The Second Grapevine Genome Is Published

 
A second version of the grapevine genome was published at PLoS ONE last week (Velasco et al. 2007). As I began to collect information on that paper I learned that another genome sequence of grapevine had been published independently last September in Nature (Jaillon et al. 2007). Before discussing the PLoS ONE paper I decided to write up a report of that August genome sequence trying to not let the second sequence influence me [The Grapevine Genome].

This gives us an opportunity to evaluate the state of genome biology and genome evolution by comparing two competing analyses of the same genome. Keep in mind that the authors of the second paper were aware of the first study when they published in PLoS ONE so they had an opportunity to correct or modify their own work in light of the previous paper. Thus, the second group is able to point out "errors" in the first sequence and correct "errors" in their own sequence before publication.

Keep this in mind as you read the second paper because it often seems as though the first group to publish did a very sloppy job. What we don't see in the published work is the evidence of sloppiness in the second study that was fixed by referring to the earlier work.

Velasco et al. (2007) also sequenced the Pinot Noir cultivar of Vitis vinifera but unlike the previous study they used a heterogeneous strain. Recall that in the September paper the sequencing team used an inbred line in order to reduce the extreme heterogeneity seen in normal wine-making strains.

The genome size is 505 Mb (505 × 10⁶ bp). This is larger than the earlier published sequence (487 Mb). The extra DNA is almost entirely due to inclusion of ribosomal RNA clusters. Velasco et al. (2007) identified 29,585 genes—only slightly fewer than the 30,434 genes reported by Jaillon et al. (2007). Both teams used fairly strict criteria for identifying and annotating genes. The number of genes in the grapevine genome is comparable to the number in Arabidopsis (26,819) but fewer than the number in poplar (45,555) and rice (41,046). We can expect this number to fall as false positives are eliminated.

There are 719 tRNA genes (including 163 pseudogenes), 89 snRNA genes, and about 1500 copies of the 18S + 5.8S + 28S ribosomal RNA repeat. There are about 175 copies of the 5S RNA gene.

The authors report 166 copies of snoRNA and 143 copies of microRNAs based on known examples in other plant genomes.

Many plants exhibit very high heterogeneity between homologous chromosomes. Sister chromosomes in the Pinot Noir cultivar differ by as much as 11% in DNA sequence, including large gaps. This gives rise to regions that are hemizygous—they contain only one copy of a DNA sequence in a diploid genome. An example of this heterogeneity is shown below.

Two almost contiguous regions of chromosome 1 are depicted. The red regions are transposons of various kinds (c=Copia, a=Gypsy/athila, etc.). You can see that many of the deletions/insertions are at transposon positions indicating that much of the heterogeneity between sister chromosomes is due to the insertion and excision of active transposons. This level of transposon activity is rare in mammalian genomes but common in flowering plants.

In order to study the evolution of the grapevine genome, Velasco et al. (2007) compared the sequences of paralogous genes. These are genes that belong to a gene family that diverged from a common ancestor. By comparing the differences in sequence between any two genes it is possible to estimate the time of divergence. In order to avoid any bias due to selection, it is preferable to only compare nucleotide substitutions that do not change the amino acid sequence (synonymous substitutions, K_s).

The results are shown in the figure above. Most of the pairs of genes are very similar with 0 or 0.1 substitutions. These genes arose from a very recent duplication event. There is a secondary peak at about 0.9 substitutions indicating that a large number of genes were duplicated at some particular time in the past. If this is evidence of a genome-wide duplication event then these pairs of genes should be clustered in syntenic regions. (Large segments of the chromosome that have the same order of genes.)

The insert (E) shows the distribution of those pairs from syntenic regions. It looks like most of the pairs have accumulated similar numbers of substitutions suggesting strongly that there was a genome-wide duplication event.

It is well known that flowering plant genomes have undergone polyploidization and/or hybridization during their evolution from a common ancestor about 200-300 million years ago. In their September paper in Nature, Jaillon et al. (2007) proposed that the grapevine genome was closer to the common ancestor of dicotyledenous plants. Their analysis suggested that all dicots arose from a hexaploid ancestor (three haploid genome equivalents). Further duplications occurred in the lineages leading to poplar and Arabidospis, according to Jaillon et al. (2007) [The Grapevine Genome].

Velasco et al. (2007) disagree. In the second genome study they claim that the ancestral dicot genome was tetraploid (one round of duplication) and that a second round of duplication (2R) occurred in the grapevine lineage after it diverged from poplar and Arabidopsis (see below). Note that in this study Arabidopsis and poplar are assumed to more closely related to each other than they are to grapevine whereas in the previous study grapevine was clustered with poplar.



A third duplication (3R) took place independently in the lineages leading to Arabidopsis and polar, according to Velasco et al. (2007).

At present, it isn't possible to say who is correct. In fact, they might both be wrong. The significance of these two studies is that it gives us some idea of the level of confidence we can place on speculations about genome evolution. How you interpret your data depends very much on how you compare sequences both within a species and between species. The data does not seem to be good enough to make confident predictions as judged by the differing opinions of these two groups.

The take-home lesson is that we need to take studies of this sort with a large grain of salt. In most cases we won't be lucky enough to have competing labs to analyze the same data and point out differing interpretations.

---

Jaillon, O., Aury, J.M., Noel, B., Policriti, A., Clepet, C., Casagrande, A., Choisne, N., Aubourg, S., Vitulo, N., Jubin, C., Vezzi, A., Legeai, F., Hugueney, P., Dasilva, C., Horner, D., Mica, E., Jublot, D., Poulain, J., Bruyère, C., Billault, A., Segurens, B., Gouyvenoux, M., Ugarte, E., Cattonaro, F., Anthouard, V., Vico, V., Del Fabbro, C., Alaux, M., Di Gaspero, G., Dumas, V., Felice, N., Paillard, S., Juman, I., Moroldo, M., Scalabrin, S., Canaguier, A., Le Clainche, I., Malacrida, G., Durand, E., Pesole, G., Laucou, V., Chatelet, P., Merdinoglu, D., Delledonne, M., Pezzotti, M., Lecharny, A., Scarpelli, C., Artiguenave, F., Pè, M.E., Valle, G., Morgante, M., Caboche, M., Adam-Blondon, A.F., Weissenbach, J., Quétier, F., Wincker, P.; French-Italian Public Consortium for Grapevine Genome Characterization (2007) The grapevine genome sequence suggests ancestral hexaploidization in major angiosperm phyla. Nature 449:463-467. [PubMed] [Nature]

Velasco, R., Zharkikh, A., Troggio, M., Cartwright, D.A., Cestaro, A., Pruss, D., Pindo, M., Fitzgerald, L.M., Vezzulli, S., Reid, J., Malacarne, G., Iliev, D., Coppola, G., Wardell, B., Micheletti, D., Macalma, T., Facci, M., Mitchell, J.T., Perazzolli, M., Eldredge, G., Gatto, P., Oyzerski, R., Moretto, M., Gutin, N., Stefanini, M., Chen, Y., Segala, C., Davenport, C., Demattè, L., Mraz, A., Battilana, J., Stormo, K., Costa, F., Tao, Q., Si-Ammour, A., Harkins, T., Lackey, A., Perbost, C., Taillon, B., Stella, A., Solovyev, V., Fawcett, J.A., Sterck, L., Vandepoele, K., Grando, S.M., Toppo, S., Moser, C., Lanchbury, J., Bogden, R., Skolnick, M., Sgaramella, V., Bhatnagar, S.K., Fontana, P., Gutin, A., Van de Peer, Y., Salamini, F., Viola, R. (2007) A high quality draft consensus sequence of the genome of a heterozygous grapevine variety. PLoS ONE 2(12): e1326. doi:10.1371/journal.pone.0001326 [PubMed] [PLoS]

The Grapevine Genome

 
The sequence of the grapevine genome was reported in Nature last September (Jaillon et al. 2007). The 56 authors are all members of the French-Italian Public Consortium for Grapevine Genome Characterization [International Grape Genome Program].

