There's no Tim Horton's. 
One of the most popular exhibits was the Leica booth. They set up a number of their most popular microscopes including the one shown in the photo. People gathered around drooling.
One of the big events for ASBMB is the Herbert Tabor JBC lecture. It was held Saturday night in one of the large ballrooms. There were about one thousand people attending.
Hunter is trying to find out how many different proteins kinases there are in humans. The latest count suggests about 900 different enzymes. This is a remarkable number when you think about it. It means that 3-4% of all genes in our genome are kinases.
Name this molecule. We need the exact name, preferably the correct one.
Poster sessions and exhibits are a big part of any scientific meeting but at big meetings such as this one the number of posters and the number of exhibitors is so huge that they can only be accommodated in a very large convention center. The photos show the main exhibit hall in the process of being set up for posters and exhibits and what it looks like when people start viewing the posters and visiting the exhibits.
There's so much going on at the Experimental Biology meeting you just can't hope to see everything. You have to be ruthless in making decisions about what to attend and what to skip. Sometimes there are important talks going on at the same time and you just can't decide. 
The Washington Convention Center is a wonderful facility. It covers four city blocks in downtown Washington just north of Massachusetts Ave. between 7th and 9th. It's about a fifteen minute walk due north of the Capitol where the Congress is housed. The neighborhoods on the South, North, East, and West sides of the building are good examples of the diversity of a typical American city.
My society has a long history of sponsoring undergraduate research and inviting undergraduates to present their work in a poster session at this meeting. I look forward to seeing these posters and meeting some of the undergraduates who did the work.
This was an impressive group of students. I had serious science discussions with about a dozen presenters. I don't think I could identify the winner because some of the topics were way outside my areas of knowledge but here are two posters that I liked very much.
Amit reasoned that the release factor had to shift from the compact form in solution to the extended form when it attached to ribosomes. He also reasoned that if he could block that shift the release factor would not work.
Beccy Joscwitz used the split ubiquitin yeast two hybrid system to look for proteins that interacted with a membrane protein in yeast [see Technology reveals 'lock and key' proteins behind diseases]. She's a very impressive student and seems to be right on top of the work. She knew most of the problems and she also knew when to ask questions. I think the judges were very impressed.
There are six societies at this meeting: American Association of Anatomists; The American Physiological Society, American Society for Biochemistry and Molecular Biology,American Society for Investigative Pathology; American Society for Nutrition; and American Society fpr Pharmacology and Experimental Therapeutics. The slogan for the conference is "Today's Research: Tomorrow's Health." 
Tam's Asian cuisine. There was nobody at the Center Plate—the station with the "healthiest" choices. Everyone was buying General Tso's Chicken .... mmmmmmm, good. Lots of calories. Lots of fat.
The Experimental Biology meetings are huge. There are thousand of people attending and one of the major road blocks at such meetings is getting registered and collecting all the material you need. It's a good idea to arrive early to avoid the rush and that's just what I did this morning. 
The program is 560 pages. I haven't read it yet. The abstract books contain short, one-paragraph, summaries of all the talks and posters. There are 1444 pages of abstracts and each one has four or five abstracts. The print is very small. I haven't read them all yet.
High school students who are taught creationism instead of evolutionary theory lack the critical thinking skills that are necessary for college, according to Stanford President Emeritus Donald Kennedy.That sounds like something sensible although I'm not sure the correlation is a cause and effect relationship. Perhaps the lack of critical thinking skills and the teaching of creationism have a deeper cause?
Kennedy is currently serving as an expert witness for the University of California Regents, who are being sued by a group of Christian schools, students and parents for refusing to allow high school courses taught with creationist textbooks to fulfill the laboratory science requirement for UC admission. After reading several creationist biology texts, Kennedy said he found "few instances in which students are being introduced to science as a process—that is, the way in which scientists work or carry out experiments, or the way in which they analyze and interpret the results of their investigations."I don't see why a college or university should be obliged to accept a creationist biology course as a legitimate science course.
Kennedy said that the textbooks use "ridicule and inappropriately drawn metaphors" concerning evolution to discourage students from formulating independent opinions. "Even with respect to the hypothesis that dominates them—namely, that biological complexity and organic diversity are the result of special creation—critical thinking is absent," he added.
