Thursday, April 09, 2009
Twisted Tree of Life Award #3
Jonathan Eisen at The Tree of Life has just awarded his third Twisted Tree of Life Award. And well-deserved it is.
New Breakthrough in Evolution Theory
Imagine a culture of yeast cells growing in a medium where sucrose is the only carbon source. Sucrose isn't the preferred carbon source for yeast but yeast can handle it if need be. Cells secrete an enzyme called invertase that breaks down sucrose to glucose and fructose
The products of the reaction, glucose and fructose, can be taken up by the cell or they may diffuse away before being taken up. Molecules produced by the invertase from one cell can be absorbed by a neighboring cell.
As the concentration of free glucose and fructose rises in the medium, cells that lack the ability to synthesize and secrete invertase may survive. Thus invertase negative mutants may accumulate because they don't need to make their own invertase in order to have a source of carbon. In game theory, such mutants are called "cheaters."
Hands up, all you people who think that the existence of a stable equilibrium of cheaters and cooperators is a new discovery in evolutionary theory.
Right, it's not.
The editors of Nature think it is, so they published the paper from the Dept. of Physics at MIT (Gore et al., 2009).
The MIT PR department thought it was revolutionary enough to warrant a press release that was picked up by ScienceDaily [Cooperative Behavior Meshes With Evolutionary Theory].
One of the perplexing questions raised by evolutionary theory is how cooperative behavior, which benefits other members of a species at a cost to the individual, came to exist.
Cooperative behavior has puzzled biologists because if only the fittest survive, genes for a behavior that benefits everybody in a population should not last and cooperative behavior should die out, says Jeff Gore, a Pappalardo postdoctoral fellow in MIT's Department of Physics.
Gore is part of a team of MIT researchers that has used game theory to understand one solution yeast use to get around this problem. The team's findings, published in the April 6 online edition of Nature, indicate that if an individual can benefit even slightly by cooperating, it can survive even when surrounded by individuals that don't cooperate.
In short, the study offers a concrete example of how cooperative behaviors can be compatible with evolutionary theory.
I agree that this is an interesting example but I don't think the public is well served by presenting it as a new contribution to evolutionary theory. The public is entitled to think that evolutionary biologists must be really stupid if they've never thought of this before. They (the public) would be really confused if they happened to read the Wikipedia entry on John Maynard Smith (1920 - 2004).
There are no references to Maynard Smith's work in the citations at the end of the Nature paper, although there is a reference to "Smith, J.M." who wrote the book Evolution and the Theory of Games.
Gore, J., Youk, H., and van Oudenaarden A. (2009) Snowdrift game dynamics and facultative cheating in yeast. Nature advance online publication 6 April 2009. [DOI: doi:10.1038/nature07921]
Wednesday, April 08, 2009
What Stephen Harper Said in 1997
I don't know where Canadian Cynic gets all this stuff but he has just posted a link to a speech by Stephen Harper in 1997 [CTV.ca]. It's worth reading the entire speech if you can stomach it. If you can't, then try this little excerpt.
OTTAWA -- The text from a speech made by Stephen Harper, then vice-president of the National Citizens Coalition, to a June 1997 Montreal meeting of the Council for National Policy, a right-wing U.S. think tank, and taken from the council's website:
Ladies and gentlemen, let me begin by giving you a big welcome to Canada. Let's start up with a compliment. You're here from the second greatest nation on earth. But seriously, your country, and particularly your conservative movement, is a light and an inspiration to people in this country and across the world.
Now, having given you a compliment, let me also give you an insult. I was asked to speak about Canadian politics. It may not be true, but it's legendary that if you're like all Americans, you know almost nothing except for your own country. Which makes you probably knowledgeable about one more country than most Canadians.
But in any case, my speech will make that assumption. I'll talk fairly basic stuff. If it seems pedestrian to some of you who do know a lot about Canada, I apologize.
I'm going to look at three things. First of all, just some basic facts about Canada that are relevant to my talk, facts about the country and its political system, its civics. Second, I want to take a look at the party system that's developed in Canada from a conventional left/right, or liberal/conservative perspective. The third thing I'm going to do is look at the political system again, because it can't be looked at in this country simply from the conventional perspective.