The species is the dicotyledonous plant Vitis vinifera and the variety is cultivar Pinot Noir. In this case, the line was a special inbred variety that was about 93% homogeneous. It was necessary to use a selfed line of plants because most field varieties are very heterogeneous and this would have made it more difficult to assemble the sequence using the shotgun strategy.

The genome has 19 chromosomes amounting to 487 Mb of DNA (487 × 10⁶ base pairs). This is comparable in size to the three other plant genomes that have been sequenced; rice, poplar, and Arabidopsis.

The published sequence is referred to as a "high-quality draft" by the authors. They report 30,434 protein-encoding genes and 600 tRNA genes. (Ribosomal RNA genes aren't included in the paper.) This is somewhat fewer genes than poplar (45,555) and rice (37,544) but more than Arabidopsis (27,029). However, this might be deceptive since the total number of identified genes tends to decrease as annotation proceeds and annotation of the Arabidopsis genome is much further along than annotation of the other genomes.

About 41% of the genome is composed of transposons—most of which are non-functional pseudogenes. Genes make up 46% of the genome (7% exons, 37% introns). This is a much lower percentage of junk DNA than typical mammalian genomes.

Vitis vinefera is a dicotyledonous plant like the poplar tree and the small flowering plant Arabidopsis. Rice is a monocot and monocots and dicots are thought to have diverged about 200 million years ago. Previous studies have suggested that grapevine should be more closely related to popular than to Arabidoposis and the genomic sequence confirms that relationship.

One of the most interesting problems in plant evolution is the tracking of various genome duplications that have occurred. Most plants show traces of recent polyploidization events and/or more ancient ones. This is most clearly seen when looking at paralogous genes in gene families and the evidence for large scale duplication comes from comparisons of large blocks of sequence. These syntenic regions (or paralogous regions) within a haploid genome are strong evidence of ancient duplications.

The figure below is taken directly from the Nature paper. It shows syntenic regions within the grapevine genome (left). Each colored region corresponds to a stretch of paralogous (homologous) genes. As you can see, chromosome 1, 14, and 17 each contain a large block of similar sequence (light green). Chromosomes 10, 12, and 19 have a different syntenic region (red).



The evidence suggests an ancient hexaploidization in the lineage leading to grapevine. When the syntenic regions of poplar (middle) and Arabidoposis (right) are mapped, you can see that the patterns get much more complicated and the regions become scrambled. The simplest explanation is that the grapevine genome is close to the ancestral genome of all dicots and the poplar and Arabidopsis genomes have undergone additional duplications accompanied by gene loss. The rice genome shows no evidence of the ancient tripling of the genome in dicots.

The phylogenetic tree looks like this—where stars represent duplication events. There has been at least one, and possibly two, duplications in the lineage leading to rice. It will be interesting to see if other monocot genomes show evidence of these duplications or whether they are specific to rice.

It appears that there have been two polyploidy events in the lineage leading to Arabidopsis from the time it diverged from the other two dicots. I don't think anyone has a good explanation for why genome duplications are so frequent in the evolution of vascular plants.¹

Note that the gene duplications give rise to larger gene families in flowering plants but what this means is that there are fewer distinct genes in plant genomes compared to mammalian genomes. Of course, plants have a number of metabolic pathways that aren't found in animals and some of the genes for these pathways are specifically amplified in the grapevine genome.

For example, there are more genes for stilbene synthases in grapevine than in poplar or Aribidopsis Stilbane synthases are essential enzymes in the resveratrol pathway. Resveratrol is the wine chemical associated with presumed health benefits coming from wine consumption.

The grapevine genome also has extra copies of the gene for terpene synthases. These are responsible for synthesis of resins, oils, and aromas that give wine its unique taste. These genes are probably the result of selected breeding over the course of several thousand years.

UPDATE: Read about The Second Grapevine Genome Is Published.

---

1. Perhaps the Intelligent Design Creationists can explain this using their "scientific" theories.

Jaillon, O., Aury, J.M., Noel, B., Policriti, A., Clepet, C., Casagrande, A., Choisne, N., Aubourg, S., Vitulo, N., Jubin, C., Vezzi, A., Legeai, F., Hugueney, P., Dasilva, C., Horner, D., Mica, E., Jublot, D., Poulain, J., Bruyère, C., Billault, A., Segurens, B., Gouyvenoux, M., Ugarte, E., Cattonaro, F., Anthouard, V., Vico, V., Del Fabbro, C., Alaux, M., Di Gaspero, G., Dumas, V., Felice, N., Paillard, S., Juman, I., Moroldo, M., Scalabrin, S., Canaguier, A., Le Clainche, I., Malacrida, G., Durand, E., Pesole, G., Laucou, V., Chatelet, P., Merdinoglu, D., Delledonne, M., Pezzotti, M., Lecharny, A., Scarpelli, C., Artiguenave, F., Pè, M.E., Valle, G., Morgante, M., Caboche, M., Adam-Blondon, A.F., Weissenbach, J., Quétier, F., Wincker, P.; French-Italian Public Consortium for Grapevine Genome Characterization (2007) The grapevine genome sequence suggests ancestral hexaploidization in major angiosperm phyla. Nature 449:463-467. [PubMed] [Nature]

[Photo Credit: Nature]

Bon Voyage Charles

 
On this day in 1831 Charles Darwin set sail from Plymouth Sound (England) on the newly refitted brig HMS Beagle. Its mission was to explore South America and survey its coast.

The ship returned to England on October 2, 1836 after circumnavigating the globe.

When the ship left England, Darwin was officially the companion of the captain, Robert FitzRoy, but by the time it returned Darwin was the official naturalist.

---

[Image Credit: The HMS Beagle Project]

Happy Holidays from Celebrity Atheists

 
The Daily Telegraph (Sydney, Australia) has a gallery of 15 celebrity atheists [Christ-miss for atheist celebs]. My favorites are Katharine Hepburn and Jodie Foster.

It is cause for billions of people to rejoice. But not these celebrity Grinches - sorry, atheists.

They are the stars who do not believe three wise men followed a star to a baby in a manger more than 2000 years ago.

What's significant about this list is not the fact that there are famous people who don't believe in God. That's been true for hundreds of years. And it's not the fact that some of them are very intelligent either—that's almost a given. (We'll ignore Angelina Jolie.)

No, the important point is that atheism is entering the mainstream. Newspaper articles like this wouldn't have been printed ten years ago. The more people learn about life in the absence of religion, the more it will come to be seen as a perfectly normal way to behave. That's a good thing.

---

[Hat Tip: Hemant Mehta at Friendly Atheist (Merry Tuesday to These Celebrities)]

Pray for France!

