Joe Who?

 
According to CBS News,

Washington - Vice presidential candidate Joe Biden says today's leaders should take a lesson from the history books and follow fellow Democrat Franklin D. Roosevelt's response to a financial crisis.

"When the stock market crashed, Franklin D. Roosevelt got on the television and didn't just talk about the, you know, the princes of greed. He said, 'Look, here's what happened,'" Barack Obama's running mate recently told the "CBS Evening News."

Except, Republican Herbert Hoover was in office when the stock market crashed in October 1929. There also was no television at the time; TV wasn't introduced to the public until a decade later, at the 1939 World's Fair.

I would have thought the bloggers would be all over this. Have I been reading the wrong blogs?

Lately I've been wondering what happened to Joe Biden. You don't see much about him on television. Now I know why. Maybe he and Sarah should take a very long trip to Afghanistan and let the big boys run for President.

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Howler Monkeys

 
Back in the olden days before blogs, we had the newsgroup talk.origins where the battle between evolution and creation was fought. The newsgroup still exists and it's still very active.

One of the most famous anti-evolutionists on talk.origins was a man named Ted Holden. He was witty and prolific, as well as being a famous internet kook. Ted didn't like the fact that he had to defend himself against attacks from scores of people so he coined the term "Howler Monkeys" to describe the chorus of evolutionists who joined in whenever a creationist appeared. (Ted wasn't exactly a creationist in the traditional sense. There was very little about Ted that was "traditional.")

Here's a posting from Ted Holden in 1995 ...

The clique which dominates talk.origins sees themselves as heroes, doing battle with the powers of darkness in an effort to prevent a return to the dark ages. I once noted that, to any outsider attempting to present anything other than the standard lock-step glop on t.o, they present what amounts to a sort of a tribal reaction, what one might expect from a tree-full of crows confronting a hawk or a tree of howler-monkeys encountering a leopard. The crew has since adopted the term "howler-monkeys" as a heraldic device, or metaphor, and refer to themselves as "howler monkeys" as a badge of honor.

Ted is right about the term "Howler Monkeys." Many people on talk.origins were proud to call themselves Howler Monkeys and meetings of talk.origins participants were called Howlerfests. We had a Toronto Howlerfest in 2005 that brought talk.origins regulars like the Canadian cousin of Prof. Steve Steve (see photo), PZ Myers, Canadian Cynic, John Wilkins, and Jeffrey Shallit who have gone on to to become bloggers. You may have heard of some of these talk.origins alumni.

Many of you don't know about Howler monkeys. Ms. Sandwalk just sent along this National Geographic video of Howler monkeys in action. I don't think she meant it as a compliment.

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How Many Genes Do Nematodes Have? - Pristionchus pacificus Genome

 

Nematodes are small wormlike creatures that live almost everywhere. Many of them are parasites but there are thousands of species that live in the soil. "... it is said that if everything on the earth were to disappear except the nematodes, the outlines of everything would still be visible: the mountains, lakes and oceans, the plants and the animals would all be outlined by the nematodes living in every habitat."¹

The free-living species Caenorhabditis elegans was chosen by Sydney Brenner as a model organism for the study of development [Nobel Laureates: Sydney Brenner, Robert Horvitz, John Sulston]. It turned out to be an excellent choice and by the mid 1990s this small metazoan (multi-cellular animal) was selected as the best metazoan candidate for genome sequencing.

The complete genome sequence was published in 1998. The genome is 100 Mb in size (= 100 million base pairs). This was smaller than the predicted size of the fruit fly genome (165 Mb) or the human genome (3,200 Mb). The first estimates of the number of genes were over 19,000 and at the time this was thought to be a reliable estimate although there were many, including me, who though that it was probably too high.

Over the years we have become more skeptical of these initial gene counts because there are many problems. The location of genes is determined by sophisticated computer programs that are trained to recognize the important characteristics of gene sequences (protein coding genes). This year marks the tenth anniversary of the publication of the C. elegans genome sequence and most people will be surprised to learn that the annotation of this sequence is just beginning to be complete.

A recent paper by James Thomas summarizes the result so far (Thomas, 2008).

Thomas points out that gene prediction suffers from the presence of false positives. One of the complications is pseudogenes, which are not easy to distinguish from real genes. Another complication is proving that a predicted gene is actually functional and not just a computational artifact. There is no better way to resolve these issues than by having real live people look at every potential gene. This is why annotation takes so long.

The latest estimate is 20,140 protein coding genes in the Caenorhabditis elegans genome. The coding regions (exons) would take up about 40 Mb of DNA or 24% of the genome. Most of the remainder is junk DNA.

