Posting Comments on PLoS One

 
Okay that's it for me. This isn't worth the trouble.

I tried posting a response on the thread "Is "prokaryotic" an outdated term?" over on PloS One and after getting bumped around to several different webpages I finally ended up with what looked like a response form. I typed in an extremely erudite and well-reasoned response that would have blown everyone out of the water then hit the "Post" button. (There's no "Preview" option on PLoS One. This is highly discriminatory—it works against people like me who need to proofread everything before posting.)

The result of trying to post a comment is the error message shown below. I can close the error window and hit "Post" again but this produces an endless cycle of error messages.


I'm not an complete idiot when it comes to using computers. I'm not going to waste any more time trying to post comments on the PLoS Website.

Is "Prokaryote" a Useful Term?

 
Coturnix (Bora Zivkovic) is the Online Community Manager at PLoS-ONE (Public Library of Science). Part of his job is to get people to post comments on the PLoS websites. [New in Science Publishing, etc.]

So when Bora suggested we get involved in a debate on "Is "prokaryotic" an outdated term?" I hopped on over to the PLoS website and read the comments. I discovered that you have to register on PLoS in order to comment so I went ahead and did that and posted a response to the question.

I don't like registering on websites, it's a painful process, especially in this case 'cause you have to answer a lot of questions. It took me about ten minutes to figure out what to do and to convince the program to let me register even though I didn't want to receive email spam from PLoS. I also had to make up a user ID—Larry_Moran, in this case—because, apparently your name isn't good enough. This is not a very open process.

Theme

The Three Domain Hypothesis
Anyway, the question is important. If you think the Three Domain Hypothesis is well established, then you believe there are two non-eukaryotic domains (Bacteria, Archaea). Furthermore, the eukaryotes cluster with the Archaea according to this hypothesis. Thus, the word "prokaryote" encompasses a paraphyletic group and becomes useless.

But we wouldn't be having this discussion if the Three Domain Hypothesis is incorrect. In that case, the root of the tree might well be a split between eukaryotes and prokaryotes. The point is that the discussion about usefulness of "prokaryote" is really a debate about the validity of the Three Domain Hypothesis and we shouldn't forget that. It's wrong to assume that your side has won that debate and then start to solidify your apparent victory by defining your opponent's point of view out of existence!

Phone this Hotline for Technical Support

 

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[Hat Tip: Canadian Cynic]

You Will Be Assimilated!

 
Canada's ongoing attempt to subvert American culture has been noted by Tegumi Bopsulai, FCD (not his real name). He sends this photograph of a Tim Horton's in Geneva, New York. It's not the one that's farthest south—that distinction goes to the Timmy's in Jamestown NY, as far as I know.

Does anyone have any other evidence of Canada's success? I believe the assimilation is more successful in states like New York than in California. I don't think we're even trying in Texas.

Happy 50th Birthday!

 
50 years ago today we were treated to the continuous "beep-beep" of the first artificial Earth satellite. Sputnik ("traveling companion") was launched by the Soviet Union on October 4, 1957. [Listen to it here.]

It was an exciting time. I remember the thrill of realizing that the space age had truly begun and like many others I tried, unsuccessfully, to find Sputnik in my telescope.

For some, the launch was a traumatic event for another reason. It signaled to the entire world that the Soviet Union was a technologically advanced country. Many interpreted this to mean that science (not technology) education in the Soviet Union was ahead of that in the West. This was not an unreasonable assumption, as it turns out, but not because of Sputnick.

Some improvements in science education were made and, according to popular belief, our students in the West rapidly caught up with those in other countries, only to fall behind again in the 1980's. The truth is certainly more complicated.

Does anyone know of a reliable study of science education in various countries over the past 50 years? What was the real effect of Sputnik in the short term and in the long term?

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[Photo credit: Astronomy Picture of the Day for October 4, 2007.]

[See Bad Astronomy for more information and links about Sputnik I.

The Goal of a University Education

 
At the University or Toronto we're about to go through one of our regular navel-gazing exercises where the administrators ask us how they should plan for the future. In this case, it's a document called "Towards 2030." It's another one of those motherhood-type essays about improving the undergraduate experience and coping with a changing research environment. After 43 years in university, it's all beginning to sound a bit repetitive.

