Calling All Adaptationists (Again)

 
Have I got a treat for you! Before getting to the special excitement, let me congratulate all of you adapationists for your outstanding performance in the last contest [Calling All Adaptationists]. You did a marvelous job of making up stories to explain homosexuality in humans. Rudyard Kipling would have been proud [Just-So Stories].

Your mission for today, should you choose to accept it, is to explain odorous urine (smelly pee).

Here's the data. Some people produce odorous urine when they eat asparagus. They can transform the chemical, asparagusic acid (1,2-dithiolane-4-carboxylic acid), into smelly compounds like methanethiol, dimethyl sulfide, dimethyl disulfide, bis(methylthio)methane, dimethyl sulfoxide, and dimethyl sulfone (Mitchell, 2001). Other people can eat asparagus 'till the cows come home and their urine remains as pleasantly smelling as usual. The allele for producing the smell is an autosomal dominant trait.

There's an additional complication. Some people can't smell the odorous urine. There's no linkage between excretors and perceivers (able to smell the urine). Some can excrete but not smell and some can excrete and smell. All permutations exist in the population.

This ability to excrete smelly compounds and the ability to smell them are both examples of visible phenotypes. They're not just some neutral variation hiding away in junk DNA. Therefore, many (most?) adaptationists will certainly insist that it has to have an adaptive role in human evolution.

This is untilled soil, as far as I can gather. For some reason the experts haven't published the explanation. At least there's nothing I could find after hunting on the internet. You could become famous if your story makes sense. Let's see what you can come up with. I'll get you started ....

Once upon a time there were naked hunter men running on the savannah while their gatherer wives collected asparagus in the deep water by the sea shore ....

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Mitchell, S.C. (2001)
Food Idiosyncrasies: Beetroot and Asparagus. Drug Metabolism and Disposition 4(2):539-543.

Are These Dappers?

 
Is the first figure a dapper? How about the second figure? What about the third Figure, isn't he dapper in his nice suit?

Check out the definition of this new word from Ryan Gregory, Dog's Ass Plots (DAPs).

The Sun Revolves Around France

 
I thought the The View would take first prize when it comes to recent stupidity on TV but here's a contender. The contestant doesn't know whether the sun goes around the Earth or not so he polls the audience. 56% of them say yes.

The French accept evolution. Now we have to work on astronomy. I sure hope Phil Plait of Bad Astronomy doesn't see this.

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[Hat Tip: Casey Luskin (really!) [The French Reject Prayer while Accepting Evolution and Geocentrism]]

Toronto Catholic District School Board Allows HPV Vaccine

 
In the fight against superstition there are good days and there are bad days. Today is one of the good days when the Toronto Catholic School Board rejected the advice of the Catholic bishops and decided to go ahead with the HPV vaccination program [Catholic trustees vote to allow HPV vaccine in schools].

TORONTO -- In a move keeping with their counterparts across the province, trustees at the Toronto Catholic District School Board overwhelmingly voted in favour of allowing public health nurses to administer the controversial HPV vaccine in its schools.

After a discussion that lasted more than 90 minutes, trustees voted 9-3 in favour of the motion, rightly putting the health of their daughters over morality, one trustee said.

"I sure don't want to know that the headlines in two decades will read 'Catholic women lead in deaths for cervical cancer,' " trustee Maria Rizzo said during a passionately delivered statement to the board.

"I have a 16-year-old daughter. I'm sorry she's not in Grade 8."

In a separate motion brought forward by Ms. Rizzo, the board also agreed to lobby other levels of government to expand the free vaccination program to all eligible women.

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[Photo Credit: The photograph shows the Most Reverend James Wingle, D.D., Bishop of St. Catharines, President of the Ontario Conference of Catholic Bishops, whose advice was rejected by the Toronto Catholic School Borad.]

Evo-Devo: Innovation and Robustness in Evolution

When I first read the paper by Ciliberti et al. (2007) I was disappointed. On the surface, the paper seems to be addressing an important issue in evolutionary theory; namely, how can you get significant innovation in light of the fact that most biological systems resist change? On closer reading, however, it seemed more complicated than that. The authors were actually dealing with a phenomenum called "robustness." This is a popular description of a simple fact—the fact that many mutations are neutral so that there can be many variants of a protein that all carry out the same function. This has been known for decades.

The people who use the word "robustness" tend to elevate it to a level of significance that makes me nervous. Furthermore, they rarely use the term "random genetic drift" or "accident" in their papers, giving the impression that "robustness" is an adaptation that favors evolution.

