental retreat where we discussed a number of things, including undergraduate education. The Biochemistry Undergraduate Student Society (BUSS) made a presentation and sent along eight students who joined the various discussion groups that we set up to talk about undergraduate teaching. It was lots of fun and very informative.

One of the issues that was raised was student evaluations. The main student group for all arts students and science students has a standard student evaluation form that they distribute in most classes. The results are published in the Anti-Calendar.

The Department of Biochemistry does not participate in this exercise and, consequently, none of our courses are in the Anti-calendar. We use our own evaluation forms with very different questions and the results are summarized for internal use within the department.

Some students suspect that the department has blocked the publication of student evaluations in the Anti-Calendar. They suspect that the reason for doing this is all of our courses have very bad ratings and we don't want students to find out how bad we are. (That kind of reasoning may actually work in our favor. Students who think like that stay out of our courses.)

The truth is that we have been doing our own evaluations for 40 years and we have different questions, and a different scale, than the ones used by the student union. That's the only reason why we're not in the Anti-Calendar.

However, even if we switched to using the standard students forms, I would remain opposed to collecting and publishing student evaluations for another reason. (The following opinion is not departmental policy, unfortunately.)

I've blogged about this is the past [Student Evaluations] [Student Evaluations Don't Mean Much]. The facts are that student evaluations don't evaluate what students think they're evaluating. Many scientific studies have been done and the evidence strongly suggests that students evaluations are based mostly on whether students like the personality of the Professor.

I teach science and scientific reasoning. I think it's important to ask whether the collecting and publication of student evaluations is a worthwhile and valid exercise. If student evaluations are scientifically justified then they should be published. If the evidence doesn't back up the claims then they are worthless. This isn't hard to follow, is it?

Publication of worthless student evaluations may actually be counter-productive. The result may turn students away from courses they should be taking and encourage them to take easy bird courses they should be avoiding.

Until it can be demonstrated that student evaluations are useful and scientifially valid, I will continue to exercise my right to block publication of my evaluations, regardless of any decision by the Department of Biochemistry. And I will continue to argue against using flawed student evaluations in tenure and promotion decisions. I will also oppose all attempts to reward faculty members for excellence in teaching based entirely—or mostly—on student evaluations. Any other position is anti-scientific, in my opinion. No competent scientist can ever justify relying on standard undergraduate student evaluations to evaluate teaching ability.

Let's hear what everyone else thinks of student evaluations.

Here are a few interesting links to stimulate discussion.

Part of the discussion requires that you understand the "Sandbox Experiment" as described in [Of What Value are Student Evaluations?].

... true believers (who too often seem to have a stake in selling institutions a workshop or an evaluation form) proclaim that student evaluations cannot be manipulated or subverted. Anyone who believes such claims needs to read the first part of Generation X Goes to College by Peter Sacks. This part is an autobiography of a tenure track experience by the author in an unnamed community college in the Northwest. Sacks, an accomplished journalist who is not a very accomplished teacher, soon finds himself in trouble with student evaluations. Sacks exploits affective factors to deliberately obtain higher evaluations, and describes in detail how he did it in Part 1 called "The Sandbox Experiment." Sacks obtains higher evaluations through a deliberate pandering, but not through promotion of any learning outcomes. For years, he manages not only to deceive students, but also peers and administrators and eventually gets tenure based on higher student evaluations. This is a brutal case study that many could find offensive, but it proves clearly that (1) student evaluations can indeed be manipulated, and (2) that faculty peer reviewers and administrators who should know better than to place such blind faith in student evaluations sometimes do not.

Read Student Evaluations: A Critical Review for a description of the Dr. Fox Effect, another one of those standard examples that every one should be aware of if they want to debate the issue of student evaluations.

This article also has a pretty good discussion of the "academic freedom" issue—which I prefer to call the "controversy conundrum." It is a very real problem. The more controversial your lectures, the more likely you are to receive lower student evaluations of faculty (SEF). Yet, teaching controversial issues is the essence of a university education.

There exist simple and well-known ways for a professor to avoid giving offense. One technique, when a class ostensibly focuses on a controversial subject matter, is to focus one's lectures on what other people have said. For example, a professor may, without raising any eyebrows, teach an entire course of lectures on ethics without ever making an ethical statement, since he confines himself to making reports of what other people have said about ethics. This ensures that no one can take offense towards him. During classroom discussions, he may simply nod and make non-committal remarks such as "Interesting" and "What do the rest of you think about that?", regardless of what the students say. (This provides the added "advantage" of reducing the need both for preparation before class and for effort during class, on the part of the professor.) Although pedagogic goals may often require correcting students or challenging their logic, SEF-based performance evaluations provide no incentive to do so, while the risk of reducing student happiness provides a strong incentive not to do so. Some students may take offense, or merely experience negative feelings, upon being corrected, whereas it is unlikely that students would experience such negative feelings as a result of a professor's failure to correct them. Overall, SEF reward professors who tell their students what they want to hear.

As far as I'm concerned, it's much more fun to tell students what they don't want to hear!

The article also makes a comment on the perception of students as consumers; and universities as businesses whose goal is to please the customer. Nothing could be further from the truth.

A fourth reason why SEF are widely used may be the belief that the university is a business and that the responsibility of any business is to satisfy the customer. Whether they measure teaching effectiveness or not, SEF are probably a highly accurate measure of student satisfaction (and the customer is always right, isn't he?). However, even if we agree to view the university as a business, the preceding line of thought rests upon a confusion about the product the university provides. Regardless of what they may themselves think at times, students do not come to college for entertainment; if they did, they might just as well watch MTV for four years and put that on their resumes. Students come to college for a diploma. A diploma is a certification by the institution that one has completed a course of study and thereby been college-educated. But that will mean nothing unless the college or university can maintain intellectual standards. A particular student may be happy to receive an easy A without having to work or learn much, but a college that makes a policy of providing such a product will find its diplomas decreasing in value.

Part of a university's responsibility may be to satisfy its students. But it is also a university's responsibility to educate those individuals whom it is certifying as educated. Unfortunately, those goals are often in conflict.

Here are some interesting comments from Professor Fich at the University of Toronto [Are Student Evaluations of Teaching Fair?].

Finally, I'd like to hear from you on the following point. Why are student evaluations anonymous? Shouldn't we be encouraging students to stand up and take responsibility for their opinions rather than hiding behind anonymity? Yes, I'm well aware of the fact that students think they will be punished for a negative evaluation. This is an unreasonable and illogical fear in most cases (i.e., at a respectable university). The point of a university education is to engage in debate and discussion. Trust me, most Professors can take it. Most students should start learning how to do the same.

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[Image Credit: The cartoon is from the ASSU Anti-Calendar]