I was wondering whether anyone had any new ideas when I saw this article in the New York Times [Academic Business]. It's written by Andrew Delbanco who is the director of American studies and Levi Professor in the Humanities at Columbia University. There's nothing new there either. It's the same old complaints that we protested about in the 1960's; namely, the transformation of the university into a corporation. Even when we became Professors we didn't succeed in reversing this trend. The latest navel-gazing exercise is a case in point. It's the administrators who act as though this is "their" university and everyone else is an employee or a customer.

But Delbanco does make a few points that I'd like to comment on.

College today is a place in which students from many backgrounds converge, and it is neither feasible nor desirable to prescribe for them some common morality. But college should be a place that fosters open debate of the ethical issues posed by modern life — by genetic screening and engineering; by the blurring of the lines dividing birth, life and death; by the global clash between liberal individualism and fundamentalism.

I just came back from a class where my students discussed evolution and creationism with me and my colleague, who happens to be a Jesuit Priest. It was a lot of fun but you know what? In a university of 72,000 students (59,000 undergraduates) this class represents only a tiny fraction of the student body. The vast majority don't want this kind of education no matter how valuable we think it is. It's simply not true that if you create the classes they will come.

It's not good enough to just mouth the words about the value of a liberal education. We need practical solutions to the problem of getting today's students to buy into the concept. Anybody got any ideas on how to do that?

Delbanco also says,

Some signs suggest that higher education is waking up to its higher obligations. There is more and more interest in teaching great books that provoke students to think about justice and responsibility and how to live a meaningful life. Applications are up at Columbia and the University of Chicago, which have compulsory great-books courses; students at Yale show growing interest in the “Directed Study” program, in which they read the classics; and respected smaller institutions like Ursinus College in Pennsylvania have built their own core curriculums around major works of philosophy and literature.

This is where I part company with the Professor of Humanities. There was a time when I thought that the old books were a wonderful way to build a good program in liberal education. But since then I've come to appreciate that part of the problem is scientific illiteracy and we don't solve that problem by focusing all our attention on dead philosophers and even deader novelists.

Don't get me wrong, I still think that philosophy is the core discipline in an university and every student should become familiar with the basic problems in philosophy. What I'm objecting to is the attitude that being literate in the humanities is all it takes to become educated. You simply can't intelligently discuss the "ethics" of genetic engineering these days if you don't learn science. And you don't learn science by reading the great books, even if one of them is The Origin of Species.

Scientists need to speak out. You can stand around at cocktail parties discussing the meaning of Moby-Dick all you want but you can't call yourself educated if you don't know what DNA is or what causes eclipses and earthquakes.

I don't know how to get students interested in science either, by the way. Does anybody? Is the problem beyond the ability of the university to solve?

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[Photo Credit: The top photograph shows a walkway in one of theolder buildings on the University of Toronto campus from the Macleans website]

[Hat Tip: Michael White at Adaptive Complexity who has some interesting comments that are worth reading(Do Universities care about more than image?)]

This is Your Brain on Spirits

 
Denyse O'Leary—Toronto's version of Bill Dembski—has written a book in collaboration with McGill researcher Mario Beauregard. It's about proving the existence of God through the study of brain waves. Denyse has been telling us about this book for over a year.

This isn't my field so I've given his book a pass although I've got no doubts about its scientific validity (none!). PZ Myers isn't nearly so shy. Read his assault review at [The Spiritual Brain]. Here's the bottom line.

Don't buy this book. Stick your brain in a blender first.

Are those the only two choices?

Nobel Laureate: Barbara McClintock

 

The Nobel Prize in Physiology or Medicine 1983.

"for her discovery of mobile genetic elements"

Barbara McClintock (1902-1992) received the Nobel Prize in Physiology or Medicine for discovering transposons, or mobile genetic elements [Transposons: Part I, Transposons: Part II].