First, facts about Canada. Canada is a Northern European welfare state in the worst sense of the term, and very proud of it. Canadians make no connection between the fact that they are a Northern European welfare state and the fact that we have very low economic growth, a standard of living substantially lower than yours, a massive brain drain of young professionals to your country, and double the unemployment rate of the United States.
In terms of the unemployed, of which we have over a million-and-a-half, don't feel particularly bad for many of these people. They don't feel bad about it themselves, as long as they're receiving generous social assistance and unemployment insurance.
2009 Canada Gairdner Awards
The 2009 Canada Gairdner Award recipients were announced last week. Each awardee gets $100,000 (CDN). The winners are ...
Richard Losick: "for the discovery of mechanisms that define cell polarity and asymmetric cell division, processes key in cell differentiation and in the generation of cell diversity"
Kazutoshi Mori: "for the dissection and elucidation of a key pathway in the unfolded protein response which regulates protein folding in the cell"
Nubia Muñoz: "for her epidemiological studies that defined the essential role of the human papilloma virus in the etiology of cervical cancer on a global level which led to the development of successful prophylactic vaccines"
David Sackett: "for his leadership in the fields of clinical epidemiology and evidence-based medicine, which have had major impacts internationally in applied clinical research and in the practice of medicine"
Lucy Shapiro: "for the discovery of mechanisms that define cell polarity and asymmetric cell division, processes key in cell differentiation and in the generation of cell diversity"
Peter Walter: "for the dissection and elucidation of a key pathway in the unfolded protein response which regulates protein folding in the cell"
Shinya Yamanaka: "for his demonstration that the key transcription factors which specify pluripotency may become reprogrammed somatic cells to pluripotent stem cells"
The awards will be presented next October at the University of Toronto. Since this is the 50th anniversary of the Gairdner Awards there will be quite a gathering. You should plan on being here.
This year The Gairdner Foundation is celebrating its 50th Anniversary in spectacular fashion.
Between March and November we will hold 7 major international symposia across the country, in Vancouver, Edmonton, Ottawa, Toronto (York), Sherbrooke, Montreal and Halifax (see under Events). The finale will occur in Toronto, where we will host 50 past Gairdner recipients, including 22 Nobel Laureates, from Oct 28-30. This will be by far the largest gathering of the world's top scientists ever held in Canada. We will also introduce the 2009 Canada Gairdner Award recipients.
Canada Gairdner Laureates will participate in lectures, panel discussions, public forums, interviews and informal talks with academics, researchers, biotech and pharma companies, government leaders, graduate and postgraduate students, high school students, the media and interested members of the general public. With the exception of the social events, all the programs will be free and open to anyone who wants to share in the excitement of leading edge biomedical science.
The 50th Anniversary will be a spectacular culmination of everything The Gairdner Foundation has achieved in becoming Canada's premier international prize, and one of the top three biomedical prizes in the world. It will be a vehicle to raise awareness of the fascinating world of biomedical science and its importance to lives.
Nobel Laureates: Mario Capecchi, Martin Evans, and Oliver Smithies
The Nobel Prize in Physiology or Medicine 2007
"for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells"
Mario R. Capecchi (1937 - ), Sir Martin J. Evans (1941 - ), and Oliver Smithies (1925 - ) won the Noble Prize in 2007 for developing techniques to transform embryonic stem cells with foreign genes integrated at a specific place in the genome, then using those cells to make transgenic mice. The Press Release describing this work is a well-written description of how the techniques was developed.
This is how to make knock-out mice.
THEME:
Nobel Laureates
Summary
This year's Nobel Laureates have made a series of ground-breaking discoveries concerning embryonic stem cells and DNA recombination in mammals. Their discoveries led to the creation of an immensely powerful technology referred to as gene targeting in mice. It is now being applied to virtually all areas of biomedicine – from basic research to the development of new therapies.
Gene targeting is often used to inactivate single genes. Such gene "knockout" experiments have elucidated the roles of numerous genes in embryonic development, adult physiology, aging and disease. To date, more than ten thousand mouse genes (approximately half of the genes in the mammalian genome) have been knocked out. Ongoing international efforts will make "knockout mice" for all genes available within the near future.