The number of genes is remarkably close to the original prediction although it should be noted that estimates of the number of genes went up after the initial draft sequence was published. Nevertheless, unlike the gene count in humans, the number of genes has held pretty steady.

The number of genes can be compared to the number in the Drosohila melanoaster genome (~15,000) and the human genome (20,500). These are the only two other eukaryotic metazoan genomes² that have been extensively annotated.

There are about 23,000 distinct transcripts from these genes. What that means is that roughly 18,000 genes produce a single transcript and about 2,000 produce two or three different transcripts by alternative splicing.

The C. elegans genes can be divided into two categories. About 8,000 of them are unique and the remainder belong to gene families. A gene family consists of multiple copies of the same gene in the same genome. The copies (paralogues) may be identical or they may be quite different but still related. Some of the gene families are very large and some have only two members.

There seem to be about 3,000 genes families contributing to the 12,000 genes that are not unique. The bottom line is that there are about 11,000 (8K + 3K) different kinds of gene in C. elegans. Interestingly, only 1800 of these genes are found in both insects (Drosophila) and primates (humans). The rest are restricted to just insets and nematodes or just nematodes (10,000 are found in other nematode species).

James Thomas points out that the determination of orthology (same genes in other species) is much more difficult than one might imagine. Many of the online databases, for example, contain erroneous entries based on faulty predictions. These false predictions propagate so that it often isn't reliable to use the database to confirm that a predicted gene actually exists. That's why he restricts his comparisons to well-annotated genomes wherever possible.

Partially annotated genome sequences of Caenorhabditis brigsae and Caenorhabditis remaneri are available. Orthologous gene comparisons indicate that the three species are remarkably dissimilar for species within the same genus. They probably diverged at least 20 My ago.

A new nematode genome sequence was published this week. The species is Pristionchus pacificus, a parasite of the oriental beetle Examala orientalis (Dieteridh et al. 2008). The authors note that there is a different species of parasitic nematode associated with almost every species of beetle, which means that there are at least as many nematodes as insects.

The Pristionchus pacificus genome is 169 Mb in size, which is considerably larger than the size of the Caenorhabditis elegans genome (100 Mb). P. pacificus has 23,500 genes.

Some of the increase in genome size is due to more genes but this is only a minor difference. Some of it is due to the presence of additional copies of repetitive DNA sequences in P. pacificus but the increase doesn't account for the extra 69 Mb of DNA.

The differences in gene number are almost entirely due to increases in the members of gene families in the P. pacificus genome. Several specific examples were given, notably 250 extra copies of ribosomal protein genes compared to C. elegans.

Another remarkable difference is in the number of genes involved in detoxification, or removal of poisonous substances. There are about 250 extra copies of gene family members in this category. The authors speculate that this expansion may be selection for detoxifying enzymes in parasites as opposed to the free-living C. elegans.

In addition to the various Caenorhabditis species, we now have a complete genome of the nematode Brugia malayi the parasite responsible for filariasis in humans. Pristionchus diverged from Caenorhabditis about 350 My (million years) ago and Brugia diverged from the others about 900 My ago according to Dietrich et al. (2008). Thomas (2008) cautions that these divergence times are based on an underestimate of mutation/fixation rates and that nematodes may be evolving more rapidly than other phyla. Nevertheless, it is clear that nematodes are an ancient, diverse, and abundant group of animals.

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1. Nematoda.

2. See the discussion in the comments for examples of other well-annotated eukaryotic genomes. Yeast is obvious but what about Arabidopsis?

[Photo Credit: Christina Beck]

Christoph Dieterich, Sandra W Clifton, Lisa N Schuster, Asif Chinwalla, Kimberly Delehaunty, Iris Dinkelacker, Lucinda Fulton, Robert Fulton, Jennifer Godfrey, Pat Minx, Makedonka Mitreva, Waltraud Roeseler, Huiyu Tian, Hanh Witte, Shiaw-Pyng Yang, Richard K Wilson, Ralf J Sommer (2008). The Pristionchus pacificus genome provides a unique perspective on nematode lifestyle and parasitism Nature Genetics DOI: 10.1038/ng.227

J. H. Thomas (2008). Genome evolution in Caenorhabditis Briefings in Functional Genomics and Proteomics, 7 (3), 211-216 DOI: 10.1093/bfgp/eln022

In the Words of Sydney Brenner

 
Sydney Brenner says,

Actually, the orgy of fact extraction in which everybody is currently engaged has, like most consumer economies, accumulated a vast debt. This is a debt of theory, and some of us are soon going to have an exciting time paying it back - with interest, I hope.