Monday's Molecule was Flavin Adenine Dinucleotide or FAD [Monday's Molecule #23]. The flavin moiety is the three ring structure at the top of the figure. It's attached to a sugar called ribitol drawn in an open chain conformation. The ribitol, in turn, is attached to a single phosphate group at the other end.
FMN and FAD are required for important reactions in all species. They are made from riboflavin (right). Riboflavin can be synthesized in bacteria, protists, fungi, plants and some animals but mammals have lost the ability to make it. Instead, we have to obtain riboflavin from our food and that's why it's a vitamin in humans (vitamin B2). (It's not a "vitamin" in other species since they can make it themselves.)
Everything we publish is freely available online throughout the world, for you to read, download, copy, distribute, and use (with attribution) any way you wish. No permission required.If large corporations like John Wiley & Sons are going to threaten to sick lawyers on bloggers like Shelley then we'll just have to ignore everything that's published in their journals. That's what I'm going to do from now on.
Tangled Bank #78 has been posted at About: Archaeology. There's a brief list of articles on the framing debate in case anyone hasn't had enough. Don't be turned off. There's lot of good stuff as well. In addition, there's a link to one of my articles but y'all have read that already.
There are three basic ways to regulate the activity of an enzyme. The cell can control the synthesis of the enzyme by regulating the expression of the gene; the enzyme activity can be modified by binding small effector molecules that alter the structure of the enzyme (allosteric regulation); or the activity can be changed by covalent modification. 
Knoechel, T.R., Tucker, A.D., Robinson, C.M., Phillips, C., Taylor, W., Bungay, P.J., Kasten, S.A., Roche, T.E., and Brown, D.G. (2006) Regulatory roles of the N-terminal domain based on crystal structures of human pyruvate dehydrogenase kinase 2 containing physiological and synthetic ligands. Biochemistry 45:402-15. [doi: 10.1021/bi051402s]
As Francis Collins, head of the project which mapped the human genome, has written of DNA sequence similarities, “This evidence alone does not, of course, prove a common ancestor” because an intelligent cause can reuse successful design principles. We know this because we are intelligent agents ourselves, and we do this all the time. We take instructions we have written for one thing and use them for another. The similarity is not the result of a blind mechanism but rather the result of our intelligent activity.This is an old argument. It ignores the fact that sequence similarities match the phylogenies determined independently from comparative morphology and the fossil record. This is the "twin nested hierachies" evidence for evolution and it's powerful evidence indeed. Furthermore, it ignores the fact that the differences in sequences correspond closely to what we expect from evolution by random genetic drift.
Some design proponents think the evidence for common ancestry is good (e.g., Michael Behe), while others—citing the fossil record, especially The Cambrian Explosion—do not. But neither group thinks that sequence similarity alone proves either common ancestry or the Darwinian mechanism, as so many science writers of our day seem eager to assume.I congratulate Logan Gage for acknowledging that there are disagreements within the Intelligent Design Creationist camp. That's not something we see very often. However, I think he may be distorting Behe's position a little bit. Perhaps he means to place all the emphasis on "similarity alone" but that seems to be a quibble. Here's what Behe says in Darwin's Black Box on pages 175-177. Judge for yourself whether Behe thinks sequence analysis provides strong support for common descent.
When methods were developed in the 1950s to determine the sequences of proteins, it became possible to compare the sequence of one protein with another. A question that was immediately asked was whether analogous proteins in different species, like human hemoglobin and horse hemoglobin, had the same amino acid sequence. [The question was asked because it was a prediction of evolution-LAM]. The answer was intriguing: horse and human hemoglobins were very similar but not identical. Their amino acids were the same in 129 out of 146 positions in one of the protein chains of hemoglobin, but different in the remaining positions. When the sequences of the hemoglobins of monkey, chicken, frog, and others became available, their sequences could be compared with human hemoglobin and with each other. Monkey hemoglobin had 5 differences with that of humans; chickens had 26 differences; and frogs had 46 differences. These similarities were highly suggestive. Many researchers concluded that similar sequences strongly supported descent from a common ancestor.The reason for bringing this up is to show that Behe accepts common descent and sequence similarity is strong evidence of common descent. It would be nice if the Intelligent Design Creationists acknowledged this and discussed the sum total of the evidence and not just the sound bite version of sequence similarity.