With gene targeting it is now possible to produce almost any type of DNA modification in the mouse genome, allowing scientists to establish the roles of individual genes in health and disease. Gene targeting has already produced more than five hundred different mouse models of human disorders, including cardiovascular and neuro-degenerative diseases, diabetes and cancer.
Modification of genes by homologous recombination
Information about the development and function of our bodies throughout life is carried within the DNA. Our DNA is packaged in chromosomes, which occur in pairs – one inherited from the father and one from the mother. Exchange of DNA sequences within such chromosome pairs increases genetic variation in the population and occurs by a process called homologous recombination. This process is conserved throughout evolution and was demonstrated in bacteria more than 50 years ago by the 1958 Nobel Laureate Joshua Lederberg.
Mario Capecchi and Oliver Smithies both had the vision that homologous recombination could be used to specifically modify genes in mammalian cells and they worked consistently towards this goal.
Capecchi demonstrated that homologous recombination could take place between introduced DNA and the chromosomes in mammalian cells. He showed that defective genes could be repaired by homologous recombination with the incoming DNA. Smithies initially tried to repair mutated genes in human cells. He thought that certain inherited blood diseases could be treated by correcting the disease-causing mutations in bone marrow stem cells. In these attempts Smithies discovered that endogenous genes could be targeted irrespective of their activity. This suggested that all genes may be accessible to modification by homologous recombination.
Embryonic stem cells – vehicles to the mouse germ line
The cell types initially studied by Capecchi and Smithies could not be used to create gene-targeted animals. This required another type of cell, one which could give rise to germ cells. Only then could the DNA modifications be inherited.
Martin Evans had worked with mouse embryonal carcinoma (EC) cells, which although they came from tumors could give rise to almost any cell type. He had the vision to use EC cells as vehicles to introduce genetic material into the mouse germ line. His attempts were initially unsuccessful because EC cells carried abnormal chromosomes and could not therefore contribute to germ cell formation. Looking for alternatives Evans discovered that chromosomally normal cell cultures could be established directly from early mouse embryos. These cells are now referred to as embryonic stem (ES) cells.
The next step was to show that ES cells could contribute to the germ line (see Figure). Embryos from one mouse strain were injected with ES cells from another mouse strain. These mosaic embryos (i.e. composed of cells from both strains) were then carried to term by surrogate mothers. The mosaic offspring was subsequently mated, and the presence of ES cell-derived genes detected in the pups. These genes would now be inherited according to Mendel’s laws.
Evans now began to modify the ES cells genetically and for this purpose chose retroviruses, which integrate their genes into the chromosomes. He demonstrated transfer of such retroviral DNA from ES cells, through mosaic mice, into the mouse germ line. Evans had used the ES cells to generate mice that carried new genetic material.
Two ideas come together – homologous recombination in ES cells
By 1986 all the pieces were at hand to begin generating the first gene targeted ES cells. Capecchi and Smithies had demonstrated that genes could be targeted by homologous recombination in cultured cells, and Evans had contributed the necessary vehicle to the mouse germ line – the ES-cells. The next step was to combine the two.
For their initial experiments both Smithies and Capecchi chose a gene (hprt) that was easily identified. This gene is involved in a rare inherited human disease (Lesch-Nyhan syndrome). Capecchi refined the strategies for targeting genes and developed a new method (positive-negative selection, see Figure) that could be generally applied.
Birth of the knockout mouse – the beginning of a new era in genetics
The first reports in which homologous recombination in ES cells was used to generate gene-targeted mice were published in 1989. Since then, the number of reported knockout mouse strains has risen exponentially. Gene targeting has developed into a highly versatile technology. It is now possible to introduce mutations that can be activated at specific time points, or in specific cells or organs, both during development and in the adult animal.
Gene targeting is used to study health and disease
Almost every aspect of mammalian physiology can be studied by gene targeting. We have consequently witnessed an explosion of research activities applying the technology. Gene targeting has now been used by so many research groups and in so many contexts that it is impossible to make a brief summary of the results. Some of the later contributions of this year's Nobel Laureates are presented below.