 
This is a public service announcement for all the creationists who have been visiting Sandwalk lately.

France is in trouble. It needs your help [Pray for France]. The country is almost 30% atheist and less than 1% evangelical Christian. This is a problem because, as everyone knows, France is a very special country.

"The kingdom of France is predestined by God to defend the Church of Christ Our Lord. This kingdom will be great among all the kingdoms of the earth. In as much as it is loyal to its calling, it will be victorious. If it proves unfaithful in this, it will be punished harshly. Nevertheless, it will remain until the end of time."

               -St. Remi at King Clovis' baptism in 498

Your task, should you choose to accept it, is to pray for 40 days.

Rampant secularization has made the spiritual battleground in France difficult. Yet, God is on the move – working through His people and drawing in the French people – one soul at a time.

Did you know that for the past 7 years thousands of French people intercede for France during the 40 days preceding Lent?

Pray for France is your access point to join French believers during these 40 Days of Prayer.

Lent begins on Ash Wednesday, which falls on February 6th in 2008. You should start praying on Feb. 6th—if you have trouble thinking of anything good to say about France the website will sell you a brochure of prayers for $3.50.

Not being religious, I can't really get into this effort to support France but I'd really like to see the rest of you participate. As it turns out, I'm going to be in France for the first half of lent and I'd sure like to think that your prayers will make for good weather, good food, and good wine.

---

[Hat Tip: Hemant Mehta at Friendly Atheist]

Oh My God!

 
According to a report in the Toledo Blade a recent survey of 1005 American adults reveals the following astonishing facts [Survey finds most Americans believe Jesus born of virgin].

--75 pecent believe that Jesus was born to a virgin. Mary

--69 percent of adults believed Jesus turned water into wine at the wedding in Cana.

--68 percent believed Jesus used five loaves of bread and two fish to feed a crowd of 5,000.

--64 percent believed the Earth was covered by a flood in which Noah, his family, and numerous animals were spared by living on an Ark.

--56 percent expressed literal belief in the Bible account of the devil, disguised a serpent, tempting Eve to eat forbidden fruit.

--49 percent accepted as accurate the Bible story of Samson losing his legendary strength when Delilah had his hair cut.

Guess what folks? This survey was not taken in 1500 AD. These are the opinions of people today in 2007!

[Photo credit: Zarna (Oh My God!)]
[Hat Tip: RichardDawkins.net]

The Human Genetic Variation "Breakthrough"

 
"Human Genetic Variation" is the scientific "breakthrough" of 2007, according to Science magazine. I have a problem with science journalism when science writers misuse the word "breakthrough" but that's topic for another posting [Breakthrough of the Year in Science].

In this thread I want to discuss the actual choice made by Science editors. Elizabeth Pennisi describes the choice in the lead article of this weeks issue [BREAKTHROUGH OF THE YEAR: Human Genetic Variation].

Equipped with faster, cheaper technologies for sequencing DNA and assessing variation in genomes on scales ranging from one to millions of bases, researchers are finding out how truly different we are from one another.

There is some truth to this statement. It's true that the details or the amount of genome-wide of variation are being added to the databases. But is it true that we only realized for the first time in 2007 that humans are different from one another?

Of course not. We've known about massive variation in populations since the the 1960's [The Cause of Variation in a Population]. We've been using DNA fingerprints to identify criminals for more than 15 years. Think about it. Would DNA fingerprinting work if we weren't all different from one another at the level of genome sequence?

The unveiling of the human genome almost 7 years ago cast the first faint light on our complete genetic makeup. Since then, each new genome sequenced and each new individual studied has illuminated our genomic landscape in ever more detail. In 2007, researchers came to appreciate the extent to which our genomes differ from person to person and the implications of this variation for deciphering the genetics of complex diseases and personal traits.

We're familiar with the writings of Elizabeth Pennisi so it shouldn't come as a big surprise that she makes statements like this. She seems to be remarkably deficient in her knowledge of scientific background and history.

It is simply not true that "In 2007, researchers came to appreciate the extent to which our genomes differ from person to person." Real scientists have known and appreciated that fact for decades. It's part of understanding junk DNA, Neutral Theory, and the importance of random genetic drift.

The true part of the statement is that by mapping more and more specific examples of variation we can do some experiments that we couldn't do before. This is an advance in technology but not an advance in our understanding of the extend of human genetic variation.

---

Breakthrough of the Year in Science

 
For the longest time science journalists have been misusing the word "breakthrough." What they usually mean is any scientific discovery that merits a press release by a university or a scientific journal. Both of these sources are biased and it's the role of competent science writers to recognize that bias and report the real significance of a scientific publication.

Science usually advances incrementally, building slowly but surely on the work of others. Real "breakthroughs" are extremely rare.

All scientists know this so it comes as a major disappointment to see the publication of the American Association for the Advancement of Science (AAAS) promoting a "Breakthrough" of the Year [Breakthrough of the Year: Human Genetic Variation]. Why couldn't this be a scientific achievement of the year or a scientific advance of the year? Either of those words gives a better impression than"breakthrough" and allows us to nominate real advances in science that aren't necessarily breakthroughs.

---

Did You Forget Why They're Called IDiots?

 
Bill Dembski and Jonathan Wells have teamed up to write a new book on Intelligent Design Creationism. By all accounts, it is no better than any of the other books that these authors have written. This shouldn't be a surprise. Putting two IDiots together does not cancel out.

Dembski was upset that the reviews on Amazon weren't as glowing as he would have liked. Even worse, the negative reviews were rising to the top of the list as more and more people ranked them as helpful. What to Do?

Well, if you're an IDiot, the first thing you think of is a way to fudge the results. You start by posting a message on the IDiot blogs asking all your follower to rush on over to Amazon and vote for the favorable reviews. Yep, that'll work all right. Except for one teeny, tiny problem.

Rational people found out about it and since there are more of them than IDiots, you can guess what happened. Now what does an IDiot do? That's right, complain about "shameless manipulation"! Here's the current position on deliberately trying to manipulate the results on Amazon.

THE DESIGN OF LIFE is being shamelessly manipulated by the Darwinists at Amazon. Not only are they posting negative reviews that give no indication that the reviewers have read the book but they are also voting up their negative reviews so that these are the first to be seen by potential buyers.

PZ Myers has the complete story [You Bastards!]. He points out the obvious ....

Wait a minute…Dembski himself shamelessly urges his acolytes to rush off and manipulate the reviews because he doesn't like the one-star reviews his book is getting, and now he shamelessly protests because we called attention to his shameless manipulation? My poor exhausted irony meter is stirring again.

Don't forget why we call them IDiots.

---

Rome Lights the Colosseum

 

From the International Herald Tribune [Rome lights up Colosseum to celebrate UN vote on death penalty, abolition in New Jersey].

The city of Rome lit up the Colosseum on Wednesday to celebrate a U.N. vote calling for a moratorium on the death penalty and a decision by the U.S. state of New Jersey to abolish capital punishment.

The ancient arena was bathed in white light as Italy celebrated the U.N. General Assembly resolution approved Tuesday despite opposition by supporters of the death penalty, including the United States, Iran and China.

Italy, a firm opponent of capital punishment, spearheaded the drive for the nonbinding resolution, which was co-sponsored by European Union states and 60 other countries.