For the most part it was shown that analogous proteins from species that were already thought to be closely related (like man and chimp, or duck and chicken) were pretty similar in sequence, and proteins from species thought to be distantly related (such as skunk and skunk cabbage) were not that similar. In fact, for some proteins one could correlate the amount of sequence similarity with the estimated time since various species were thought to have last shared a common ancestor and the correlation was quite good. Emile Zuckerkandl and Linus Pauling then proposed the molecular clock theory, which says that the correlation is caused by proteins accumulating mutations over time. The molecular clock has been vigorously debated since it was proposed, and many issues surrounding it are still contended. Overall, however, it remains a viable possibility....
The three general topics of papers published in JME [the Journal of Molecular Evolution]—the origin of life, mathematical models of evolution, and sequence analysis—have included many intricate, difficult, and erudite studies. Does such valuable and interesting work contradict this book's message? Not at all. To say that Darwinian evolution cannot explain everything in nature is not to say that evolution, random mutation, and natural selection do not occur, they have been observed (at least in cases of microevolution) many different times. Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form? No one has ever explained in detailed, scientific fashion how mutation and natural selection could build the complex, intricate structures discussed in this book.
First, my apologies to anyone who's responded to Larry's comment. I deleted it, because I don't want him dirtying up my blog.I've decided not to read Mixing Memory any more. I'm thinking that Chris has gone off the rails and I don't want to be the one that tips him over the edge.
Next, Matt, I have nothing but contempt or the nouveau atheists (I use that phrase to convey their tackiness, in case that wasn't apparent). I have been saying as much for about 6 months now, and will continue to do so. I won't apologize for it, either. They deserve nothing but contempt. And it should be noted that contempt for a relatively small, privileged group does not entail contempt for anyone else (I do have contempt for other groups, of course, but most people on the planet I'm OK with) or a broad sense of superiority. Do I feel superior to them? Anyone who's read a few books would. Do I feel superior to everyone else? Certainly not.
Mike, atheists should respond by pointing out how insane that kind of talk is. They should note that saying a group is not really American, or doesn't matter, sounds more and more like, say, Nazi antisemitic rhetoric when it's used by people in power (and that includes people in the media, who are, obviously, in positions of power). Of course, one doesn't have to call all religious people stupid, and advocate for the eradication of religion (which, I should add, also sounds a lot like Nazi rhetoric) to do so. I have nothing against being mean by itself. I have something against being mean, stupid, and totalitarian (little "t").
Richard, my point is that, by and large, they aren't even being "rude" in the same way. Instead, what they're trying to do is force their narrow world view on the entire rest of the world (go read Moran and others' talk of ridding the world of superstition, by which they mean all religious beliefs, on their blogs), through aggression and violence. Granted, it's rhetorical aggression and violence, but it's still aggression and violence. And perhaps worst of all, it is rhetoric with no obligation to facts or truth. Perhaps a better name for the nouveau atheists would be "evangelical" or "proselytizer" atheists.
Name this molecule. It's related to last week's theme on pyruvate and pyruvate dehydrogenase.
I started a little controversy over on Greg Laden's blog when I responded to the umteenth claim that militant approaches to a debate never achieve anything [Larry Moran]. I said,Everyone keeps repeating this mantra as though it were the gospel truth. The historical evidence says otherwise. There are dozens of examples of things that used to be “militant” approaches that have become accepted standards today.PZ liked the suffragette idea and expanded on it [We Aim to Misbehave] and [Rude Ladies].
Here’s just one example. Do you realize that women used to march in the streets with placards demanding that they be allowed to vote? At the time the suffragettes were criticized for hurting the cause. Their radical stance was driving off the men who might have been sympathetic to women’s right to vote if only those women had stayed in their proper place.