Gene targeting has helped us understand the roles of many hundreds of genes in mammalian fetal development. Capecchis research has uncovered the roles of genes involved in mammalian organ development and in the establishment of the body plan. His work has shed light on the causes of several human inborn malformations.
Evans applied gene targeting to develop mouse models for human diseases. He developed several models for the inherited human disease cystic fibrosis and has used these models to study disease mechanisms and to test the effects of gene therapy.
Smithies also used gene targeting to develop mouse models for inherited diseases such as cystic fibrosis and the blood disease thalassemia. He has also developed numerous mouse models for common human diseases such as hypertension and atherosclerosis.
In summary, gene targeting in mice has pervaded all fields of biomedicine. Its impact on the understanding of gene function and its benefits to mankind will continue to increase over many years to come.
[Photo Credits: Mario Capecchi: Reuters,DayLife, Sir Martin J. Evans: Reuters, DayLife, Oliver Smithies: University of North Carolina, Chapel Hill.]
The images of the Nobel Prize medals are registered trademarks of the Nobel Foundation (© The Nobel Foundation). They are used here, with permission, for educational purposes only.
Tuesday, April 07, 2009
On the Evolution of Bacterial Chromosomes
This is a story about two cultures; the old biologists who grew up with the 'phage group and bacterial genetics, and the younger biologists who didn't.
It's also a story about science journalism and the reporting of science in the 21st century.
We've known about plasmids in bacteria for a very long time. Plasmids are small circular DNA molecules that carry a number of genes, such as those for antibiotic resistance, or sex. Some of them are present in multiple copies while others are present in only a single copy. In the case of single-copy plasmids, their replication is coupled to that of the chromosome and the daughter plasmids segregate to the daughter cells just like the newly replicated chromosomes do.
Genes can hop from chromosomes to plasmids and back again. This phenomenon was discovered in the 1950's by Jacob and Adelberg (1959). Several well-known plasmids carrying certain chromosomal genes were studied, including a famous one known as F-lac—an F plasmid containing the lac operon.
By the time the first E. coli Bible was published in 1987, there were dozens and dozens of examples of gene transfer between chromosomes and plasmids (Holloway and Low, 1987).
During the 1970s and 80s, the DNA contents of many difference species of bacteria were published. It soon became apparent that certain classes of bacteria (e.g. Rhizobiaceae) contained large plasmids called megaplasmids. Sometimes it was difficult to tell the difference between a plasmid and a chromosome (bacterial chromosomes are usually circular).
As a general rule, plasmids were dispensable. The bacteria could be "cured" of a plasmid and still survive. When the plasmid acquired essential genes, as they did from time to time, they became chromosomes. Some species of bacteria had two or more chromosomes. It was part of general knowledge that plasmids could evolve into chromosomes as described in a 1998 review by Moreno.
Animal intracellular Proteobacteria of the alpha subclass without plasmids and containing one or more chromosomes are phylogenetically entwined with opportunistic, plant-associated, chemoautotrophic and photosynthetic alpha Proteobacteria possessing one or more chromosomes and plasmids. Local variations in open environments, such as soil, water, manure, gut systems and the external surfaces of plants and animals, may have selected alpha Proteobacteria with extensive metabolic alternatives, broad genetic diversity, and more flexible and larger genomes with ability for horizontal gene flux. On the contrary, the constant and isolated animal cellular milieu selected heterotrophic alpha Proteobacteria with smaller genomes without plasmids and reduced genetic diversity as compared to their plant-associated and phototrophic relatives. The characteristics and genome sizes in the extant species suggest that a second chromosome could have evolved from megaplasmids which acquired housekeeping genes. Consequently, the genomes of the animal cell-associated Proteobacteria evolved through reductions of the larger genomes of chemoautotrophic ancestors and became rich in adenosine and thymidine, as compared to the genomes of their ancestors. Genome organisation and phylogenetic ancestor-descendent relationships between extant bacteria of closely related genera and within the same monophyletic genus and species suggest that some strains have undergone transition from two chromosomes to a single replicon. It is proposed that as long as the essential information is correctly expressed, the presence of one or more chromosomes within the same genus or species is the result of contingency. Genetic drift in clonal bacteria, such as animal cell-associated alpha Proteobacteria, would depend almost exclusively on mutation and internal genetic rearrangement processes. Alternatively, genomic variations in reticulate bacteria, such as many intestinal and plant cell-associated Proteobacteria, will depend not only on these processes, but also on their genetic interactions with other bacterial strains.Given this context, I was interested in a recent press release: Evolutionary origin of bacterial chromosomes revealed. "Hmmm," I thought., "I wonder what new mechanism has been discovered?"