There's much to criticize in the field of evolutionary developmental biology or evo-devo. Some of the "theories" are little more than wide-eyed speculation. I'm thinking particularly of The Plausibility of Life by Marc Kirschner and John Gehart.
Animal Chauvinism
That's one of the problems I have with this paper. The other problem is that it's a modeling paper. The authors create a model of evolution and demonstrate that their model produces systems that evolve. I have a problem with these models. While a mathematical model is useful to show that a mechanism can work, it does not prove that it does work.

Let me give a quick example to show you why I'm skeptical of claims by modelers. It is possible to model a Lamarckian process where species inherit acquired characteristics. The result will be evolution but that does not mean that the inheritance of acquired characteristics is a real mechanism of evolution. This point is not always made clearly in papers that describe mathematical models of evolution. To often, the fact that the model produces evolution is taken as evidence that the assumptions in the model are correct and it is an accurate representation of real biological evolution. This is the same problem with just-so stories [Just-So Stories].

Let's see how Ciliberti et al. (2007) set up their experiments in the introduction to the paper.

Biologists increasingly realize that genetic systems need to be robust to both genetic and nongenetic change (7–14). Robustness means that a system keeps performing its function in the face of perturbations. For example, many proteins can continue to catalyze chemical reactions, regulate transcription, communicate signals, and serve other roles despite mutations changing many amino acids; regulatory gene networks continue to function despite noisy expression of their constituent genes; embryos continue to develop normally even when faced with substantial environmental variation. Mutational robustness means that a system produces little phenotypic variation when subjected to genotypic variation caused by mutations. At first sight, such robustness might pose a problem for evolutionary innovation, because a robust system cannot produce much of the variation that can become the basis for evolutionary innovation.

The language sounds a little strange to me but I soon realized that there were many other authors who talked about "robustness" in this way. To me, the fact that there's neutral genetic variation in a population is just a natural consequence of chance mutation and random genetic drift. I don't see why biologists think that systems "need" to be robust and I don't see why the presence of neutral variation poses a "problem" for innovative change. It's perfectly acceptable to have beneficial mutations occurring on a background of neutral variation.

The "problem" seems to be more serious for evolutionary developmental (evo-devo) biologists than for others. It has given rise to much speculation about the evolution of evolvability. If you are interested in that sort of thing you should read the book The Plausibility of Life by Marc Kirschner and John Gelhart. (Warning, the contents may not be suitable for pluralists.)

The authors of the paper (Ciliberti et al.) claim that far from being a "problem" the existence of neutral variation is actually required for innovative evolution to occur.

As we shall see, there is some truth to this appearance, but it is in other respects flawed. Robustness and the ability to innovate cannot only coexist, but the first may be a precondition for the second.

This is pretty much where I stopped reading the first time. However, Michael White over on Adaptive Complexity has highlighted this paper in a posting put up yesterday [Evolution's Balancing Act]. This suggest that the paper resonates with some evolutionary biologists and piques my interest.

The paper describes a model of an evolutionary system. It happens to be gene regulatory networks but it could be just about anything. Ciliberti et al. (2007) show that if you have a single system with no variation then the possibility for innovative change is limited. On the other hand, if you have a robust system where there are many different variants—in different species—then there are more pathways to innovative change. Seems like a pretty trivial conclusion to me. It's the sort of thing Sewell Wright was talking about (Wright, 1932).

The course of evolution through the general field [adaptive landscape-LAM] is not controlled by direction of mutation and not directly by selection, except as conditions change, but by a trial and error mechanism consisting of a largely nonadaptive differentiation of local races (due to inbreeding and by occasional crossbreeding) and a determination of long time trend by intergroup selection.

The paper doesn't mention Wright, random genetic drift, or neutral mutations; although it does talk about neutral networks.

Instead, the paper seems to be fitting in with the evo-devo concepts of evolvability and facilitated variation. In other words the idea here seems to be getting very close to the concept that the variations in different species are selected because they increase the long term potential for innovative evolution. This is very different from what Wright was saying. He said—and I agree with him—that the variation is strictly accidental and just happens to provide potential for future evolution. The distinction is important for our understanding of evolution. Does evolution see into the future? Is there a hidden purpose?

Is "robustness" selected? I doubt that any of the authors would answer yes if the question was put directly but the paper certainly gives the impression that there's something positive going on. So does the description offered by Michael White when he says thing like,

Evolution carries out an incredibly tricky balancing act: the genetic program of a species has to be resistant to small changes, yet also susceptible to the adaptive remodeling of natural selection ....

So how does evolution maintain both stability and the potential for innovation?

This could be just metaphoric. The personification of "evolution" as acting to creat robustness may be excusable on that grounds. Nevertheless, a lot of this sort of language is creeping into the evo-devo literature and I wonder if it doesn't mean something more.