Barbara McClintock began her interest in genetics while she was an undergraduate at Cornell in 1921. That was a time when genetics as a discipline was just being recognized [autobiography]. McClintock went on to earn a Ph.D. from Cornell in 1927 and then stayed on to lecture in genetics undergraduate courses. In 1936 she moved to the University of Missouri where she was a Professor until 1941 when she took a position at the Carnegie Institution of Washington, with a lab at the Cold Spring Harbor Laboratories (New York, USA). She remained there in an official position until 1967 but was still a frequent visitor until well into the 1970's.

Most of her scientific work was in the field of maize cytogenetics where she quickly established a reputation as a good experimenter with a very sharp mind. She received many accolades and awards throughout her career and was elected to the National Academy of Sciences (USA) in 1944. In 1945, she became the first female president of the Genetics Society of America.

Her work on mobile genetic elements in maize began in 1944 and this work soon led to the discovery of two transposons, Dissociator (Ds) and Activator(Ac).

The presentation speech was given by Professor Nils Ringertz of the Karolinska Institute and it explains, in easy-to-understand terms, the significance of McClintock's work.

Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,

The Nobel prize in Physiology or Medicine for 1983 recognizes a great discovery about the organization of genes on chromosomes and how these genes, by changing places, can alter their function. This discovery, made while investigating blue, brown, and red spots on maize kernels, resulted in new knowledge of great medical importance - information which provides the key to problems as diverse as hospital infections, African sleeping sickness and chromosome changes in cancer cells. In order to explain this link, we must start at the beginning; namely with Barbara McClintock's investigations of coloured spots on maize kernels.

The maize cobs that we buy at the supermarket usually have yellow kernels. This is not always the case with wild forms of maize. In Central and South America where maize originated, one can still find primitive types of maize where the kernels are blue, brown or red. The colour depends on pigments in the surface layer of the kernel endosperm. The endosperm is the food store for the developing seedling. The synthesis of kernel pigments is controlled by the genes of the maize plant. In some cases one finds differently coloured kernels on the same cob. The explanation for this is that the cob is formed from a group of female flowers. Each of these female flowers may be fertilized independently by a pollen gram from a male flower. Maize cobs with differently coloured kernels arise when the pollen grains do not carry the same genes for endosperm pigments. All these phenomena can be explained on the basis of the laws of the inheritance stated by Gregor Mendel in 1866. What cannot be explained, however, and what puzzled plant breeders in the 1920's, was that maize kernels sometimes have numerous spots or dots, rather than being evenly coloured as would be expected. It was suspected that the dots on the kernels were due to the instability of genes involved in the pigment synthesis. These genes were believed to undergo mutations during the development of the kernel. Should such a mutation be inherited by several generations of daughter cells it would result in a differently coloured spot. This idea received further support when it was found that maize with variegated kernels also had broken chromosomes. The problem of variegation in maize was of slight importance from a practical point of view, but it fascinated Barbara McClintock because it evidently could not be explained on the basis of Mendelian genetics.

McClintock analyzed this phenomenon by studying chromosome changes and the results of crossing experiments in maize with different patterns of variegation. She was able to identify a series of genes on chromosome number 9 that determine pigmentation and other characteristics of the endosperm. She found that variegation occurred when a small piece of chromosome 9 moved from one place on the chromosome to another close to a gene coding for a pigment. The usual effect was to switch off the gene, and furthermore, the chromosome frequently showed a break at the site of integration. McClintock called these types of genetic material "control elements" since they clearly altered the function of neighbouring genes. In a series of very advanced experiments carried out between 1948 and 1951, McClintock mapped several families of control elements. These elements affected not only the pigmentation pattern of the maize kernels but other properties as well. She also pointed out that mobile genetic elements were probably present in insects and higher animals. In spite of this, her observations received very little attention. This was because her findings, when first presented, were overshadowed by the discovery that the DNA molecule stores the genetic information in its structure. It also became evident that mutations involving only one change in one of the building blocks in the DNA molecule could have serious effects. Under these circumstances, it is not surprising that few geneticists were prepared to accept that genes could jump in the irresponsible manner that McClintock proposed for controlling elements. The "state of the art" in molecular genetics at that time made it difficult to accept "jumping genes", and thus McClintock had to await the development of methodological tools powerful enough to verify in biochemical terms her great discovery.