Italy also hailed the signing Monday of a law abolishing the death penalty in New Jersey, making it the first U.S. state to abolish capital punishment in more than 40 years.

Rome's Colosseum, once the arena for deadly gladiator combat and executions, has become a symbol of Italy's fight against capital punishment. Since 1999, the 1st century monument has been lit up every time a death sentence is commuted somewhere in the world or a country abolishes capital punishment.

About 133 civilized countries have abolished the death penalty but there are still 100 countries that retain it. According to Amnesty International, 90% of all executions worldwide take place in only six countries: Chain, Iraq, Iran, the United States, Pakistan and Sudan [UN Assembly calls for moratorium on death penalty].

---

Tangled Bank #95

 
The latest version of the Tangled Bank has been posted by ouroboros [Tangled Bank 95: Here I stand and can do no other].

Welcome to the 95th installment of Tangled Bank, a blog carnival devoted “to science and medicine, broadly defined.”

The installment’s title was inspired by its issue number, and comes from a probably apocryphal line almost definitely never uttered by Martin Luther, the author of the 95 Theses — in honor of Tangled Bank founder PZ Myers‘ deep love for Christianity (or possibly for just nailing things into churches).

If you’re visiting Ouroboros for the first time: Greetings! The site is devoted to reviewing research literature in the biology of aging. Feel free to poke around and stay a while. If you like what you see, subscribe to our RSS feed.

---

Nobel Laureates: Paul Boyer and John Walker

 

The Nobel Prize in Chemistry 1997.

"for their elucidation of the enzymatic mechanism underlying the synthesis of adenosine triphosphate (ATP)"



In 1997, Paul D. Boyer (1918 - ) and John E. Walker (1941 - ) won the Nobel Prize in Chemistry for working out the details of the "binding change" mechanism in the synthesis of ATP by ATP synthase [How Cells Make ATP: ATP Synthase].

Boyer elucidated the chemical mechanism in the 1970's and 1980's and Walker provided confirmation when he solved the structure of the ATP synthase components a number of years later.

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

Nobel Laureates

Your Majesty, Royal Highnesses, Ladies and Gentlemen.

Life requires energy. Our muscles require energy when we move. We need energy to think. Energy input is required for the production of new biological molecules. This year's three Nobel laureates in Chemistry have contributed in different ways to our knowledge of how living organisms can obtain and utilize energy. Common to their discoveries is the unique adenosine triphosphate (ATP) molecule, which can store and transport energy in all organisms, whether it be a simple bacterium, a dandelion, a finch or a human being. Large quantities of ATP must be formed and consumed. Each day an adult converts a quantity of ATP roughly equivalent to his or her own body weight, and in case of physical exertion, many times more.

All energy on earth originates from the sun. Green plants can absorb sunlight and convert it into chemical energy through the process of photosynthesis, in which carbon dioxide and water form sugar, starch and other complex carbon compounds. Other organisms, such as humans and animals, are in turn dependent on these carbon compounds as sources of energy, and they burn them with the help of oxygen. That is why we breathe. Nature can thus be said to have chosen a combination of solar and coal-fired power plants for its energy supply. Although these two energy conversion systems may seem different in purely technical terms, in many respects they operate in the same way in living cells. The most important similarity is that the energy released is utilized with the help of the ATP molecule.

According to Peter Mitchell, the 1978 Nobel Laureate in Chemistry, the energy released in photosynthesis and cell respiration initiates a stream of positively charged hydrogen ions. These hydrogen ions, in turn, drive the production of ATP with the aid of a membrane-bound enzyme called ATP synthase. Two of this year's laureates, Paul Boyer and John Walker, have studied this important enzyme and have shown that it functions in a unique way. Among other things, they have demonstrated that ATP synthase can be compared to a molecular machine, whose rotating bent axle is driven in a step-wise process by "biological electricity" - that is, the flow of hydrogen ions. Because of the asymmetry of the rotating axle, three subunits of the enzyme assume different forms and functions: a first form that hinds adenosine diphosphate (or ADP) and phosphate building blocks, a second form where these two molecules are chemically combined into a new ATP molecule, and a third form where the ATP that has been formed is released. In the next twist of the axle, the three subunits switch form and thus also function with each other, and another ATP molecule can be formed, and so on. This "binding change mechanism" was put forward by Boyer in the late 1970s, but only in 1994 did his ingenious model gain general acceptance among researchers. In August of that year, Walker and his colleagues published three-dimensional images of ATP synthase that had been obtained by X-ray analysis of enzyme crystals. These X-ray images, magnified several million times, showed how an asymmetrically elongated protein molecule interacted with three other protein units that all showed mutually different forms. Walker had finally revealed the detailed blueprint of the molecular machine and shown that Boyer's theory of ATP formation was correct.

....

Dr. Boyer, Dr. Skou and Dr. Walker,

I have tried to describe how your pioneering studies on the enzymology of ATP metabolism have contributed to our understanding of how living cells can store and make use of energy. Your work has revealed new principles for enzyme function, opened up new areas of chemical research as well as providing the basis for biomedical applications for the benefit of mankind. In recognition of your services to chemistry the Royal Swedish Academy of Sciences has decided to confer upon you this year's Nobel Prize for Chemistry.

On behalf of the Academy, I wish to convey to you our warmest congratulations and I now ask you to receive the Prize from the hands of His Majesty the King.

---

The Top 100 Science Blogs

 
John Wilkins takes note of the fact that his blog Evolving Thoughts is #20 on the Wikio list of top 100 science blogs [Wilko on Wikio]. Wilkins thinks this is a bit strange for a philosophy blog.

I thought I'd check to see if Sandwalk is listed. Here's the blog ranking for science blogs. Sandwalk didn't make the top 100.

How are these listings generated? Here's what wikio says,

The position of a blog in Wikio's classification depends on the number and value of the links that point towards them. These links are dynamic, meaning that it is a question of backlinks or of posted links inside the items themselves.

The blog lists (blogrolls) are not taken into account and the period of validity of the links themselves is limited to the past 120 days, in order to be as most representative of the current influence of the blogs as possible, knowing that the Top blogs are all updated all the first ones of the month.

I don't really understand this method of ranking blogs. Can someone explain it to me?

While scanning the list, I began to notice something a bit strange. It turns out that 35 of the top 50 science blogs are part of the SEED consortium (ScienceBlogs^TM). The #3 blog is Pharyngula and this seems reasonable but the #7 science blog is Dispatches from the Culture Wars and this is not reasonable. Ed Brayton's blog may be interesting but it ain't a science blog.

Looking further down the list I see that Framing Science comes in at #39. Oops, there's something seriously wrong here.

I checked out Sandwalk again and discovered that it isn't a science blog. It's listed under the "General" category. That's strange. What about Bad Astronomy Blog? It didn't make the list of top 100 science blogs either. Let's see how that blog is categorized—yep, it's also under "General."

Hmm ... what about other blogs that don't make the list under the "Sciences" category? The Panda's Thumb and Genomicron aren't science blogs either. They're "General" blogs.

This is ridiculous. I tried to let wikio know that Sandwalk was in the wrong category but it turned out to be impossible to register as a science blog. Can someone from ScienceBlogs^TM let me know how they did it?

---

What Is Intelligent Design Creationism?