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S. Ciliberti, s., Martin, O.C. and Wagner, A. (2007) Innovation and robustness in complex regulatory gene networks. Proc. Natl. Acad. Sci. (USA) 104:13591-13596. Abstract

Wright, S. (1932) The roles of mutation, selection, inbreeding, crossbreeding, and selection in evolution. Proc. VI Intl. Cong. Genet. 1:356-366.

Sherri Shepherd of The View Doesn't Believe in Evolution

 
The earlier clip showed that Sherri Shepherd doesn't know if the Earth is flat. Here's a longer version where she admits to not believing in evolution. Whoopi seems to have a problem with this. So do I. There's something about this video clip that's deeply disturbing.

Catholic Public Schools: Constitutional Right or Archaic Privilege

 
Come to the lecture [Centre for Inquiry]. Unfortunately, I'll be out of town but I'm counting on many of you to attend and tell me all about it.

Starts: Friday, September 21st at 7:00 pm
Ends: Friday, September 21st at 10:00 pm
Location: University of Toronto, MacLeod Auditorium (Room 2158), Medical Sciences Building, U of Toronto, 1 King's College Circle.

CATHOLIC PUBLIC SCHOOLS: CONSTITUTIONAL RIGHT OR ARCHAIC PRIVILEGE

A FREE PUBLIC EVENT

Why did the UN condemn Ontario twice for human rights violations?

Why are we spending $0.5 billion/year on a second educational bureaucracy?

Is it true public catholic schools have the right to fire a teacher who isn't catholic?

But aren't separate catholic schools guaranteed indefinitely in the constitution?

And doesn't multiculturalism mean the best solution is to religiously segregate?

Learn why a secular democracy SHOULD NOT publicly fund catholic or other faith based schools and how we can fix the current situation

University of Toronto, Fri, Sept 21, 7pm, MacLeod Auditorium (Room 2158),Medical Sciences Building, U of Toronto, 1 King's College Crl.

Jan Johnstone, Progressive trustees network and trustee for the Bluewater District School Board,
Co-sponsored by University of Toronto Secular Alliance

(also Tues, Sept 18 at U of Guelph and Tues, Sept 25 at Carleton U - see web calendar)

A member of the Green Party-strong one school system supporters-will speak at each event

Learn the truth behind the ongoing debate on the #1 provincial election issue of 2007!

Get your questions answered and engage in a public forum on this crucial issue.

Is the World Flat?

 
Sherri Shepherd doesn't believe in evolution. She's not sure whether the world is flat or not. After watching this clip of The View you have to wonder about the intelligence of people on television. This really is flabbergasting. If I didn't know any better, I'd say it was all an act. Nobody could possibly be that stupid.

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[Hat Tip: BigHeathenMike (Sherri Shepherd Is a Retard)]

Catholic Bishops Block HPV Vaccinations

 
The Ontario government will provide free access to Gardasil®, a vaccine aginst Human Papillomavirus (HPV), for all Grade 8 girls in the province. The vaccine protects against 70% of all cervical cancers. HPV is acquired through sexual activity.

The vaccine will be administered in the public schools in three separate injections spread out over 6 months. The normal cost of the vaccine is $400. Once the series of shots is complete, women will be immune to the virus for many years.

See update
below.
The program is proceeding in the public schools but some Roman Catholic schools are threatening to block the vaccination of their young female students [Catholic schools debating moral issue of HPV shot]. The opposition in the Catholic schools is being stimulated by a letter from the Roman Catholic Bishops who oppose the vaccination program on the grounds that adolescent teenage girls should not be having sex in the first place.

Let's look at the letter sent to district school boards from the Ontario Council of Catholic Bishops [A message to Directors of Education of Catholic School Boards and to the Catholic educational community].

In August 2007, the Government of Ontario announced the introduction of the Human Papilloma Virus (HPV) vaccine into the publicly funded immunization program. This means that female students in all grade 8 classrooms in our school system will be offered the vaccine over the course of this year. This is a voluntary program and parents have the final decision on whether their daughters will be vaccinated.

The Bishops affirm that parents have the right and responsibility to decide whether their daughters should be vaccinated. We encourage parents to keep in mind some important considerations.

First, infection with HPV or other sexually transmitted diseases can occur only through sexual activity, which carries with it profound risks to a young person's spiritual, emotional, moral, and physical health. The Bishops note that, at best, a vaccine can only be potentially effective against one of these risks, that to physical health, and may have other unintended and unwanted consequences. Sexuality is a great and powerful gift. Sexual activity is appropriate only within marriage. Outside of marriage, abstinence is not only clearly the choice that leads to spiritual and moral wellbeing, but it is obviously the best protection against risks of disease.

Now, abstinence may be the choice that the Bishops have made but it's not a choice that's going to appeal to most teenagers. The Bishops can't really be this stupid, can they? Do they really think that most of their students are going to refrain from all sexual activity until they get married? What planet are they living on?