In the mid-sixties, mobile genetic elements were found to play an important role in the spreading of resistance to antibiotics from resistant to sensitive strains of bacteria. This type of transferable drug resistance is a serious problem in hospitals since it causes infections that are very difficult to treat. During the 1970's, more support was found for the medical significance of mobile genetic structures. It was found, for instance, that the transposition of genes is an important step in the formation of antibodies. It has always been a mystery how the body, using a limited number of genes, can form an almost endless number of different antibodies to foreign substances. Nature has solved this problem according to the building block principle. When an individual is born, the chromosomes carry a set of mobile building blocks for antibody genes. By recombining these blocks in various ways in different cells, the body is able to generate millions of genes for antibodies.

During the last few years mobile genetic structures have attracted great interest in cancer research. In certain forms of cancer, growth regulating genes called oncogenes, are transposed from one chromosome to another. Tumour viruses in birds and mice have been found to carry oncogenes which they, in all likelihood, originally picked up from a host cell. If a virus then introduces these genes in the wrong place on the chromosomes of a normal cell, the latter is transformed into a cancer cell.

McClintock's discovery of mobile genetic elements in maize, therefore, has been found to have counterparts also in bacteria, animals and humans.

What led McClintock to devote her research to the variegation of maize kernels was that it did not lit in with Mendelian genetics. With immense perseverance and skill, McClintock, working completely on her own, carried out experiments of great sophistication that demonstrated that hereditary information is not as stable as had previously been thought. This discovery has led to new insights into how genes change during evolution and how mobile genetic structures on chromosomes can change the properties of cells. Her research has helped to elucidate a series of complicated medical problems.

Dr. McClintock,

I have tried to summarize to this audience your work on mobile genetic elements in maize and to show how basic research in plant genetics can lead to new perspectives in medicine. Your work also demonstrates to scientists, politicians and university administrators how important it is that scientists are given the freedom to pursue promising lines of research without having to worry about their immediate practical applications. To young scientists, living at a time of economic recession and university cutbacks, your work is encouraging because it shows that great discoveries can still be made with simple tools.

On behalf of the Nobel Assembly of the Karolinska Institute I wish to convey to you our warmest congratulations and I ask you to receive your Nobel prize in Physiology or Medicine from His Majesty the King.

[Photo Credit (top): The Barbara McClintock Papers]

Transposons: Part II

 
There are many eukaryotic transposons that resemble the simple bacterial transposons described in Transposons: Part I. The classic examples are the P-factor transposon in Drosophila melanogaster and the AC-like elements in maize.

Both of these transposons have many of the characteristics of the bacterial transposons including the presence of a transposase gene. Like the bacterial transposons described earlier, this type of transposon jumps from one location to another. The original genome site is restored when the transposon is excised.

Transposons were first discovered in plants because there are many plant transposons that are quite active (they jump a lot) and they frequently land in genes that become disrupted. The disrupted gene can cause a visible phenotype that plant breeders have taken note of.

One example is shown on the left. The top figure is a yellow (colorless) kernel of corn. The wild-type purple color is not produced because of a transposon (Spm) inserted into one of the genes for the production of the pigment anthocyanin. Unfortunately for the plant breeder, this mutant isn't stable and from time to time the kernels "revert" back to purple as shown in the lower figure. The purple color is not evenly distributed because the "reversion" only occurs in small clusters of cells.

It was Barbara McClintock who first recognized that this pattern was due to "jumping genes" back in the 1940's. She based her conclusions on work she was doing with a number of genes in corn where the genetics could not be reconciled with standard Mendelian transmission. We now know that the reversion to production of anthocyanin is due to excision of the Spm transposon that was disrupting the gene. This excision occurs spontaneously in the somatic cells during the development of the kernel. McClintock received the Nobel Prize in 1983 for the discovery of mobile genetic elements.

There are many other examples of transposon mediated mutations in plants, as well as in other eukaryotes, such as yeast and Drosophila melanogaster. Another plant pigment example was shown in Monday's Molecule #45. The picture of the patterned petunia flower is reproduced below. It is taken from University of Bern website.