Now I’m not saying that all militant approaches are going to win in the end. Far form it. Most of them are destined for the dustheap of history. What I am saying is that trying to shut down the “militants” on the grounds that they are counter-productive is not logical. It’s a way of “framing” the discussion to make it sound like your opposition to the militants has a scientific basis.
I see the Feminists For Life and their horrible project of trying to rewrite history so that suffrage-era feminists come across as pleasantly enamored of servitude is going well. It’s hard to generalize at all about suffragists, since, you know, the struggle went on for decades and incorporated thousands of women. One thing you can say with certainty is they were rude and offensive by definition, since for a woman to be proper, she had to accept second class citizenship uncomplainingly. But seriously, atheists aren’t even waving placards, much less holding hunger strikes, firebombing, or whipping some jujitsu on some cops.Please don't lose sight of the main point about the comparison between the women's suffrage movement and atheists like Dawkins, PZ, and me. We're not trying to justify our position by comparing it to that of the suffragettes (suffragists). All we're trying to do is destroy this silly myth that all social change came about by speaking softly and being nice to everyone. There are lots of examples where "militant" behavior triggered social change. It doesn't always justify "militant' behavior but if you're going to fight Dawkins then at least use sensible arguments.
More to the point, suffragists didn’t actually get very far until they did in fact start openly insulting men. Mere equality between men and women wasn’t considered reason enough to extend the franchise to women, but when the purity movement latched onto suffrage and started pushing the message that women were better than men, then things changed. Men were considered drunken, violent assholes who needed women’s civilizing hand to get them in shape. It was a sorry thing that it had to get to that point in order for women to get the vote, and hopefully the lesson has been learned for future reference.* Now, as PZ notes, the way different levels of oppression certainly demanded different reactions, so there’s no reason to fault the suffragists for any radical action they had to take in order to obtain justice. But it’s silly to think of them as sweet little old ladies who’d never hurt a fly. They put up with a lot of shit, from having vegetables pelted at them in public to having police arrest them in ways that maximized the violence and humiliation.
In this discussion with D.J. Grothe, Nisbet explores the issue of “framing science” in the public mind, how scientists may be failing at effectively communicating the importance of the implications of science for society, and steps the science community may take to more expertly sell their science to a disinterested public. He also argues about Richard Dawkins and his effect on the public appreciation of science, and the impact of linking atheism with science for issues such as stem-cell research, teaching evolution in the public schools, and global warming.Nisbet links to the podcast on his website [Podcast: More on Framing (and Dawkins)] where he says,
In this week's show, host DJ Grothe and I engage in a lively forty-five minute discussion. You can listen here.I take that to mean that Nisbet thinks he did a good job of explaining these things during the interview.
I offer more details on:
--> the nature of framing and media influence.
--> does framing mean false spin?
--> the likely negative impact of Dawkins.
--> communication strategy specific to the teaching of evolution in schools.
--> what the Discovery Institute understood about framing (also see this post.)
--> the role of framing in the debates over climate change and stem cell research.
--> the use of "science navigators" in communication campaigns.
-->an effective means for engaging the broader American public on atheism.
The gene for E1α: is called PDHA1 and it's located on the X chromosome at p22.2-p22.1 [Entrez Gene = 5160]. There are more than three dozen alleles that give rise to symptoms ranging from mild lactic acidosis to developmental defects. The accumulation of lactate is due to the fact that it can't be converted to pyruvate because the defect in pyruvate dehydrogenase causes buildup of pyruvate in the cell [Pyruvate]. Males often die at an early age. (Note that males are homozygous for mutant alleles because the gene is on the X chromosome) [OMIM 300502]. Females are also affected because only one X chromosome is active and if it happens to be the one carrying the mutations the entire cell is affected [Calico Cats].
BCOADH is found in all species. It is the most "primitive" enzyme. Like PDC it has a complex structure with three different subunits. E1 catalyzes the decarboxylation reaction. E2 catalyzes the formation of acyl-CoA—it has the lipoamide swinging arm. E3 catalyzes the oxidation of the lipoamide and the reduction of NAD+.
Recall that the E2 subunits form the core of the complex (left). They contain the lipoamide swinging arm that carries substrate to three different active sites. The E3 subunits of the three enzymes are identical. There is only one E3 gene and it supplies the dihydrolipoamide dehydrogenase activity for BCOADH, PDC, and OADH.