Second, there is no consensus among those involved in public health in Canada that HPV vaccination is the most prudent strategy in terms of allocating health care resources to address the goal of preventing deaths resulting from cervical cancer.

As we discussed in class today, when confronted with powerful scientific evidence—in this case that the vaccine prevents cancer—the goal is to discredit the data in any way possible. Here the Bishops are raising the issue of better cures. The implication is that parents should not support the HPV vaccination program because the the government could possibly have developed a "more prudent" strategy. Do the Bishops know of a better way to prevent cervical cancer? If so, why aren't they telling us?

The argument is bogus for two reasons. First, the real reason for opposition is that the vaccine may encourage promiscuity. Anything else is a red herring. Second, the program is under way and it's known to work. Refusing to protect our children from a known cancer using a known available treatment on the ground that there may have been something better is—how shall we say—really stupid.

Note the use of the "controversy" tactic. By bringing up the point that there may not be a consensus among public health officials, you cast doubt on the validity of the program. This gives you an excuse to criticize it without having to look like a prude who's completely out of touch with reality.

Further research is required. The Bishops of Ontario encourage parents to learn the medical facts concerning this vaccination.

This is classic spin framing. Make it sound like there's a real scientific problem here even if there isn't. What's the harm in waiting? Well, I'll tell you what's the harm. Cervical cancer.

Although the HPV vaccination program properly leaves the choice of participation to parents, the Bishops of Ontario regret its introduction without further opportunity for thorough study of all of the effects of this program. The best interests of children demands that parents and guardians be fully informed before granting consent.

The Bishops don't want to vaccinate young girls because those young girls shouldn't behaving sex. Everything else is obfuscation. You can tell it's obfuscation because this debate is not going on in the public schools were the vaccination is underway. If there really was legitimate concern about the safety of the vaccine then surely it would be debated in the public schools.

Parents and educators want to prepare children well for their future in all aspects of their lives. A proper education in chastity helps young people to embrace their sexuality with confidence and joy. We ask that Catholic school boards include this message in the information package that parents receive
concerning the program.

That's better. The real reason the Bishops are against protecting their young women against cancer is because chastity helps them embrace their sexuality. (There's a pun in there somewhere but I'm not going to touch it.)

Yours in Christ
Most Reverend James Wingle,
Bishop of St. Catharines
President
Ontario Conference of Catholic Bishops

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[Photo Credit: St. Thomas Aquinas is in the Halton Catholic District School Board next to where I live. he Halton board narrowly rejected the recommendation of the Bishops and decided to go ahead with the vaccinations. The lower photo is from the Toronto Star website.]

UPDATE: Jennifer Smith of Runesmith's Canadian Content lives in Halton district. She is relieved that her school district came to their senses and rejected the request of the Bishops [Health Trumps Religon]

Nobel Laureate: Thomas Hunt Morgan

 

The Nobel Prize in Physiology or Medicine 1933.

"for his discoveries concerning the role played by the chromosome in heredity"

Thomas Hunt Morgan (1866-1945) received the Nobel Prize in Physiology or Medicine for his work on the genetics of the fruit fly Drosohila melanogaster. Morgan is responsible for elucidating the basic mechanims of inheritance—especially sex-linked genes. His lab constructed the first genetic maps of chromosomes.

Morgan's influence was enormous. During the middle part of his career he ran a fly lab at Columbia University where he attracted people like Alfred Sturtevant, Calvin Bridges and H.J. Muller. Later on when the Morgan lab moved to CalTech he became head of the Biology Division and hired some notable scientists like; George Beadle, Boris Ephrussi, Edward L. Tatum, Linus Pauling and Sidney W. Fox. Morgan is known and respected as much for his influence on others as for his own work in the lab [see Thomas Hunt Morgan and His Legacy by E.B. Lewis].

Morgan was not able to be present at the award ceremony in Sweden because of administrative duties at CalTech where he was setting up the Biology Division. The presentation speech was delivered by F. Henschen of the Royal Caroline Institute, on December 10, 1933.

Your Majesty, Your Royal Highnesses, Honourable Audience.

As long as human beings have existed they will have observed children's resemblance to their parents, the resemblance or non-resemblance of brothers and sisters, and the appearance of characteristic qualities in certain families and races. They will also early have asked for an explanation of these circumstances, which has produced a kind of primitive theory of heredity chiefly on a speculative basis. This has been characteristic of the theories of heredity right up to our time, and as long as there existed no scientific analysis of the hereditary conditions, the mechanism of fertilization remained impenetrable mysticism.

Old Greek medicine and science took much interest in these questions. In Hippocrates, the father of the healing art, you can find a theory of heredity that probably can be traced back to primitive ideas. According to Hippocrates, inherited qualities, in some way or other, must have been transmitted to the new individual from different parts of the organisms of the father and the mother. Similar ideas of the transmission of qualities from parents to children are to be found in other Greek scientists, and, modified, also in Aristotle, the greatest biologist of the olden times.