 
Over on Uncommon Descent there are a group of adolescents pretending to be scholars. Most of them are patting each other on the back saying what good fellows they are. The highest level of scientific knowledge they possess comes from reading Michael Behe (which they consistently misinterpret). One thing they've mastered is quote mining—do all creationists take a course in effective quote mining or do they just copy the quotes from some website?

My short foray into dumpster diving didn't provoke much in the way of intelligent discourse over there except for one poster named "gpuccio." He made some points that are worth responding to [Uncommon Descent]. I think his version of Intelligent Design Creationism may be very different from what I read. Maybe he's a cut above the rest. (Warning, don't get too excited before you read the rest of the posting.)

You are, maybe unwillingly, misunderstanding the words in Granville Sewell’s post. I think you are confused about the meaning of the word "mechaninsm". What Sewell obviously means is that we don’t know any theory which can explain the "causal mechanism" of the generation of information in biological beings which is usually termed "evolution". All your stuff of arrogantly citing natural selection and genetic drift, as though Sewell ot all of us are not aware of them, is simply pointless.

Now this could be interesting. Naturally I was aware of the fact that Sewell was not using real scientific terms when he implied that scientists know nothing about the mechanisms of evolution. That was partly the point in responding the way I did.

But in this response we have the beginnings of something significant. Maybe for the first time we are going to see a real scientific discussion of those other "causal mechanisms" that the creationists have been so cagey about.

In case you have not understood that, the whole point of ID theory is that RM, NS, genetic drift, and any other kind of random variation, have not trhe power to generate that kind of information that we observe in biological beings. You may agree or not (I suppose you don’t), but simply stating that natural selection and genetic drift are the mechanism of evolution doesn’t answer the point of ID.

I'm guessing that gpuccio is talking about special mutations here. It looks like he's redefining evolution in terms of an Intelligent Design Creationism version of information.

Before continuing, let me make one thing perfectly clear. When Granville Sewell demanded that scientists admit that they know nothing about the mechanisms of evolution it seems fair to assume that he's talking about scientific definitions of "evolution" and "mechanisms of evolution." I made that assumption and showed that Granville Sewell was just plain wrong if he was talking about science.

I think we're about to learn what Intelligent Design Creationists mean when they use those words. While this will be interesting, it's not really all that relevant when talking science to scientists.

To answer the point of ID, you should understand why we are convinced that your so called “mechanisms” are not mechanisms at all, and then demonstrate that we are wrong, and that you are right. Pretendong that we are only “invoking the supernatural”, because science can’t explain everything in detail, s only a lie. It will not do, not here. We know that’s not true. You can repeat that lie in your blog, where other darwinists are ready to support it, but not here. Here, if you want you must discuss.

Whatever. Please get to the point.

I mentioned that I lecture about evolution and I use examples like the irreducibly complex citric acid cycle and plant photosynthesis complexes to show probable evolutionary pathways to complexity. gpuccio replies with this,

Really? Can you explain a molecular pathway to all that you say? Please, explain that to us. Let’s verify the credibility of your "mechanisms" in your supposed molecular pathway. Let’s calculate the probabilitys of your supposed events. Lets’ reason, as every scientist should do, in terms of cause and effect, if we are talking necessity, and in terms of probabilities, if we are talking randomness. If you invoke natural selection, let’s verify which step of you supposed mechanism is selected, why and in what times. You see, nobody wants that you can explain everything, or have the e4vidence for everything, but just that you give a credible, detailed mechanism which "could" be believed, and for which there is at least some solid evidence.

Hmmm ... this sounds an awful lot like typical creationist screed. Whenever we mention some evidence for evolution they all of a sudden want all the excruciating details, or it doesn't count. Where are those demands when it comes to the Intelligent Design Creationist explanation of the citric acid cycle, huh?

Anyway, we see here the typical confusion of the creationist. They can't distinguish between evolution the concept, evolutionary theory, and the unique history of life on this planet. When gpuccio says "mechanisms" above, he doesn't mean mechanisms of evolution. He means detailed descriptions of events that took place several billion years ago. Nothing else will do for the creationist mindset. If we can't supply the complete historical account then it can't be evolution—God must have done it. Can you say "God of the gaps?'

gpuccio, you don't get to redefine "mechanisms of evolution" just because it suits your rhetorical purpose.

When you say that ID focuses on some complex structures, while many others are well understood, you show that you have not understood anything of ID. ID has focused on the bacterial flagellyum just because it is an easy example. But we could discuss practically any complex structure in biology, and show that it could not come into existence by your "mechanisms".

I'm sorry gpuccio but there's no polite way to say what I'm about to say.

That's just bullshit. You are lying.

Even Michael Behe has abandoned the citric acid cycle because he knows we have a reasonable evolutionary explanation. The same is true of dozens of other complex structures and pathways. There's a reason why 99% of creationist literature focuses on bacterial flagella and one or two other complex structures. It's because that's where you see the gaps and that's where your God can hide. For now.

Incidentally, I'm rejecting your use of the word "mechanism" to describe unique historical events.

You ask:

"Let me ask you a question. Did the intelligent designer allow naturalistic evolution to do most of the work, saving a few well-chosen examples for special attention? Did he (making an assumption here) let photosynthesis and the citric acid cycle—and dozens of other things that we understand—evolve on their own but step in to design bacterial flagella or whatever other complex you have chosen as the evolution problem of the day?"

No. Absolutely not. Again, you have understood nothing of ID. ID maintains that practically all "macroevolution" is the product of design. Only some patterns of "microevolution" (some kinds of bacterial resistance, and so on) can be ascribed to your "mechanisms". Please, read Behe’s last book for the details, and then answer that. Bu please, stop pretending that ID says things that it has never said.

Oh dear. Turns out that this creationist is no more intelligent than all the others. Now he's reduced to stomping his feet on the ground and shouting "no macroevolution allowed! that's what Intelligent Design Creationism is all about."

Okay, I understand. You have an intellectually bankrupt position. You say macroevolution never happens and that's what real Intelligent Design Creationism maintains. How does one debate such a position?

You say:

"Do you see the point? Scientists have plenty of good examples to choose from. From those examples they extrapolate to others where there is less information available."

Wrong again. See discussion above. The point is not, and has never been, how much information scientists have about something or something else. The point is how scientists have regularly deformed and forced the interpretation of facts to support an unlikely and unbielievable theory of supposed causal mechanisms.

So, what your saying is that you don't give a damn how much evidence scientists have about evolution and the history of life. It's all lies. Now that's an intelligent response.

Maybe I was wrong about you. Maybe you are an IDiot just like the rest.

You say:

"ID proponents, on the other hand, do the opposite. They take all of the well-studied examples and throw them in the waste basket because they are an embarrassment to their worldview. Then they taunt scientists with the more difficult cases and conclude that everything must be supernaturally created when scientists can’t give them a detailed answer to their specific example."

False. Irrational. You discuss your fantastic view of ID. Id has never said or done what you say. It is really offensive how you superficially and irrespectfully lie about serious scientists and thinkers like Dembski, Behe, and others. I respect you for having come here to say what you say, but not for saying this kind of things.

I don't think this "discussion" is going anywhere. All you keep doing is insisting that what I say about Intelligent Design Creationism is wrong. I don't think so. I'm beginning to think that it's you who doesn't understand Intelligent Design Creationism. Let me give you a clue. Intelligent Design Creationism is all about proving that some special examples of complex things can't possibly have evolved by the known mechanisms of bioloical evolution. Therefore, God exists.