The pattern of colored stripes seen in petunia flowers (left) is due to the presence of transposon Tph1. The species Petunia hybrida line W138 contains a disrupted rt locus due to the insertion of transposon dTph1 (Kroon et al. 1994). The mutation blocks production of anthrocyanin pigments and gives rise to a white flower.

During development of the flower, the Tph1 transposon excises in certain cells and pigment production is restored. The pie-shaped pattern of cells reveals that the flower grows outward from a small number of cells in the center of the primordial flower head.

The W138 line can be used to isolate additional mutants since Tph1 excises and reintegrates into other genes at an appreciable rate (van Houwelingen et al. 1998).

Plant genomes harbor many transposons since they have a huge amounts of junk DNA where transposons can hide without causing damage. In fact, much of this junk DNA may have originated from ancient transposons that acquired mutations rendering them unable to excise and jump to another site. Over time other transposons inserted themselves into the defective transposons and the amount of junk DNA grew. The recent sequencing of the genomes of several plants has revealed an abundance of sequences related to transposons. These sequences appear to be inactive.

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[Photo Credit: The pictures of the corn kernels are from Moran, Scrimgeour et al. Biochemistry 1998.]

Kroon, J., Souer, E., de Graaff, A., Xue, Y., Mol, J. and Koes, R. (1994) Cloning and structural analysis of the anthocyanin pigmentation locus Rt of Petunia hybrida: characterization of insertion sequences in two mutant alleles. Plant J. 5:69-80. [PubMed]

van Houwelingen, A., Souer, E., Spelt, K., Kloos, D., Mol, J. an Koes, R. (1998) Analysis of flower pigmentation mutants generated by random transpson mutagenesis in Petunia hybrida. Plant J. 13:39-50. [PubMed]

Transposons: Part I

 
Transposons are segments of DNA that can move (transpose) within the genome. They are also known as mobile genetic elements, transposable elements, jumping genes, or selfish DNA. Transposons often encode the enzymes necessary to catalyze their relocation and duplication in the genome. They don't usually have any function other than replicating themselves and jumping around in the genome. That's why they're sometimes called "selfish DNA." Selfish DNA is not the same as the "selfish genes" of Richard Dawkins. Those are real genes that perpetuate themselves through a beneficial effect on the organism they inhabit.

There are many different types of transposon. The best characterized ones are found in bacterial genomes where they are called insertion elements (IS). An example is shown below.
This example exhibits most of the characteristics of simple transposons. The grey bars at each end represent the genomic DNA into which the transposon is inserted. The yellow bars indicate a short stretch (~5 bp) of genomic DNA that's repeated on either side of the insertion element. This short repeat is almost always associated with insertion and excision of the transposon and it's a diagnostic feature of mobile genetic elements.

The red bars are inverted repeats at the ends of the transposon. This is another feature that's common to most transposons and it is required for copying and insertion/excision. This particular example contains a gene for the enzyme "transposase" (green).

The mechanism of transposition is shown in the figure below. Transposase catalyzes the excision of the transposon from the genome. It also cuts the DNA at the target site creating staggered ends with single-strand extensions, much like the cleavage sites of some restriction endonucleases [Restriction, Modification, and Epigenetics].


The excised transposon is integrated into the DNA that has been cut at the target site, then the single-stranded gaps are filled in by DNA polymerase and sealed by DNA ligase. The result is an integrated transposon with a short stretch of duplicated genomic DNA at each end.

In this case, the transposon can really be said to "jump" from one location to another. The original site is completely restored and the transposon moves to another location.

Many bacteria contain composite transposons that contain additional genes. The best known ones are those that carry genes for drug resistance, such as tetracycline resistance (transposon Tn10) or chloramphenicol resistance (Tn9). One of the reasons why drug resistance spreads in bacterial populations is because the resistance gene is on a mobile genetic element that can integrate into foreign DNA or into a plasmid that can be readily transferred.

There are usually not many transposons in a typical bacterial genome. This is because there are not many sites of integration that aren't lethal. In most cases when a transposon jumps it lands in a gene and inactivates it. This is usually lethal. Thus, most bacterial transposons reside in parts of the genome that are non-essential and there isn't much of that in bacteria.