Later on, this so-called transmission theory has been dominating. The only theory of heredity that has perhaps rivalled it, is the so-called preformation theory, an old scholastic idea that can be followed back to Augustine, the father of the Church. This theory maintained that, by the creation of the first woman, all following generations were also preformed in this first mother of ours. In modified form the preformation theory dominated the biology of the eighteenth century. Nevertheless, the transmission theory survived. Its last great representative was Darwin. He also seems to have understood heredity as a transmission of the personal qualities of the parents to the offspring through a kind of extract from the different organs of the body.

This conception, however, that is thus deeply rooted in the biology of past times and that will still be adopted rather generally, is fundamentally false; it has been reserved to the genetic researches of our time to prove this.

Modern hereditary researches are of a recent date, they are not yet seventy years old. Their founder is the Augustine monk Gregor Mendel, Professor at Brünn, who published (1866) his experiments on hybridization among plants, fundamental for this whole science. In the same year, in Kentucky, the man was born, who became Mendel's heir and founder of the school in heredity researches that has been called higher Mendelism, the winner of this year's Nobel Prize in Physiology or Medicine, Thomas Hunt Morgan.

Mendel's observations are of revolutionizing importance. As a matter of fact they completely upset the older theories of heredity, although this was not at all appreciated by his contemporaries. Mendel's discoveries usually are stated in two heredity laws or better rules of heredity. The first of his rules, the cleaving rule, means that if two different hereditary dispositions or hereditary factors (genes) for a certain quality - for instance for size - are combined in one generation, they separate in the following generation. If, for instance, a constantly tall race is crossed with a constantly short race, the individuals of next generation become altogether medium-sized, or, if the factor «tall» is dominant, exclusively tall. In the following generation, however, a cleaving takes place, so that once more the size of the individuals becomes variable according to certain numerical proportions, then of four descendants: one tall, two medium-sized, and one short.

The second of Mendel's rules, the rule of free combinations, means that, when new generations arise, the different hereditary factors can form new combinations independent of each other. If, for instance, a tall, red-flowered plant is crossed with a short, white-flowered one, the factors red and white can be inherited independent of the factors large and small. The second generation then, besides tall red-flowered and short white-flowered plants, produces short red-flowered and tall white-flowered ones.

Mendel's immortal merit is his exact registration of the special qualities and consequent following of their appearance from generation to generation. In this way he discovered the relatively simple, recurrent, numerical proportions, which give us the key to a true understanding of the course of heredity. The experimental genetics of our century then has proved that, taken as a whole, these Mendel rules are applicable to all many-celled organisms, to mosses and flowering plants, to insects, mollusks, crabs, amphibia, birds, and mammals.

Mendel's rules, however, met with the same fate as many other great discoveries that have been made before their time. Their significance was not understood, they fell into oblivion, and after pater Mendel had died in 1884, nobody mentioned them any more. Darwin apparently knew nothing about his great contemporary; otherwise he could have made use of Mendel's works for his own researches, and the rediscovery of Mendel's work was made only about 1900.

By that time, however, the qualifications for the application and perfection of Mendel's theories were quite different from those of their first publication. The general biological attitude had changed, and, above all, the knowledge of the cell and the cell nucleus had made excellent progress. The mechanism of fertilization had been discovered by Hertwig in 1875, and in the eighteen-eighties Weismann had asserted the opinion that the nuclei of the sex cells must be the bearers of the hereditary qualities. The indirect or mitotic cell division and the chromosomes - the strange, threadlike, colourable structures that then appear - had been discovered by Schneider in 1873 already. Only several decades later, however, was the meaning of the remarkable cleaving, wandering, and fusion of these chromosomes during the different phases of the cell division and the fertilization understood.

When, at last, Mendel's discoveries came to light, their significance was soon perceived. Behind Mendel's rules there must be some relatively simple, cellular mechanism for the exact distribution of the hereditary factors at the genesis of the new individual. This mechanism was found just in the proportion of chromosomes in the sex cells before and after the fertilization. The opinion that the chromosomes are the real bearers of heredity was first clearly pronounced by Sutton in 1903, and by Boveri in 1904. This opinion was enthusiastically received by the students of the cell. Only by this discovery organic life got the unity, the continuity that human thought demands and that is more real and more provable than the hypothetic common descent of Darwinism.

The further development of the chromosome theory during the first decade of this century may here be skipped. However, the soil was well prepared when, in 1910, the American zoologist Thomas Hunt Morgan began his researches in heredity. These soon led him to the great discoveries regarding the functions of the chromosomes as the bearers of heredity that have now been rewarded with the Nobel Prize for Medicine in 1933.