The final straw is when you refer to Dembski as a "serious scientist." Now I know you're just pulling my leg.

Goodbye.

---

How Cells Make ATP: ATP Synthase

 
In our previous posting we saw how cells can make ATP from ADP + P_i by substrate-level phosphorylation [How Cells Make ATP: Substrate-Level Phosphorylation].

This is not the most important route to ATP synthesis. Most of the ATP inside a cell is made by a membrane-bound enzyme called ATP synthase.

ATP synthase is found embedded in the inner membranes of mitochondria and chloroplasts and the inner membrane of bacterial cells. In all three cases, a membrane-associated electron transport system pumps protons (H⁺) across the membrane from the inside to the outside. In this case "outside" is actually the space between the inner and outer membranes. Protons accumulate in this space creating a protonmotive force. You can think of this "force" as the "pressure" of protons to move back into the cells because of the high concentration that has been created in the intermembrane space.

The protonmotive force is what drives synthesis of ATP. As protons move back into the cell they pass through a channel in the a subunit of ATP synthase. This subunit acts like a small motor driving the rotation of the c subunits (rotor) in the membrane. For every three protons that cross the membrane enough energy is given up to move the rotor through 120°. It takes 9 protons for one complete rotation.

The rotor (c subunits) is connected to a rod made up mostly of the γ subunit of ATP synthase. The rod rotates inside the head, which is a hexamer composed of three α and three β subunits. The head of ATP synthase doesn't rotate. It is fixed to the motor through the b subunits.

The γ rod is asymmetric as shown in the figure by depicting it with a kink. As it rotates inside the head it alters the conformation of the α and β subunits. The active site of the ATP synthase is located on the outside surface between an α and a β subunit. The spinning rod shifts the conformation of the active site between three states.


The first state is called the "open" state. In the "open" state ADP and P_i can bind to the active site. In the second state, called the "loose" state, ADP and P_i are locked in place and cannot be released. In the third state (the "tight" state") ATP is formed as ADP and P_i are squeezed together.

Since there are three active sites in each head, the effect of rotating the γ rod is to sequentially change each of the three sites from "open" to "loose" to "tight" for each 360° rotation of the rotor. Nine protons are used up in one rotation and three ATP's are synthesized. This works out to one ATP molecule for every three protons.

This mechanism of ATP synthesis is called the binding change mechanism. It was first worked out by Paul Boyer. The mechanism was confirmed by X-ray crystallographic studied done by John Walker. Boyer and Walker received the Nobel Prize in 1997.

---

[Image Credits: The images are from Horton et al. Principles of Biochemistry 4th edition ©Pearson/Prentice Hall]

[The animated gif is from Wikipedia]

How Cells Make ATP: Substrate-Level Phosphorylation

Monday's Molecule #56 was adenosine 5′-diphosphate, or ADP. ADP is the precursor for synthesis of adenosine 5′triphosphate, or ATP. ATP is one of the most important cofactors in biochemistry. It carries energy that drives other reactions to completion.

The synthesis reaction looks like this, where P_i is inorganic phosphate.

This reaction is the reverse of the energy-producing reaction where ATP is hydrolyzed to ADP and H₂O. Since the energy-producing reaction produces a lot of energy (~45 kJ mol^-1 under normal cellular conditions), it follows that the synthesis reaction requires the input of a great deal of energy.

There are several different ways that cells can make ATP from ADP and inorganic phosphate (P_i). one of the more common ways is when the phosphate group is transferred to ADP from a molecule that is more energetic than ATP. This form of biosynthesis is called substrate-level phosphorylation. The formation of ATP is coupled to the removal of a phosphate group from another molecule.

Here's an example from the gluconeogenesis/glycolysis pathway. The reaction catalyzed by phosphoglycerate kinase is readily reversible inside the cell. (In biochemistry courses, we say that it is a near-equilibrium reaction.)


When glucose is being synthesized (gluconeogenesis) the reaction goes from right to left and a molecule of ATP is used up to create 1,3-bisphosphoglycerate. During glycolysis, when glucose is being broken down, the reaction goes from left to right and a molecule of ATP is produced when the phosphate group on 1,3-bis phosphoglycerate is transferred to ADP.

This is an example of ATP synthesis by substrate-level phosphorylation. It's one of two such reactions in glycolysis and it's the main reason why the degradation of glucose can be used to produce useful energy. For example, when glucose is taken up from the blood stream by muscle cells and degraded to produce ATP that can be used in muscle contraction.

---

Bruce Alberts Is the New Editor-in-chief of Science

 
The board of directors of the American Association for the Advancement of Science (AAAS) announced yesterday that Bruce Alberts will take over as editor-in-chief of Science magazine, effective March 1, 2008 [Prominent cell biologist will take reins on 1 March].

Alberts will retain his UCSF faculty position and expects to devote half of his time to Science. "I view Science magazine as a critical venue for maintaining the standards of science, as well as for spreading an understanding and appreciation for science around the world," says Alberts. "With the tremendous challenges we face today, both of these important aims need constant attention."

As many of you know, Bruce is interested in science education and this is a marvelous opportunity for him to improve the quality of science journalism [Bruce Alberts in Toronto]. I happen to know that he is also curious about blogging and its effect on science education so maybe there will be more press about bloggers in future editions of Science.

---

They Also Edit Comments on Uncommon Descent - Then You're Banned!

 
One of the more despicable practices of bloggers is to edit the words of people who comment on their blog. I already took notice of this practice on "Dr." Sharon's Blog.

Now the same thing is happening on Uncommon Descent. I posted a message there saying "Some of the more intelligent IDiots (I realize that's an oxymoron) ..."

When the comment finally appeared it said, "Some of the more intelligent ID proponents ..."

Would it surprise you to learn that this comment from "gpuccio" didn't get edited?

Larry Moran has clearly shown the intellectual and moral level od darwinist arguments: failure to answer any pertinent question, and readyness to grossly insult any adversary, are really their only weapons. While their moral failures can always be pardoned (after all, man is not a perfect being), their intellectual stupidity and arrogance are much more difficult to excuse.

No? I didn't think you be surprised. Why is it that creationists are so willing to dish it out but so cowardly when they're on the receiving end?

Anyway, they won't have to worry about it from now on since Patrick has just posted the following message.

Since you guys apparently want to debate Larry Moran in this thread–are you guys masochists? ;) –I temporarily let his comments through but edited them for insults and such (the ones that were not entirely insults). Otherwise, Larry is banned as usual.

This will surely be followed by dozens of comments attacking me and what I said in the edited comments that were allowed to appear. I won't be able to respond to them no matter how IDiotic they are. Isn't that strange?

---

See "Gordo" at the ROM

DINOs are back at the Royal Ontario Museum in Toronto (Canada). The new James and Louise Temerty Galleries of the Age of Dinosaurs has just opened and the star attraction is a Barosaurus fossil. That's a drawing of Barosaurus above, courtesy of Mike Skrepnick. A complete description of the exhibit can be found on the ROM website [Natural History Galleries.