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I spent 20 years sharing an office with Francis Crick and many new and exciting ideas (both right and wrong) were generated from our conversations.

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I was asked by a student what ethical standards should be adopted by life scientists. I could immediately think of two prescriptions. The first, common to all scientists, is to tell the truth. The second is to stand up for all humanity.

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The attitude of my generation that all problems can be solved in the next decade, and should be solved in the next decade—these expectations are changed. Maybe science should be done better, but more slowly. I think a large number of mediocre people are in science today, and carried along by the system. General concepts are rare. Nobody publishes theory in biology—with few exceptions. Instead they get out the structure of still another protein. I'm not saying it's mindless. But the mind only acts on the day-to-day.

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There will be no difficulty in computer's being adapted to biology. There will be Luddites. But they will be buried.

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There is a strong and widely held belief that all organisms are perfect and that everything within them is there for a function. Believers ascribe to the Darwinian natural selection process a fastidious prescience that it cannot possible have and some go so far as to think that patently useless features of existing organisms are there as an investment for the future ...

Even today, long after the discovery of repetitive sequences and introns, pointing out that 25% of our genome consists of millions of copies of one boring sequence, fails to move audiences. They are all convinced by the argument that if this DNA were totally useless, natural selection would already have removed it. Consequently, it must have a function that still remains to be discovered. Some think that it could even be there for evolution of the future—that is, to allow the creation of new genes. As this was done in the past, they argue, why not in the future? ...

Some years ago I noticed that there are two kinds of rubbish in the world and that most languages have different words to distinguish them. There is the rubbish we keep, which is junk, and the rubbish we throw away, which is garbage. The excess DNA in our genomes is junk, and it is there because it is harmless, as well as being useless, and because the molecular processes generating extra DNA outpace those getting rid of it. Were the extra DNA to become disadvantageous, it would become subject to selection, just as junk that takes up too much space, or is beginning to smell, is instantly converted to garbage.

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The Sydney Brenner quotations above are from Stephen Jay Gould's book The Structure of Evolutionary Theory

Most of what I have said over the years has probably been wrong or uninteresting and deserves to be ignored and forgotten. Consequently I was pleasantly surprised when I recently received a request for a reprint of one of my old columns, published elsewhere, with the exciting news - to me - that it had been quoted by the late Stephen J Gould in his massive book The Structure of Evolutionary Theory and that it had caused him to change his mind on one important issue. I had acquired the book on publication with the intention that as soon as I could find the time I would get down to read all 1,464 pages. Needless to say, all I have now read are the pages that refer to my column.

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I learnt very quickly that the only reason that would be accepted for not attending a committee meeting was that one already had a previous commitment to attend a meeting of another organization on the same day. I therefore invented a society, the Orion Society, a highly secret and very exclusive society that spawned a multitude of committees, sub-committees, working parties, evaluation groups and so on that, regrettably, had a prior claim on my attention. Soon people wanted to know more about this club and some even decided that they would like to join it. However, it was always made clear to them that applications were never entertained and that if they were deemed to qualify for membership they would be discreetly approached at the appropriate time.

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...we need to put everything into an evolutionary framework, simply because complexity arises in biological systems by accretion and modification and not by reinvention. Thus, the properties of many of the components in our cells, whether these are mRNAs or proteins, will be conditioned not only by processes of selection for specified activities and levels because these are positively required but may also take up any value because there are no negative consequences for the organism. This ‘don't care’ condition will almost certainly be present because it is a cheap solution to the regulation problem of complex systems. Thus a 20% or a twofold increase, or indeed the very presence, of a protein may be very significant or totally irrelevant depending on whether it is following a ‘don't care’ condition. Only experiment can decide that.

I once made the remark that two things disappeared in 1990: one was communism, the other was biochemistry and that only one of these should be allowed to come back. Of course, biochemistry never really went away but continued to flourish in the thousands of unread pages of biochemical journals. Protein interactions will not be solved by proteomics or protein chips but by protein biochemistry. The genome sequences tell us about the proteins we can expect to find in cells and give us the tools to make large amounts of the proteins for reconstitution studies and for detailed structural analysis. We do not have to resurrect biochemistry, and it will flourish because it provides the only experimental basis for causal understanding of biological mechanisms. That is why this article is not called ‘The return of biochemistry.’ [from "Biochemistry Strikes Back"]

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Nobel Laureates: Sydney Brenner, Robert Horvitz, John Sulston

 

The Nobel Prize in Physiology or Medicine 2002.