Genomes that contain lots of non-essential DNA (junk) are likely to carry many transposons.

Mythical PNAS Papers

 
Here's part of a Harvard University Press release issued yesterday.

Beyond a 'speed limit' on mutations, species risk extinction

Genomes of various organisms lose stability with more than 6 mutations per generation

CAMBRIDGE, Mass. -- Harvard University scientists have identified a virtual "speed limit" on the rate of molecular evolution in organisms, and the magic number appears to be 6 mutations per genome per generation -- a level beyond which species run the strong risk of extinction as their genomes lose stability.

By modeling the stability of proteins required for an organism's survival, Eugene Shakhnovich and his colleagues have discovered this essential thermodynamic limit on a species's rate of evolution. Their discovery, published this week in the Proceedings of the National Academy of Sciences, draws a crucial connection between the physical properties of genetic material and the survival fitness of an entire organism.

This sounds very interesting. The limit of six mutations per genome per generation is far less than the calculated mutation rates for mammalian genomes [Mutation Rates] so it looks like another genetic load argument in favor of junk DNA.

So, I set off to retrieve the article that, according to the press release was published in this week's issue of PNAS. But it wasn't. You can see for yourself by looking at the current issue on the website [Sept. 25, 2007].

Not a problem. I've encountered this discrepancy before. What they mean is the issue that's about to be published and the article is available online in prepublication format. All you have to do is check the "Early Edition" (in this case the Oct. 2, 2007 edition) by clicking on the link from the PNAS home page. Except that the paper isn't there either.

Thus, in spite of what it says in the press release, this paper has not been published by PNAS in either the paper issue or online. This is not the first time this has happened. Over the past few months I've tried to find half a dozen mythical PNAS papers that are prominently mentioned in press releases.

Wait a minute ... look at the fine print on the early edition page [Early Edition]. The version that I'm looking at right now says "Last updated October 2, 2007." Right below that is the following statement.

Because PNAS publishes daily online, you may read about an article in the news media on Monday or Tuesday, but the article may not publish online until later in the week. You may use the CiteTrack feature to set up an e-mail alert to notify you as soon as the article you are interested in publishes.

This is unacceptable. If PNAS can't guarantee that a paper will be available when the press release embargo is lifted then they should change the embargo date. Most other journals have a restriction on press releases that delays the promotion of a paper until it is published and we can see for ourselves whether the hype and the reality match. Apparently PNAS is aware of this problem but instead of fixing it by moving the embargo date to Friday they choose to ignore publishing etiquette. This is wrong.

Three Cheers for October's SEED Magazine

 
One of my pet peeves is the misuse of the term "Central Dogma of Molecular Biology" [Basic Concepts: The Central Dogma of Molecular Biology]. Most people define it as the flow of information from DNA to RNA to protein. Many then go on to declare that the Central Dogma has been overthrown because of reverse transcriptase, alternative splicing, microRNA, epigenetics, or whatever.

This month's issue of SEED has a tear-out summary (cribsheet) of "Genetics." In one of the boxes titled "The Central Dogma of Molecular Biology" there's a drawing of the major pathways of information flow. The caption says.

There are nine ways information can theoretically flow between DNA, RNA, and protein. Of these, three are seen throughout nature, DNA to DNA (replication), DNA to RNA (transcription), and RNA to protein (translation). Three more are known to occur in special circumstances like viruses or laboratory experiments (RNA to RNA, RNA to DNA, and DNA to protein). Flows of information from protein have not been observed. The trend is clear: information flow from DNA or RNA into protein is irreversible. This is known as the "central dogma," and forms the foundation of molecular biology.

Yeah! As far as I know this is the only popular magazine to get it right.

MMP: Debunking the Myths, Chastising the Fearmongers

 


The amount of misinformation being spread about the Mixed Member Proportional voting system is truly frightening. I thought the citizens of Ontario deserved better than that. This is an important referendum and it shouldn't be decided by people who misrepresent the truth. There are legitimate arguments on both sides of the issue but it would be a real shame if voters were frightened into rejecting MMP by lies and distortions.