One of the highlights is “Gordo”, the Museum's massive 27-metre (90-foot) Barosaurus skeleton, the largest dinosaur on permanent display in Canada and one of only two Barosaurus skeletons on display in the world. Several of the dinosaurs on display are long-time ROM residents that have been remounted for the new display including Albertosaurus, Corythosaurus and a number of hadrosaurs that are easily recognizable by their distinctive tubular head crest, some measuring over one metre long. The most well-known hadrosaur, Parasaurolophus, a very rare species, is one of the ROM's best and most complete specimens. Other featured specimens on display include the full skeleton cast of a Tyrannosaurus rex and a real Triceratops skull.

---

[Image Credit: Barosaurus drawing courtesy of Mike Skrepnick, used with his permission.]

[Hat Tip: Brian Switek at Laelaps (Meet "Gordo" the Barosaurus)]

Monday's Molecule #56

 
Most students are busy at this time of year so I'm going to give you a break today. This is a very well-known molecule. You have to name it, giving me the common name and the correct systematic IUPAC name.

There's a direct connection between this molecule and Wednesday's Nobel Laureate(s). Your task is to figure out the significance of today's molecule and identify the relevant Nobel Laureate(s). I don't think this one is very difficult.

The reward goes to the person who correctly identifies the molecule and the Nobel Laureate(s). Previous winners are ineligible for one month from the time they first collected the prize. There is only one ineligible candidate for this week's reward because Sandwalk readers have not been very successful in recent weeks. 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 (with the correct IUPAC name) and the Nobel Laureate(s). Correct responses will be posted tomorrow along with the time that the message was received on my server. I may select multiple winners if several people get it right.

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

UPDATE: We have a winner! The molecule is ADP or 5-(6-aminopurin-9-yl)
-3,4-dihydroxy- oxolan-2-yl methoxy-hydroxy- phosphoryl oxyphosphonic acid. The Nobel Laureates are the men who worked out how ATP synthase makes ATP using ADP as a substrate. Alivia Day was the first person to get the right answers.

---

It's All About Giving

 
Have you seen the ads on television? The stores want to convince you that the Christmas spirit is all about giving. Of course they do. And it's not just any sort of "giving" that counts; it only counts if it's expensive and new and you can put it under the tree in a pretty box. The more "giving" you do, the better it will be for Wal*Mart and Sears.


How many of you are "trapped" into buying presents for people who don't really need them? How many of you are only "giving" because you know you're going to "get" and you would feel guilty if you didn't reciprocate? Why not tell people that next year you don't need to exchange gifts in order to demonstrate your friendship?

One or two presents for close family members—more for young children—that's all we need for Chritsmas.

---

[Hat Tip: PZ Myers The atheist marketing failure]

Sandwalk 2007

 
John Lynch of Stranger Fruit started a trend last year when he posted the first sentence of the first blog of each month for the entire year. He's done it again this year [My year in blogging. I couldn't do it last year for obvious reasons so here's my summary for 2007.

• January: Brits Losing After American Invasion: According to recent reports red squirrels in Britain are facing extinction.


• February: Another Canuck Blogger There's a really good blog called Primordial Blog. As far as I can tell the author (Brian) lives in the Yukon—that's part of Canada (barely) so he must be Canadian.


• March: Evolution Is a Fact DaveScot over at Uncommon Descent writes in "Theory of Evolution as well tested as…"


• April: Public Scientific Debates Sean Carrol has posted an article about pubic debates over the validity of string theory [String Theory is Losing the Public Debate].


• May: My Six Months Are Up! I started Sandwalk six months ago. The goal was to give it six months to see how things worked out.


• June: Matthew Nisbet and Chris Mooney Video on Framing Science Chris Mooney has challenged me to respond to a video (see below the fold) of a talk that he and Matt Nisbet gave on framing. Over on his blog, Chris criticizes PZ Myers who couldn't sit through the whole hour [PZ, You Can Do Better Than This....]. Neither could I, but at least I got to the 50 minute mark which was more than twice as far as PZ.


• July: Visible Mutations and Evolution by Natural Selection A recent posting [Darwin Still Rules, but Some Biologists Dream of a Paradigm Shift] raised the issue of adaptationism. The controversy is over the main mechanism of genetic change in evolving populations.


• August: Heme Groups Monday's Molecule #37 is the heme group found in myoglobin and hemoglobin.


• September: Theories of Speciation In order to understand real evolution you have to understand speciation. This fact usually comes as a great surprise to adaptationists who tend not to think of such things.


• October: Do You Think Iran Will Get the Messsage? Here's a scary report from the New York Daily News [ Bush eyes 'surgical' strikes vs. Iran, sez mag].


• November: Can You Smell Isovaleric Acid? Isovaleric acid [3-Methylbutanoic acid] smells like sweat. It is responsible for some of the odor in a locker room, for example.


• December: Seymour Benzer (1921 - 2007) Seymour Benzer died last Friday. In the 1950's and 1960's Benzer was a prominent member of the 'phage group founded by Max Delbrück and Salvador Luria [The Nobel Prize in Physiology or Medicine 1969.].

---

Sharon Moalem Exposed

 
The Unexamined Life is a blog written by a student in one of the Life Sciences Programs here at the University of Toronto.

This student was curious about the strange behavior of "Dr." Sharon Moalem when confronted with scientific errors on Dr. Sharon's Blog. So our student did some digging and posted the results [Sharon Moalem, "medical maverick"].

It turns out that Dr. Sharon isn't a medical doctor—he has a Ph.D. and he's currently a 33 year old finishing his medical degree in New York. While it's perfectly legitimate to call yourself Dr. Sharon if you have a Ph.D., it seems very clear that "Dr." Sharon is strongly implying that he is a medical doctor on his blog and on the cover of his book.

It also turns out that "Dr." Sharon has found God. He now thinks that science is a way of revealing God. (Sharon Moalem is an Orthodox Jew.) The fact that he is a true believer probably explains his unethical behavior since it is typical of believers to censure contrary opinions on their blogs, demonstrate a lack of knowledge about science, and misrepresent their credentials.

UPDATE: "Dr." Sharon doesn't stop at refusing to post critical comments and editing his original postings to remove uncomfortable links. Now our favorite undergraduate blogger has documented him editing comments! [Sharon Moalem, self-destructing before our eyes] He's becoming more and more like a creationist.

UPDATE: PZ Myers has posted a short review of Survival of the Silliest. He doesn't like it. What a surprise! :-)

---

Gene Genie #22

 
This is the 22nd edition of Gene Genie and the second time it has been hosted on Sandwalk. The beautiful logo was created by Ricardo at My Biotech Life.

The purpose of this carnival is to highlight the genetics of one particular species, Homo sapiens. All of the accepted submissions concern humans. Quite often this means looking at how our genes influence our behavior and many of this week's submissions certainly fit that category.

Tali Shapiro at Helium - Where Knowledge Rules asks whether biology or environment have the stronger influence on gender identity. The posting discusses an usual, and ultimately tragic, case of gender switching [Size
Matters].

Is love in your genes? That's the question Christian Bachmann of Med Journal Watch asks [Love is in the genes when it comes to style].

It's not only love that's in your genes. There's more and more evidence linking all sorts of altruistic behavior to certain genes. Razib posts on the main Gene Exprsssion website. The candidate gene in this case is AVPR1a a polymorphism tied to variation in altruism.