"for their discoveries concerning 'genetic regulation of organ development and programmed cell death'"

Sydney Brenner (1927 - ), H. Robert Horvitz (1947 - ), and John E. Sulston (1942 - ) received the Nobel Prize in Physiology or Medicine for making the nematode Caenorhabditis elegans into a model system that is now studied in hundreds of labs all over the world.

Bob Horvitz was a post-doc with Brenner in Cambridge in the mid-1970s and John Sulstron held a junior staff position at Cambridge under Brenner. Although there were other post-docs and graduate students who began working on C. elegans at this time, Horvitz and Sulstron were the ones making key contributions toward working out the total cell lineage. They were able to trace the fate of each cell from the zygote right through to the adult worm [see Monday's Molecule #89 for an example of a cell lineage].

The Nobel Prize was actually awarded for this achievement and not for establishing C. elegans as an experimental system but most people recognize that Brenner's many achievements had to be recognized in some way or another. The cell lineage work was clearly of Nobel Prize quality, but so were many other things that Brenner did in his career.

If there was a Nobel life-time achievement award, Brenner would have won that.

The press release announcing the 2002 Nobel Prizes does an excellent job of describing the work so I've included the entire thing below.

THEME:
Nobel Laureates

7 October 2002

The Nobel Assembly at Karolinska Institutet has today decided to award The Nobel Prize in Physiology or Medicine for 2002 jointly to

Sydney Brenner, H. Robert Horvitz and John E. Sulston

for their discoveries concerning "genetic regulation of organ development and programmed cell death"

Summary

The human body consists of hundreds of cell types, all originating from the fertilized egg. During the embryonic and foetal periods, the number of cells increase dramatically. The cells mature and become specialized to form the various tissues and organs of the body. Large numbers of cells are formed also in the adult body. In parallel with this generation of new cells, cell death is a normal process, both in the foetus and adult, to maintain the appropriate number of cells in the tissues. This delicate, controlled elimination of cells is called programmed cell death.

This year's Nobel Laureates in Physiology or Medicine have made seminal discoveries concerning the genetic regulation of organ development and programmed cell death. By establishing and using the nematode Caenorhabditis elegans as an experimental model system, possibilities were opened to follow cell division and differentiation from the fertilized egg to the adult. The Laureates have identified key genes regulating organ development and programmed cell death and have shown that corresponding genes exist in higher species, including man. The discoveries are important for medical research and have shed new light on the pathogenesis of many diseases.

Sydney Brenner (b 1927), Berkeley, CA, USA, established C. elegans as a novel experimental model organism. This provided a unique opportunity to link genetic analysis to cell division, differentiation and organ development – and to follow these processes under the microscope. Brenner's discoveries, carried out in Cambridge, UK, laid the foundation for this year's Prize.

John Sulston (b 1942), Cambridge, England, mapped a cell lineage where every cell division and differentiation could be followed in the development of a tissue in C. elegans. He showed that specific cells undergo programmed cell death as an integral part of the normal differentiation process, and he identified the first mutation of a gene participating in the cell death process.

Robert Horvitz (b 1947), Cambridge, MA, USA, has discovered and characterized key genes controlling cell death in C. elegans. He has shown how these genes interact with each other in the cell death process and that corresponding genes exist in humans.
Cell lineage – from egg to adult

All cells in our body are descendents from the fertilized egg cell. Their relationship can be referred to as a cellular pedigree or cell lineage. Cells differentiate and specialize to form various tissues and organs, for example muscle, blood, heart and the nervous system. The human body consists of several hundreds of cell types, and the cooperation between specialized cells makes the body function as an integrated unit. To maintain the appropriate number of cells in the tissues, a fine-tuned balance between cell division and cell death is required. Cells have to differentiate in a correct manner and at the right time during development in order to generate the correct cell type.

It is of considerable biological and medical importance to understand how these complicated processes are controlled. In unicellular model organisms, e.g. bacteria and yeast, organ development and the interplay between different cells cannot be studied. Mammals, on the other hand, are too complex for these basic studies, as they are composed of an enormous number of cells. The nematode C. elegans, being multi-cellular, yet relatively simple, was therefore chosen as the most appropriate model system, which has then led to characterization of these processes also in humans.

Programmed cell death

Normal life requires cell division to generate new cells but also the presence of cell death, so that a balance is maintained in our organs. In an adult human being, more than a thousand billion cells are created every day. At the same time, an equal number of cells die through a controlled "suicide process", referred to as programmed cell death.

Developmental biologists first described programmed cell death. They noted that cell death was necessary for embryonic development, for example when tadpoles undergo metamorphosis to become adult frogs. In the human foetus, the interdigital mesoderm initially formed between fingers and toes is removed by programmed cell death. The vast excess of neuronal cells present during the early stages of brain development is also eliminated by the same mechanism.