Morgan's greatness and the explanation of his astonishing success is partly to be found in the fact that, from the beginning, he has understood to join two important methods in hereditary research, the statistic-genetic method adopted by Mendel, and the microscopic method, and that he has always looked for an answer to the question: which microscopic processes in cells and chromosomes result in the phenomenons appearing at the crossings?

Another cause for Morgan's success is no doubt to be found in the ingenious choice of object for his experiments. From the beginning Morgan chose the so-called banana-fly, Drosophila melanogaster, which has proved superior to all other genetic objects known so far. This animal can easily be kept alive in laboratories, it can well endure the experiments that must be made. It propagates all the year round without intervals. Thus a new generation can be had about every twelfth day or at least 30 generations a year. The female lays about 1,000 eggs, males and females can easily be distinguished from each other, and the number of chromosomes in this animal is only four. This fortunate choice made it possible to Morgan to overtake other prominent genetical scientists, who had begun earlier but employed plants or less suitable animals as experimental objects.

Finally, few have like Morgan had the power of assembling around them a staff of very prominent pupils and co-operators, who have carried out his ideas with enthusiasm. This explains to a large extent the extraordinarily rapid development of his theories. His pupils Sturtevant, Muller, Bridges, and many others stand beside him with honour and have a substantial share in his success. With perfect justice we speak about the Morgan school, and it is often difficult to distinguish what is Morgan's work and what is that of his associates. But nobody has doubted that Morgan is the ingenious leader.

As Mendelism can be summed up in Mendel's two rules, Morganism, at least to a certain extent, can be expressed in laws or rules. The Morgan school usually speaks of four rules, the combination rule, the rule of the limited number of the combination groups, the crossing-over rule, and the rule of the linear arrangement of the genes in the chromosomes. These rules complete the Mendel rules in an extraordinarily important way. They are all inextricably connected, and form together a close biological unity.

It is true that Morgan's combination rule, according to which certain hereditary dispositions are more or less firmly combined, limits to a large degree Mendel's second rule that, at the formation of new hereditary substances, the genes may be freely combined. It is completed by the rule of the limited number of the combination groups, which has turned out to be corresponding to the number of chromosomes. On the other hand, the combination rule is confined by the strange phenomenon that Morgan calls crossing-over or the exchange of genes, which he imagines as a real exchange of parts between the chromosomes. This crossing-over theory has met with much resistance. During the last few years, however, it has got a firm support through direct microscopic observations. Also the theory of the linear arrangement of the hereditary factors seemed in the beginning a fantastic speculation, and the publication of Morgan's so-called genetic chromosome map, upon which the different hereditary factors are checked in the chromosomes like beads in a necklace, was greeted with justified scepticism. The fact was that Morgan had arrived at these sensational conclusions by statistic analysis of his Drosophila crossings and not by direct examination of the chromosomes, which, besides, is possible only in exceptional cases. But also on this point later researches have acknowledged him to be in the right, and nowadays also other genetic scientists admit that the theory of the localization of the hereditary factors within the chromosomes is not an abstract way of thinking but corresponds to a stereometric reality.

The results of the Morgan school are daring, even fantastic, they are of a greatness that puts most other biological discoveries into the shade. Who could dream some ten years ago that science would be able to penetrate the problems of heredity in that way, and find the mechanism that lies behind the crossing results of plants and animals; that it would be possible to localize in these chromosomes, which are so small that they must be measured by the millesimal millimetre, hundreds of hereditary factors, which we must imagine as corresponding to infinitesimal corpuscular elements. And this localization Morgan had found in a statistic way! A German scientist has appropriately compared this to the astronomical calculation of celestial bodies still unseen but later on found by the tube - but he adds: Morgan's predictions exceed this by far, because they mean something principally new, something that has not been observed before.

Morgan's researches chiefly occupy themselves with the family of Drosophila, and perhaps it may seem strange that his discoveries have been rewarded with the Nobel Prize for Medicine, which is to be bestowed on the man who «has done the greatest service to mankind» and «has made the most important discoveries in the field of physiology or medicine». To this may first be alleged that numerous later examinations of other genetic objects, of lower and higher plants and animals, have given evidence of the fact that, as a principle, Morgan's rules are applicable to all many-celled organisms.

Further, comparative biological research has for a long time shown a far-extending fundamental correspondence between man and other beings. We can therefore consider it as a matter of course that also such an elementary function of the cell as the transmission of hereditary dispositions is similar, that, in other words, Nature uses the same mechanism with man as with other beings to preserve species, and that Mendel's and Morgan's rules thus are applicable also to man.