I've already tried to explain why the Sunday Toronto Star was wrong in its editorial [The Toronto Star Endorses First-Pass-the-Post], but others have done a better job.

Here's an article in The National Post by Andrew Coyne [PR:Debunking the fearmongers]. Coyne says,

... we are told that changing the system will result in chronic instability, a series of minority governments, one falling after the other; or else that it will lead to chronic gridlock, a legislature divided into dozens of smaller parties, some extremist, who would use their bargaining power to hijack the political process, demanding that one or other of the mainstream parties adopt their agenda in return for their support. The spectre of Israel and Italy are often invoked, as if to cinch the argument.

We can dispose of the last easily enough. One: Israel and Italy are uniquely divided societies, and were long before they adopted PR. Two: Neither country has ever used anything like the mixed system proposed for Ontario, but rather adopted much more extreme forms of PR, with no threshold for support.

As for the more specific fears, they would perhaps be more tenable were we the first country ever to try proportional representation -- were it not already in use, in one form or another, in most of the democratic world. But in fact it is, and in no country have any of the scare stories come to pass.

Read the entire article to see just how misleading the opponent of MMP have become.

Then there's the press releases on the Vote for MMP website. The first one addresses the claim that party lists would be drawn up by party bosses and would favor hacks. This accusation was made in the Toronto Star editorial, but it's popular fodder for all opponents of MMP. Here's the truth from REALITY CHECK: VOTEFORMMP.CA CALLS ON TORONTO STAR TO CLEAN UP MISLEADING REPORTING.

VoteForMMP.ca is accusing the Toronto Star of fear-mongering and inaccurate journalism in the Star's editorial today against electoral reform.

In today's editorial, the Toronto Star repeated the misleading claim that under Ontario's proposed new MMP system, the new province-wide candidates “could simply be appointed by party bosses.”

"This argument is regularly being used falsely by unthinking defenders of the status quo to deter support for needed electoral reform," said Rick Anderson, campaign chair of VoteForMMP.ca. "It's a shame that a media organization with the Star's credentials is not more careful with the facts regarding such an important question confronting voters."

...

In today's system, parties are left to determine their own methods for democratically nominating local candidates. Likewise, the Citizens’ Assembly left it to the individual parties to determine their own methods of nominating both riding and provincial candidates in the future, with the provisos that the parties are required to nominate their candidates publicly before voters vote and to publish the details of their candidate nomination processes in a clear, democratic and transparent fashion.

"In the other jurisdictions which use MMP all parties have adopted democratic candidate nomination processes for proportional candidates, just as they have for local candidates. Moreover, even in advance of the new system being adopted three of Ontario's four parties have already made public statements affirming they will follow democratic practices to nominate MMP candidates." (See backgounder below.)

"The notion that under MMP candidates would be appointed is simply hogwash," said Anderson. "Star readers should demand greater accuracy from their paper. Informed voters require a higher standard than this inaccurate sloganeering."

The important point here is that Ontario parties will almost certainly adopt democratic practices in drawing up their lists. It makes sense and it's what other countries do. Let's not hear any more fearmongering about party lists. From now on, people who use that argument are not guilty of mere ignorance.

What about the idea that a Mixed Member Proportional voting system would lead to political chaos? This is another of the arguments used in the Toronto Star editorial and it's widely believed to be true. Here's the real truth based on available facts [REALITY CHECK #2 TORONTO STAR WRONG ABOUT WHETHER FPTP OR MMP LEADS TO POLITICAL CHAOS].

VoteForMMP.ca says the Toronto Star owes it to voters to do its homework on whether first-past-the-post (FPTP) or mixed member proportional (MMP) leads to better political consensus.

In an editorial today, the Toronto Star claimed that “Jurisdictions that have adopted some form or other of proportional representation – think of Italy, Israel, Germany, Belgium – have become notorious for chaotic politics and legislature gridlock.”

More than 80 countries use proportional voting systems, with some for more than a century. If colourful anecdotes suffice for “evidence”, does that mean Zimbabwe or Nigeria prove that FPTP is “notorious” for producing oppressive and corrupt regimes?