The seminal breakthrough in our understanding of programmed cell death was made by this year's Nobel Laureates. They discovered that specific genes control the cellular death program in the nematode C. elegans. Detailed studies in this simple model organism demonstrated that 131 of totally 1090 cells die reproducibly during development, and that this natural cell death is controlled by a unique set of genes.

The model organism C. elegans

Sydney Brenner realized, in the early 1960s, that fundamental questions regarding cell differentiation and organ development were hard to tackle in higher animals. Therefore, a genetically amenable and multicellular model organism simpler than mammals, was required. The ideal solution proved to be the nematode Caenorhabditis elegans. This worm, approximately 1 mm long, has a short generation time and is transparent, which made it possible to follow cell division directly under the microscope.

Brenner provided the basis in a publication from 1974, in which he broke new ground by demonstrating that specific gene mutations could be induced in the genome of C. elegans by the chemical compound EMS (ethyl methane sulphonate). Different mutations could be linked to specific genes and to specific effects on organ development. This combination of genetic analysis and visualization of cell divisions observed under the microscope initiated the discoveries that are awarded by this year's Nobel Prize.

Mapping the cell lineage

John Sulston extended Brenner's work with C. elegans and developed techniques to study all cell divisions in the nematode, from the fertilized egg to the 959 cells in the adult organism. In a publication from 1976, Sulston described the cell lineage for a part of the developing nervous system. He showed that the cell lineage is invariant, i.e. every nematode underwent exactly the same program of cell division and differentiation.

As a result of these findings Sulston made the seminal discovery that specific cells in the cell lineage always die through programmed cell death and that this could be monitored in the living organism. He described the visible steps in the cellular death process and demonstrated the first mutations of genes participating in programmed cell death, including the nuc-1 gene. Sulston also showed that the protein encoded by the nuc-1 gene is required for degradation of the DNA of the dead cell.

Identification of "death genes"

Robert Horvitz continued Brenner's and Sulston's work on the genetics and cell lineage of C. elegans. In a series of elegant experiments that started during the 1970s, Horvitz used C. elegans to investigate whether there was a genetic program controlling cell death. In a pioneering publication from 1986, he identified the first two bona fide "death genes", ced-3 and ced-4. He showed that functional ced-3 and ced-4 genes were a prerequisite for cell death to be executed.

Later, Horvitz showed that another gene, ced-9, protects against cell death by interacting with ced-4 and ced-3. He also identified a number of genes that direct how the dead cell is eliminated. Horvitz showed that the human genome contains a ced-3-like gene. We now know that most genes that are involved in controlling cell death in C. elegans, have counterparts in humans.

Of importance for many research disciplines

The development of C. elegans as a novel experimental model system, the characterization of its invariant cell lineage, and the possibility to link this to genetic analysis have proven valuable for many research disciplines. For example, this is true for developmental biology and for analysis of the functions of various signaling pathways in a multicellular organism. The characterization of genes controlling programmed cell death in C. elegans soon made it possible to identify related genes with similar functions in humans. It is now clear that one of the signaling pathways in humans leading to cell death is evolutionarily well conserved. In this pathway ced-3-, ced-4- and ced-9-like molecules participate. Understanding perturbations in this and other signaling pathways controlling cell death are of prime importance for medicine.

Disease and programmed cell death

Knowledge of programmed cell death has helped us to understand the mechanisms by which some viruses and bacteria invade our cells. We also know that in AIDS, neurodegenerative diseases, stroke and myocardial infarction, cells are lost as a result of excessive cell death. Other diseases, like autoimmune conditions and cancer, are characterized by a reduction in cell death, leading to the survival of cells normally destined to die.

Research on programmed cell death is intense, including in the field of cancer. Many treatment strategies are based on stimulation of the cellular "suicide program". This is, for the future, a most interesting and challenging task to further explore in order to reach a more refined manner to induce cell death in cancer cells.

Using the nematode C. elegans this year's Nobel Laureates have demonstrated how organ development and programmed cell death are genetically regulated. They have identified key genes regulating programmed cell death and demonstrated that corresponding genes exist also in higher animals, including man. The figure schematically illustrates the cell lineage (top left) and the programmed cell death (below) in C. elegans. The fertilized egg cell undergoes a series of cell divisions leading to cell differentiation and cell specialization, eventually producing the adult organism (top right). In C. elegans, all cell divisions and differentiations are invariant, i.e. identical from individual to individual, which made it possible to construct a cell lineage for all cell divisions. During development, 1090 cells are generated, but precisely 131 of these cells are eliminated by programmed cell death. This results in an adult nematode (the hermaphrodite), composed of 959 somatic cells.