Human hereditary researches have already made great use of Morgan's investigations. Without them modern human genetics and also human eugenics would be impractical - it may be that eugenics still chiefly remain a future goal. Mendel's and Morgan's discoveries are simply fundamental and decisive for the investigation and understanding of the hereditary diseases of man. And considering the present attitude of medicine and the dominating place of the constitutional researches, the role of the inner, hereditary factors as to health and disease appears in a still clearer light. For the general understanding of maladies, for prophylactic medicine, and for the treatment of diseases, hereditary research thus gains still greater importance.

Mr. Steinhardt. The Caroline Institute regrets very much that Professor Morgan is not able to be here today in person. I beg Your Excellency, as the official representative of the United States of America, to accept the Nobel Prize for Professor Morgan. May I also ask Your Excellency, in forwarding the prize to him, to convey with it the admiring congratulations of our Institute.

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[Photo Credit: The top photo is from the Nobel Prize website [Thomas Hunt Morgan and His Legacy]. The bottom photograph is from Imaginal Discs.]

Vote for your favorite life science blogs

 
The Scientist has an article about good science blogs [Vote for your favorite life science blogs]. Read the article and vote for Sandwalk your favorite science blogs.

I voted but I'm not going to tell you which blogs I named.

Eye Color in Fruit Flies

 
Monday's Molecule #43 is drosopterin, a major pigment in the eyes of the fruit fly, Drosophila melanogaster.

The biochemical pathway shown below is an updated figure similar to one taken from an undergraduate lab manual where students identify the pigments by thin layer chromatography [Thin Layer Chromatography of Eye Pigments of Drosophila melanogaster].

There are two kinds of pigments required for the normal red eyes. The ommochrome pathway produces a brown pigment and the drosopterin pathway produces a bright red (scarlet) pigment. Both pigments are transported to the site of eye formation by a common transport system.

The precursor of ommochrome is the amino acid tryptophan and the initial precursor in the drospterin pathway is the nucleoside guanine. Guanine and tryptophan need to be transported into the site of synthesis by specific membrane transporters.

Mutations in the transport system block the transport of the pigments and result in flies with white eyes (left) and various other colors such as brown and scarlet.




One of the proteins in the both the guanine and tryptophan transport system is the product of the white gene. Mutations in this gene result in white eyes because neither of the pigments is made. The other subunit of the guanine transporter is the product of the brown gene. Defects in this gene will only affect synthesis of drosopterin and the resulting eyes will be brown. The second subunit of the tryptophan transporter is encoded by the scarlet gene. Defects in that gene will block production of the brown ommochrome pigment and give rise to scarlet eyes because only drsopterin is present.

Examples of these three mutants are shown on the right from a paper by Mackenzie et al. (1999). The wild-type fly is the one at the lower left. Scarlet and white are on top and the brown mutant is in the lower right position.

Four other eye color mutants, Punch, purple, sepia and clot disrupt the activities of enzymes in the pathway from guanine to drosopterin (Kim et al., 2006).

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Kim, H.J., Kang, C.H., Kim, Y.T., Sung, S.W., Kim, J.H., Lee, S.M., Yoo, C.G., Lee, C.T., Kim, Y.W., Han, S.K., Shim, Y.S., Yim, J.J. (2006) Identification and characteristics of the structural gene for the Drosophila eye colour mutant sepia, encoding PDA synthase, a member of the Omega class glutathione S-transferases. Biochem J. 398:451-460.

Mackenzie, S.M., Brooker, M.R., Gill, T.R., Cox, G.B., Howells, A.J., Ewart, G.D. (1999)Mutations in the white gene of Drosophila melanogaster affecting ABC transporters that determine eye colouration. Biochim Biophys Acta. 1419:173-85.

Monday's Molecule #43

 
We have a winner!!! (see comments)


Today's molecule is a real biologically relevant molecule but it's a bit unusual. You have to supply the common name and the complete IUPAC name. There's an obtuse, indirect connection between this molecule and Wednesday's Nobel Laureate(s). (Hint: The Nobel Prize winner did not go to Sweden to get the prize.)


The reward goes to the person who correctly identifies the molecule and the Nobel Laureate(s). Previous free lunch winners are ineligible for one month from the time they first collected the prize. There are two ineligible candidates for this Wednesday's reward. Both of them are waiting to collect their prize this week or next week. The prize is a free lunch at the Faculty Club.

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(s). Correct responses will be posted tomorrow along with the time that the message was received on my server. This way I may select multiple winners if several people get it right.

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

PZ Rants About Science Textbooks

This is a posting about science textbook publishing. I have a vested interest in this debate because I'm the co-author of two biochemistry textbooks published by Pearson/Prentice Hall—one of the largest textbook publishers in the world.