The respected comparative studies show countries with proportional representation enjoy stable, effective, representative, accountable governments, which tend to produce legislation more in line with majority viewpoint while maintaining strong economic performance.

Notwithstanding colourful politics, Italy is actually a fairly stable and successful country, as vibrant in its political culture as it is in so many other ways, and hardly a failing state. The periodic reorganizations of its governing coalitions are sometimes colourful to be sure, but are generally accomplished without elections or even changes of government, more akin to what we think of as cabinet shuffles than anything else. (See: minority governments in Canada for more disruptive examples of chaos). Where does the Star get off treating Italy this way - and forgiving what happens here in Canada when voters are divided in their preferences?

Germany is an example which directly disproves the Star's supposed point. When the 2005 elections produced a split outcome, and smaller parties demanded high concessions as the price of coalition support, the two largest parties instead agreed to collaborate together in forming a successful government. The Star should check its facts.

...

The Star is perpetuating two misleading myths: one that FPTP is relatively stable and the other that PR is not. The facts are generally the opposite of the Star's comfortable prejudice in favour of the status quo.

Gathering of the Godless

 
"Gathering of the Godless" is one of the subtitles in an ABC News story about last weekend's atheist meeting in Virginia (USA) [The Rise of Atheism].

For another, more interesting, version read Hermant's summary on FriendlyAtheist [Atheist Alliance International Convention 2007 (Recap)]. Find out he got to be Daniel Dennett.

Superoxide Dismutase Is a Really Fast Enzyme

PhilipJ has posted the latest "Molecule of the Month" on Biocurious [Molecule of the Month: Superoxide Dismutase]. The molecule is superoxide dismutase from cow (Bos taurus) drawn by David Goodsell from the 2SOD (formerly 1SOD) structure in the Protein Data Bank. This structure is from 1980.

The formal name of this enzyme is copper-zinc superoxide dismutase in order to distinguish it from other, unrelated, superoxide dismutases. As noted on the Biocurious website, the main reason for having this enzyme is to get rid of dangerous free radical forms of oxygen that are produced in a number of cellular reactions; notably, membrane-associated electron transport and photosynthesis. (Superoxide dismutase is found in all species.)

The reaction involves a copper ion (Cu²⁺) at the active site of the enzyme (E). A free radical, such as the toxic superoxide radical anion, binds to the coper ion and an electron is transferred from the superoxide radical to the copper ion. This leads to the reduction of the copper ion from the +2 form to the +1 form as it picks up a single negative charge from the electron. In the second step, this electron is passed from the copper ion back to another superoxide anion which then combines with two protons to make hydrogen peroxide (H₂O₂). Hydrogen peroxide can be easily converted to water + molecular oxygen by ubiquitous catalase enzymes.


Superoxide dismutase is an important enzyme and it's role in scavenging free radicals would be more than enough to justify its inclusion in biochemistry textbooks. But there's another reason why this enzyme is discussed. It's one of the fastest enzymes known to biochemists as shown in the table below.



I suspect that most of you aren't familiar with the Michaelis-Menten constants k_cat and K_M but that doesn't matter. Trust me, these are very fast enzymes.

In fact, superoxide dismutase is faster than it has any right to be. The maximum rate of an enzymatic reaction was thought to be limited to the rate of diffusion inside the cell. This makes sense since the substrate (superoxide anion) has to collide with the active site copper ion before a reaction can occur. But measurements of the actual enzymatic rate gave a result that was faster than theoretically possible given the diffusion rates inside the cell.

It wasn't until the structure of the enzyme was solved that this mystery was cleared up. Look at the structure shown above. This is the human version of copper-zinc superoxide dismutase from 2003 [1HL5]. The structure is drawn in a way that highlights the charges on the surface of the enzyme. Red side chains are negatively charged and blue side chains are positively charged. The entry channel to the copper ion (green) at the active site is lined with positively charged amino acid residues. These suck in the negatively charged oxygen radicals like a vacuum cleaner and feed them to the active site. That's how the enzyme can operate so fast.