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McCain Snubs Letterman

 
Ms. Sandwalk often watches David Letterman but I don't.¹ Last night John McCain called up David Letterman at the last minute to cancel his appearance. Apparently McCain had to rush back to Washington to save the country.

I was told in no uncertain terms that I had to start watching David Letterman because I had missed a good show last night. Well, as it turns out, the best part is already on YouTube. Not a good idea to piss off David Letterman.

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1. It's past my bedtime.

Discussing Junk DNA with an Adaptationist

Adaptationists are scientists who like to find adaptive explanations for all features of organism. For them the concept of junk DNA is difficult to swallow in spite of abundant scientific evidence and in spite of the fact that counter-explanations do not account for the data. Nils Reinton is a molecular biologist working in the field of medical diagnostics and he has been challenging the concept of junk DNA in the comment section of a recent posting. The title of that posting, Everything Is There for a Reason?, was direct response to an earlier posting from Nils where he claimed that we shouldn't label DNA as "junk" because it's a science stopper.

During the discussion in the comment to my posting, I challenged Nils to answer a number of questions. He has responded on his blog SciPhu with Hey junk people, I accept your challenge (part I).

Here are the first four questions with my personal summary of his answers.

Q: Why do pseudogenes and most of the transposon-related sequences look so much like broken genes?

A: They may look like broken genes but they probably have some function.

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Q: Why is the DNA sequence in most of our DNA not conserved?

A: It's not conserved because it's a reservoir for evolution. In addition, it probably contains genes for small RNAs and, as we all know, those predicted small RNA genes are not conserved.

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Q: Why can we delete large segments of mammalian DNA with no observable effect?

A: There is an effect. We just haven't found it yet.

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Q: Why is there so much variations in repetitive DNA within a species? Some people have segments that are ten times longer than segments found in other people. Are all of the nucleotides in the longer segments functional?

A: There are some examples of differences in repeats that do make a difference. Therefore, it is wrong to conclude that most of the variation has no effect. Furthermore, the discovery of copy number variation is a new phenomenon and it may turn out the have profound effects.

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Nils concludes Part 1 by repeating his earlier complaint ..

This belief that there’s hidden function to be found, treasures to unearth if you will, is the difference between those advocating these parts of DNA as “junk” and me. In my opinion, It’s not the details of what is junk and what isn’t, ..- and how much, that bothers me…..

It’s the attitude. To dismiss something as junk is contrary to my idea of science being driven out of curiosity and the need to explore. Curiosity may kill a cat every now and then, but I’ll take that risk and continue to praise the scientist who recognize possibilities in the junk rather than dismissing it.

This is nonsense but I already covered that complaint in my previous posting.

Nils seems to think that the adaptationist program is the only way to remain curious and excited about science. This is in direct contrast to the original Spandrels paper by Gould and Lewontin. They argued that strict application of the adaptationist program prevents people from seeing other possibilities. It's a science stopper.

Gould and Lewontin argued that a pluralist worldview was far superior because it considers a wider range of possible explanations.

Personally, I'm as excited about the possibility that our genome could be 95% junk as I am about the possibility that there may be strange new features that we don't know about. At least the tentative conclusion that much of it is junk has the advantage of being a superior explanation of the data.

The conclusion that most of the DNA has some unknown function in spite of much evidence to the contrary strikes me as non-scientific. To justify it on the ground that such a belief is required in order to maintain an interest in the subject is almost unbelievable.

Incidentally, despite some initial skepticism¹, Richard Dawkins—not usually thought of as the best example of a pluralist—has now resorted to using junk DNA as one of his arguments against Intelligent Design Creationism.

Gene duplications have occurred from time to time throughout the genomes. It is by these, and similar means, that genome size can increase in evolution. But remember the distinction between the total capacity of the whole genome, and the capacity of the proportion that is actually used. Recall that not all the globin genes are actually used. Some of them, like theta in the alpha cluster of globin genes, are pseudogenes, recognizably kin to functional genes in the same genomes, but never actually translated into the action language of protein. Genomes are littered with with nonfunctional pseudogenes, faulty duplicates of functional genes that do nothing, while their functional cousins (the word doesn't even need scare quotes) get on with their business in a different part of the same genome. And there's lots more DNA that doesn't even deserve the name pseudogene. It, too, is derived by duplication, but not duplication of functional genes. It consists of multiple copies of junk, "tandem repeats," and other nonsense that may be useful for forensic detectives but which doesn't seem to be useful in the body itself.
            Richard Dawkins in "The "Information Challenge",
            The Skeptic magazine, 1998

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1. The Extended Phenotype p. 157

What Happened to 30 Biochemistry Graduate Students at Yale?