Over on Living the Scientific Life GrrlScientist took note of the fact that a personalized genetics company published a claim that Jim Watson's genome was 1/16th African [Ebony, Meet Irony]. This result has been questioned on other blogs. For example, John Hawks of john hawks weblog wonders if it's a good idea for a private company to engage in this sort of cheap shot [Will the Watson "gotcha" moment bring down public genomics?].

Were you breastfed? Are you smart? Did you know that there might be a correlation between being breastfed as an infant and your IQ as an adult? Caroline Wright of phgfoundation discusses a recent paper on this subject [Correlation between IQ and breastfeeding moderated by genetics].

The confusion about the relative influence of genes and environment has a semantic component. Coturnix at A Blog Around the Clock asks Has the word "gene" outlived its usefulness?.

Did you know that your response to social stress might be determined by a single nucleotide change in your BDNF gene? Check out what John Fossella has to say in rs6265 (A) is my bodyguard. John runs the blog Biomarker driven mental health 2.0, which is dedicated to supporting consumer-driven personalized medicine.

Meanhwhile, the interest in personalized genetic testing prompted a CBC television show about [The DNA Genealogy Scam], which I blogged about on Sandwalk]. Later on I wondered whether science bloggers shouldn't be more cautious about promoting private testing services [23andMe - More Hype from Genetic Testing Services].

George Church is also a bit skeptical about some aspects of personalized genomics [George Church on Personal Genomics]. The posting is on Epidemix.

Bertalan Meskó weighs in with an opinion on ScienceRoll [Personalized Genetics: Back to the Personal Genome Project ].

Maybe we should all be worried since You Can Now Buy a Genetic Test at Rite-Aid.

One of the problems with personalized genetic testing is that it might reveal something you don't want to know. Matt Mealiffe of DNA and You asks Who's your daddy?.

What if you learn that you have a pre-disposition to cancer, or something worse? Does the information from one of these genetic testing companies prompt life altering changes? PredictER Blog wonders whether people really take these tests seriously [To Blog or To Jog? Genetic Tests and "Life-Changing" Decisions].

DNA direct is a genetic testing and educational services company. It has a blog called DNA Direct Talk and they've submitted an article that addresses the competition between their company and the new companies that have just started up [Opinions on 23andMe, deCODEme, Navigenics: Personal Genomics Services]. The posting was written by Lisa E. Lee, director of content at DNA Direct,

If you are interested in submitting a DNA sample to one of these companies then Hsien-Hsien Lei (Eye on DNA) has some advice for you [How to Prepare Yourself for a Genetic Test].

Gene therapy is when patients with genetic problems are cured by inserting a good copy of the defective gene. There have been several successes, but also some failures. Shelley Batts discusses one of the failures, noting that Gene Therapy Patient Wasn't Killed By the Therapy. Shelley blogs at Retrospectacle.

Speaking of gene therapy, can anything be done about hereditary blindness? Ruth has the story on The Biotech Weblog. She reports on clinical trials that are currently underway [Gene therapy for Hereditary Blindness on Phase I Clinical Trials].

Over on Gene Expression Razib brings up the OAC2 gene, once again. The question is how much do alleles of this gene contribute to eye color and skin color? [OCA2, blue eyes and skin color].

The sickle cell allele of the &beta:-globin gene is another favorite that's been discussed many times in Gene Genie submissions. The latest contribution is by Yann Klimentidis over on Yann Klimentidis' Weblog. The question is when was the sickle cell allele introduced into East Africa? [The sickle cell gene's recent introgression into East Africa]

BRCA1 is another popular gene. Mutations in this gene have been linked to many cancers but the biochemistry hasn't been worked out in most cases. A posting on Genetics & Health looks at one of the latest studies [50% BRCA 1 genes have PTEN mutations]. Elaine Warburton posted the summary.

Steve Murphy has a rather graphic description of Toxic epidermal necrolysis (TEN). This disease may be associated with alleles at the HLA locus and this raises questions about the results of genetic tests [Toxic Epidermal Necrolysis and Pharmacogenomics]. The article is on Gene Sherpas, another blog devoted to personalized genetics.

How many diseases can be cured by gene therapy? In order to answer that question you have to know how many genes we have. Most of you know that the number of known genes in our genome has been dropping steadily since the first drafts of the sequence were published. But do you know how far they've dropped? Keith Robison does and he's posted an article about it on OMICS! OMICS!. You might be surprised to hear what the latest number is [The Incredible Shrinking Human Genome].

Other heath-related articles look at the influence of infection and environment on human health. For example, FitBuff.com asks What is MRSA? Symptoms and Prevention. I hope I won't be giving too much away if I reveal that MSA is methicillin-resistant Staphylococcus aureus.

Some of us are interested in human evolution and that's fair game on Gene Genie. Greg Laden at Greg Laden's Blog discusses the results in a recent PLoS Genetics paper in Origin of Native America. These latest results suggest a single migration at some indeterminate date that's likely to be more than 10,000 years ago. You can bet this isn't the end of the controversy. Read Greg's summary and comments.

A recent paper in PNAS has stimulated a lot of blogging. Greg Laden submits his view of the peper at [Study Suggests Increased Rate of Human Adaptive Evolution]. My own submissions began with questions about the study at [Are Humans Evolving Faster?] and [Accelerated Human Evolution] and continued with more questions that provoked a discussion with the primary author of the study (John Hawks, see comments) [Is Evolution Linked to Environmental Change?]

The next edition of Gene Genie will be published at ScienceRoll. You can submit articles at Blog Carnival: Gene Genie.

---

Granville Sewell Needs My Help

 
Over on Uncommon Descent, one of the IDiots (Granville Sewell) confesses his ignorance and asks for help [Jean Rostand on Evolution].

It is becoming harder and harder to find Darwinists willing to make a serious attempt to defend their theory, and explain how it could account for the complexity of life, they are almost entirely in attack mode. Their three main arguments are 1) ID is not science 2) ID is not science and 3) ID is not science. I believe ID is science, but I can understand the concern many have about it being taught in science classrooms, so I would like to propose a compromise. How about we simply "have the courage to recognise that we know nothing of the mechanism" of evolution, and leave it at that? Each student can decide for himself/herself what the most likely explanation might be.

Maybe I can help. I'm not a Darwinist but I do know a thing or two about the important mechanisms of evolution.

In natural selection the frequency of an allele increases in the population because the presence of the allele confers a selective advantage on the individual who carries it. This individual will survive and reproduce more frequently than individuals possessing the other allele of the gene in question. Over many generations the beneficial allele has a higher than normal probability of becoming fixed in the population

In random genetic drift an allele will increase in frequency due to chance alone and not because it confers a selective benefit. In most cases the allele will be nearly neutral with respect to its phenotype. Over a long period of time, these non-selected alleles will become fixed relative to other similar alleles in the genome.

There are many other things that you need to learn about evolution, Granville, but these two important concepts will do for now. Good descriptions of these mechanisms are easy to find on the internet. I'm surprised that you've never heard of them before. I guess that's why you're an IDiot.

---

Merry Christmas from the Turtle Creek Chorale

 
The Turtle Creek Chorale is a men's choir based in Dalls, Texas (USA). Their mission, among other things, is: "Celebrating a positive image of the gay community and partnering with artists and organizations that share our values and mission."

Here's how they celebrate by singing their own special version of the Hallelujah Chorus, from Handel's Messiah. I wish we could have taken our children to see this version instead of the ordinary version.

---