Schreiner, M.E., Fiur, D., Holatko, J., Patek, M. and Eikmanns, B.J. (2005) E1 enzyme of the pyruvate dehydrogenase complex in Corynebacterium glutamicum: molecular analysis of the gene and phylogenetic aspects. J Bacteriol. 187:6005-18.
Schnarrenberger, C. and Martin, W.. (2002) Evolution of the enzymes of the citric acid cycle and the glyoxylate cycle of higher plants. A case study of endosymbiotic gene transfer. Eur J Biochem. 269:868-83.
Recall that the pyruvate dehydrogenase complex catalyzes the conversion of pyruvate to acetyl-CoA. This is an important reaction in all living cells because acetyl-CoA is required for fatty acid synthesis. The reaction is important in animals because acetyl-CoA enters the citric acid cycle where it is broken down to carbon dioxide and the energy is captured by the mitochondrial electron transport system in the form of ATP. This step isn't so important in most bacteria because they don't have a citric acid cycle. Most species can also save the two carbon atoms of the acetyl group in acetyl-CoA and use them to build carbohydrates such as glucose. Animals can't do this.
You would think that the pyruvate dehydrogenase complex (PDC) must be ubiquitous since it catalyzes such an important reaction. Not so. PDC is the only enzyme in eukaryotes but some bacteria have another enzyme that can make acetyl-CoA. As you might expect, the bacteria that gave rise to mitochondria do have a PDC that's related to the eukaryotic enzyme. This is because the genes were transferred from those bacteria to their eukaryotic hosts when the endosymbiotic event occurred about two billion years ago.
The structure of many ferredoxins have been solved. The one shown on the left is from Pseudomonas aeruginosa. It's a typical example (Giastas et al. 2006). The protein is quite small and most ferredoxins contain two iron-suflur (Fe-S) complexes. These are box-like structures formed from iron molecules (red) and sulfur molecules (yellow). They are bound to the protein through the sulfhydyl groups of the amino acid cysteine. Electrons are carried by the iron ions.Fe3+ + e- → Fe2+There's another important reason why PFOR is important in some bacteria. Look at the PDC reaction shown above. The arrow points in one direction indicating that this reaction is essentially irreversible. It can't be used to fix carbon dioxide by combining it with the acetyl group to make pyruvate. That's not true of the much simpler PFOR reaction. In fact, the reverse reaction is the main CO2 fixing reaction in many photosynthetic bacteria and in methanogens (bacteria that use methane as a carbon source).
Chabriere, E., Vernede, X., Guigliarelli, B., Charon, M.H., Hatchikian, E.C. and Fontecilla-Camps, J.C. (2001) Crystal structure of the free radical intermediate of pyruvate:ferredoxin oxidoreductase. Science 294:2559-63.
Garczarek, F., Dong, M., Typke, D., Witkowska, H.E., Hazen, T.C., Nogales, E., Biggin, M.D., and Glaeser, R.M..(2007) Octomeric pyruvate-ferredoxin oxidoreductase from Desulfovibrio vulgaris. J Struct Biol. 2007 Feb 17; [Epub ahead of print] .
Giastas, P., Pinotsis, N., Efthymiou, G., Wilmanns, M., Kyritsis, P., Moulis, J.M., and Mavridis, I.M..(2006) The structure of the 2[4Fe-4S] ferredoxin from Pseudomonas aeruginosa at 1.32-Å resolution: comparison with other high-resolution structures of ferredoxins and contributing structural features to reduction potential values. J. Biol. Inorg. Chem. 11:445-58.
An article in our local newspaper (The Toronto Star) suggests a link between the mass kill off of bees and cellular phones [Cellular phone uses linked to bee deaths]. A similar report appeared in The Independent in the UK [ Are mobile phones wiping out our bees?].Weatherall, a retired Toronto police officer who was forced out of his Woodstock, Ont., home after high levels of radio waves from nearby hydro-electric poles and cellphone towers made him electro-hypersensitive, is better able than most to understand the German study, which shows that bees refuse to return to their hive when cellphones are placed nearby.Near the end of the story in the Toronto Star the reporter also checks with Ernesto Guzman, an expert on bees at the University of Guelph in Ontarion, Canada. Guelph is one of the top schools in veterinary medicine and agriculture.