 
In 1991 there were 30 young people beginning graduate school in the Molecular Biophysics and Biochemistry Progam at Yale University. Where are they now? How many have tenure at a university? The answer might surprise you. Read about the fate of these students in this week's issue of Science [And Then There Was One].

Looking at my own department, there are about 10 Ph.D.'s from a similar cohort and four of them have academic positions in 2008.

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[Hat Tip: Chance and Necsssity]

The Value of Science Blogs

 
Three well-known science bloggers, Shelley Batts (Of Two Minds), Nicholas Anthis (The Scientific Activist), and Tara Smith (Aetiology) have just published an article in PLoS Biology entitled Advancing Science through Conversations: Bridging the Gap between Blogs and the Academy.

I agree with most of what they have to say but there are a couple of problems that aren't addressed in the article. First, the more science blogs we have the more difficult it is to read them all. I'm currently trying to follow 104 science blogs on a daily basis and it's quite a chore. How are we going to sort out the wheat from the chaff and what are we going to do when there's too much wheat?

The second problem concerns the definition of a science blog. We all know that strictly science blogs aren't nearly as entertaining as those that branch off into religion, politics, and other non-science topics. All three of the authors know this because their own blogs are an interesting mix of real science and other things. The authors propose that institutions, such as universities, encourage more science blogging but that will only work for the strictly science blogs and we know that those kind of blogs aren't very popular. Institutions are reluctant to be directly associated with the more popular science blogs, like Pharyngula, because they don't want to be seen as endorsing the private views of faculty members.

The PLoS Biology article says,

Institutions may wish to implement more formal vetting mechanisms, however, such as periodic review by institutional moderators or peer review by official committees of blog-literate individuals, established scientists, and bloggers. Institutions might use one of a variety of mechanisms to confer a visible token of this review—such as a “blog badge”—in order to both reward quality bloggers and help readers identify trusted blogs. A blog badge is simply a small picture or icon that is prominently featured on the blog and represents an award or achievement. Such badges are usually given as awards (such as the “Weblog Awards” or the “MedBlog Awards”), and are awarded to particular outstanding blogs in a variety of categories, such as “Best Group Blog,” “Most Informative,” and “Best Translation of Published Research.” Traditional blogging awards are conferred by a committee who invites submissions until a deadline, reviews them, and then posts the winners on their Web site. The winners can then download the badge to post on their blog. Institutions might find it useful, and bloggers might find it motivating, if institutional blog badges were conferred for particularly insightful posts or as a token for passing their test or review periods. Accumulating these badges would be a public and official way for the institution to reward and validate the blogger, while conferring authority to the blog by letting readers know it has met the criterion for institutional peer review.

I think this may be missing the point of blogs. Their value is based on the fact that there's no "institutional" control or monitoring. There is no peer review. This is the internet and it's free-wheeling and opinionated. I don't know of an "institution" that can officially attach its name to those kind of blogs—although they must tolerate them in the name of academic freedom. (Besides, if we use science press releases as our criterion for judging institutional accuracy, then institutional blog badges aren't going to be worth very much.)

I think we need to rely on bloggers themselves to identify the best blogs.

UPDATE: DrugMonkey does a better job of discussing some of these same issues at Blogging in the Academy: Batts et al, 2008, In addition, the conflict between anonymous blogging—is it desirable?—and institutional support is raised in the article and in the comments.

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[Hat Tip: John Dennehy]

Which Animal Phylum Has the Most Species?

 
I bet almost all of you think it's Arthropoda since there are so many insects and especially beetles, which God was very fond of.¹

However, recent advances in taxonomy have suggested that there are one million species of nematode. This is about the same number of species as arthropods so the primacy of insects has been challenged.

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1. This is a reference to a famous quip by J.B.S. Haldane. When asked to name the most important thing he has learned about God from studying biology he reportedy said, "I'm not sure, but He seems to be inordinately fond of beetles."

[Photo Credit: Iowa State University Plant Disease]

Happy Autumnal Equinox

 
If I've got this right then today at 11:44 AM EST (i.e. right now!) is the Autumnal Equinox. Have a very happy one!



Most people think that the Spring and Fall equinoxes are the days when there are equal amounts of daylight and night. If that's true then why is the Autumnal Equinox at 11:44 in the morning?