PZ Myers posted an article about the high cost of textbooks [Textbooks, again]. He says,

Everyone in academia knows it: textbook publishers abuse the system. Jim Fiore decries the high cost of college textbooks, and I have to agree completely. Basic textbooks at the lower undergraduate levels do not need a new edition every year or two, not even in rapidly changing fields like biology.

There are two points here. The cost of textbooks is determined by the market and lots of other factors. As a general rule, the publishers are not making outrageous profits on individual college textbooks. They try to make their money on volume.

Most people don't understand that a large part of the cost of a textbook is due to the mark-up at the retailers. Much of the rest of the price is due to the cost of production and marketing. Look at the list of people who contribute to a textbook. You'll usually find them listed on the back of the title page. There are artists and editors as well as people who manage the project and people who market the books. Each new edition of a major textbook like biology can cost close to $1 million dollars these days. You have to sell more than 20,000 copies just to recover the production costs. (Really popular books will sell more than 100,000 copies but the difference isn't all profit.)

So let's understand and agree that the original price of a textbook is not unreasonable. My biochemistry textbook in 1965 was Conn & Stumpf and it cost $9.95. This works out to $65.80 in 2007 dollars using the handy-dandy inflation calculator on the US Dept. of Labor website. The 1965 textbook was much smaller, covered less material, and had no color figures. Modern biochemistry textbooks cost about $120-150 and they are very much better than the books published 40 years ago.

Even if we didn't want to make substantive changes in each edition and even if there were no second-hand market, we would still be forced to update our books because of pressure from competitors. Those other authors are hard at work revising and improving their books and if you don't follow suit you'll soon end up having no market share. What I'm saying here is that there are many reasons for new editions and it's very simplistic to attribute the cause to ripping off students. That's not how it works.

PZ's second point is more complex. Textbooks come out with new editions every few years. A typical cycle is four years—not the "year or two" that PZ suggests. While it is true that some of the pressure to produce new editions comes from a desire to eliminate the second-hand book market, that's not the only reason. There really is new material to add and new ways to approach the subject. In my case we're into the 4th edition of my Principles of Biochemistry textbook. The dates of publication are: 1992, 1996, 2002, and 2006. The next edition is scheduled for 2010. We're just about to start work on it. The differences between these editions are not trivial: they're part of a plan to transform the way we teach biochemistry. This is not unusual.

Churning editions is just a way for the publisher to suck more money out of a captive audience. It makes it difficult for students to sell off their used textbooks, it gives faculty the headache of having to constantly update their assignments, and if you allow your students to use older editions, it means we have to maintain multiple assignments. It's extraordinarily annoying, and to no good purpose at the university (to great purpose at the publisher, though).

This is simply not accurate. It's part of the urban myth about publishing. Everyone likes to blame someone else for the cost of textbooks.

I'm surprised that PZ would complain about having to update his assignments. You can't have it both ways, PZ. Either the new editions are trivial, in which case you don't have to change much, or they contain substantive changes, in which case your complaint about it being motivated to rip off students is unjustified. If you were using my textbook then be aware of the fact that my goal is to get you to change the way you've been teaching biochemistry. That's why I have new editions.

PZ, it sounds like you would never consider switching textbooks because it would be too much trouble for you to change your teaching. Is this a correct assumption?

On the plus side of their ledgers, though, I also urge the students to keep their textbooks once the course is over. These are valuable reference books that they may well find handy throughout their college careers and in their life afterwards. I've never quite understood the rush to dispose of those books the instant the semester ends — I kept my undergraduate biology and chemistry books until they fell apart (another gripe: the increasingly cheap bindings of these books), and I still have several of my old history texts on my shelves.

I'm with you on that one, PZ. I have all my old college textbooks. They are my friends. I never, ever, thought of selling them. They are full of notes in the margins and text highlights that reflect how I learned the material and what was important or controversial. I don't understand why students want to get rid of their textbooks when the course ends. Unless, of course, they never really cared about the subject in the first place and just needed a grade to graduate or get into medical school. But that's probably being too cynical.

Vote for your favorite BPR3 icon

 
Bloggers for Peer-Reviewed Research Reporting is a fledgling organization that's going to try and impose some standards on the reporting of peer-reviewed papers by bloggers. Here's their mission statement at [BPR3.org].

Bloggers for Peer-Reviewed Research Reporting strives to identify serious academic blog posts about peer-reviewed research by developing an icon and an aggregation site where others can look to find the best academic blogging on the Net.

The idea is to list all blog posts about peer-reviewed scientific literature on one site (with an RSS feed) and to identify all such blogs with a copyrighted icon. I've expressed some skepticism about this attempt to organize bloggers (sort of like herding cats) [Bloggers for Peer-Reviewed Research Reporting] but let's see how it works out.

Here are the three finalist in the icon contest from BPR3 website. Vote below.