Despite the new German research, bee researchers remain skeptical of the impact of radio waves on bees. They claim it is just one of several theories that include global warming and genetically modified crops.Personally, I will take Guzman's word over that of a retired police officer suffering from "electro-sensitivity." If I were writing the headline it would be "Cellphone link to bee deaths discredited by expert." I guess it all depends on how you want to
"All of these are speculation. They deserve to be investigated. They are good hypotheses, some of them. Others are out of reality, in my opinion," said Ernesto Guzman, associate professor with the University of Guelph's department of environmental biology.
Guzman, a specialist in bee research, says he believes stress is the major factor in the situation south of the border while in Canada a combination of poor weather on fall food supply levels and an influx of mites is the likely cause.
That's a thought, but I think the answer is much simpler: PZ and Larry Moran are not primarily interested in promoting science.It's not a simple as that Chad. I try to do both things. I try to write about science with the hope that I'm telling people something they don't know. If you would take the time to look at my blog I think you might see the occasional posting on science-related topics. Religion isn't mentioned.
"That's crazy," you say. But here it is from the horse's mouth, Larry Moran in Chris Mooney's comments:I think religion is the problem and I'll continue to make the case against religion and superstition. One of the many ways where you and Nisbet go wrong is to assume that people like PZ, Dawkins, and me are primarily fighting for evolution. That's why you argue that in the fight to save evolution it's "wrong" (e.g., not part of your frame) to attack religion.That's the beginning and end of the problem. The entire problem with "framing" is that Nisbet and Mooney are looking for the best way to promote science, while PZ and Larry are looking for the best way to smash religion. The goals are not the same, and the appropriate methods are not the same-- in particular, Nisbet and Mooney argue that the best way to promote science would be to show a little tact when dealing with religious people, and that runs directly counter to the real goals of PZ and Larry.
When are you going to realize that our primary goal in many cases is to combat the worst faults of religion? Asking us to stop criticizing religion is like asking us to give up fighting for something we really care about. That's not "framing," it's surrender.
John Logsdon over at Sex, Genes, and Evolution recommends a new book, The Origins of Genome Architecture by Michael Lynch. John also points us to a review article by Lynch [The Origins of Eukaryotic Gene Structure]. I second both recommendations. Read the article. Buy the book.Despite the enormous progress in molecular genetics over the past 50 years, no general theory for the evolution of the basic architectural features of genes has been formulated. Many attempts have been made to explain the features of genes, genomes, and genetic networks in the context of putatively adaptive cellular and/or developmental features, but few of these efforts have been accompanied by a formal evolutionary analysis. Because evolution is a population-level process, any theory for the origins of the genetic machinery must ultimately be consistent with basic population-genetic mechanisms. However, because natural selection is just one of several forces contributing to the evolutionary process, an uncritical reliance on adaptive Darwinian mechanisms to explain all aspects of organismal diversity is not greatly different than invoking an intelligent designer.Some of you will probably see why I like this guy! He warns against "uncritical reliance on adaptive Darwinian mechanisms."
This paper represents a first step toward the formal development of a general theory for the evolution of the gene that incorporates the universal properties of random genetic drift and mutation pressure. Although the ideas presented are unlikely to be correct in every detail, at a minimum they serve as a null model. For if verbal adaptive arguments are to provide confident explanations for any aspect of gene or genomic structure, something must be known about patterns expected in the absence of selection. This is a significant challenge because at this point it is difficult to reject the hypothesis that the basic embellishments of the eukaryotic gene originated largely as a consequence of nonadaptive processes operating contrary to the expected direction of natural selection. A significant area of future research will be to take these observations on gene and genome complexity to the next level, to evaluate whether natural selection is a necessary and/or sufficient force to explain the evolution of the cellular and developmental complexities of eukaryotes.Everyone needs to start paying attention. Random genetic drift is just as important for evolution as natural selection. That's not speculation. As far as I'm concerned, it's hard incontrovertible fact.