Here's the answer from Wikipedia. It's the sort of thing I would have expected to find on Bad Astronomy but, if it's there, I couldn't find it.

An equinox in astronomy is the moment in time (not a whole day) when the centre of the Sun can be observed to be directly above the Earth's equator, occurring around March 20 and September 23 each year.

More technically, at an equinox, the Sun is at one of two opposite points on the celestial sphere where the celestial equator (i.e., declination 0) and ecliptic intersect. These points of intersection are called equinoctial points—the vernal point and the autumnal point. By extension, the term equinox may be used to denote an equinoctial point.

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[Image Credit: eSky]

Monday's Molecule #89

 

You may have noticed that this week's "molecule" isn't exactly a molecule. It's something else entirely. In order to win the fabulous prize you need to tell me what the figure represents and what species it refers to.

There's a direct connection between today's "molecule" and a Nobel Prize. I'm looking for the people who contributed to the work shown in the figure. One of them could have won a Nobel Prize for several other key discoveries but this is the one the Nobel Prize committee decided to pick. A wise choice, in my opinion.

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

THEME:

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

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

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

UPDATE: This week's winner is Brad Hersh of Clemsen University. The figure is the cell lineage of the nematode Caenorhabditis elegans and the Nobel Laureates are Sulston, Horvitz, and Brenner (2002). Congratulations Brad!

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Joseph Mallord William Turner (1775–1851)

 
Turner was an English artist who did most of his work in the first half of the nineteenth century. I'm a fan of most of Turner's paintings but I particularly like the seascapes that show Napoleonic era battleships.

John Pieret visited the Turner exhibition at the Metropolitan Museum of Art in some big city south of the border. He was mean kind enough to post pictures on his blog at Page Turner. It's hard to imagine how someone can have such good taste in art and such a bad

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Yes, Virginia, there is a Santa Claus

 
Yesterday was 111th anniversary of an editorial published in The New York Sun. The author was Francis Pharcellus Church. See the article on Wikipedia for the complete history of Yes, Virginia, there is a Santa Claus.

Most people don't know what Frances Pharcellus Church actually wrote so here it is ...

Virginia,

Your little friends are wrong. They have been affected by the skepticism of a skeptical age. They do not believe except they see. They think that nothing can be which is not comprehensible by their little minds. All minds, Virginia, whether they be men’s or children’s, are little. In this great universe of ours, man is a mere insect, an ant, in his intellect as compared with the boundless world about him, as measured by the intelligence capable of grasping the whole of truth and knowledge. Yes, Virginia, there is a Santa Claus. He exists as certainly as love and generosity and devotion exist, and you know that they abound and give to your life its highest beauty and joy. Alas! how dreary would be the world if there were no Santa Claus! It would be as dreary as if there were no Virginias. There would be no childlike faith then, no poetry, no romance to make tolerable this existence. We should have no enjoyment, except in sense and sight. The eternal light with which childhood fills the world would be extinguished. Not believe in Santa Claus! You might as well not believe in fairies. You might get your papa to hire men to watch in all the chimneys on Christmas eve to catch Santa Claus, but even if you did not see Santa Claus coming down, what would that prove? Nobody sees Santa Claus, but that is no sign that there is no Santa Claus. The most real things in the world are those that neither children nor men can see. Did you ever see fairies dancing on the lawn? Of course not, but that’s no proof that they are not there. Nobody can conceive or imagine all the wonders there are unseen and unseeable in the world. You tear apart the baby’s rattle and see what makes the noise inside, but there is a veil covering the unseen world which not the strongest man, nor even the united strength of all the strongest men that ever lived could tear apart. Only faith, poetry, love, romance, can push aside that curtain and view and picture the supernal beauty and glory beyond. Is it all real? Ah, Virginia, in all this world there is nothing else real and abiding. No Santa Claus! Thank God! he lives and lives forever. A thousand years from now, Virginia, nay 10 times 10,000 years from now, he will continue to make glad the heart of childhood.

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Does Science Need Religion?

 
That's the question asked by Scott Hatfield on Monkey Trials. He discusses a recent statement by Malcolm Brown who is Director of Mission and Public Affairs for the Church of England. Scott also responds to criticisms of Brown's position from Jason Rosenhouse. You can find all the links at GOOD SCIENCE, GOOD RELIGION along with an excellent analysis by Scot.

For what it's worth, I agree with much of Scot's analysis and with Jason Rosenhouse. Malcolm Brown is expressing a position that's very common among theists even though it is often denied. For the believer, science has to make room for God and accommodate religion because the two working together are superior to either one on its own. Brown is worried about those who claim to compartmentalize religion and science and keep them separate.

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