Imagine my surprise to read ...
Most bacteria have only one chromosome. The Rhizobiaceae is an unusual bacterial family in that all of its members have either two chromosomes or one chromosome and very large plasmids. Until this study, it was not clear how such multichromosomal architectures had evolved.That's not new. The idea that large megaplasmids in Rhizobiaceae could become plasmids by acquiring essential genes has been around for three decades, at least. Surely these workers known their history? The press release must be an exaggeration of what's in the paper.
João Setubal, associate professor at the Virginia Bioinformatics Institute and the Department of Computer Science at Virginia Tech, commented: "Thanks to the efforts of the Agrobacterium Genome Sequence Consortium and the wider research community, we have sufficient sequence data available from different bacterial species to allow the inference of a general model for bacterial genome evolution. It appears that the transfer of genes from chromosomes to large plasmids mediates second chromosome formation."
So I looked up the paper (Slater et al., 2009). These workers sequenced the genomes of a number of related bacterial species containing chromosomes and plasmids. They announce the "surprising" discovery that genes can transfer between chromosomes and plasmids.
While it has long been known that gene transfer can occur between organisms, the picture that emerges from our study shows a group characterized by composite genomes in which genes of all classes are not only migrating between organisms, but also intracellularly among chromosomal and plasmid replicons.It sounds like they never heard of F-lac or any of the other F′ or R′ plasmids. It sounds like they are completely unaware to the fact that transfer of genes from chromosomes to plasmids is an old established fact.
The authors propose a "general model for bacterial genome evolution" in which plasmids evolve into chromosomes.
This is not an isolated phenomenon. There seem to be lots of cases where today's scientists are unaware of the history of their field. A consequence of this ignorance is that the wheel is being constantly reinvented, with all the associated hype of a modern breakthrough.
Another example is the recent "discovery" of regulatory RNAs. Bacterial and 'phage examples have been known for forty years.
Why is this happening? Why do reviewers let it pass?
[Image Credit: Jessica Snyder Sachs]
Holloway, B. and Low, K.B. (1987) F-Prime and R-Prome Factors. in Escherichia coli and Salmonella typhimurium: Cellular and Molecular Biology. F.C. Neidhardt ed. vol.2.
Jacob, F. and Adelberg, E.A. (1959) Transfer of Genetic Characters by Incorporation in the Sex Factor of Escherichia coli. Comptes Rendus 249:189-191.
Moreno, E. (1998) Genome evolution within the alpha Proteobacteria: why do some bacteria not possess plasmids and others exhibit more than one different chromosome? FEMS Microbiol 22(4):255-275. [PubMed]
Slater, S.C., Goldman, B.S., Goodner, B., Setubal, J.C., Farrand, S.K., Nester, E.W., Burr, T.J., Banta, L., Dickerman, A.W., Paulsen, I., Otten, L., Suen, G., Welch, R., Almeida, N.F., Arnold, F., Burton, O.T., Du, Z., Ewing, A., Godsy, E., Heisel, S., Houmiel, K.L., Jhaveri, J., Lu, J., Miller, N.M., Norton, S., Chen, Q., Phoolcharoen, W., Ohlin, V., Ondrusek, D., Pride, N., Stricklin, S.L., Sun, J., Wheeler, C,, Wilson, L,, Zhu, H., and Wood, D.W. (2009) Genome Sequences of Three Agrobacterium Biovars Help Elucidate the Evolution of Multi-Chromosome Genomes in Bacteria. J. Bacteriol. 2009 Feb 27. [Epub ahead of print] [PubMed] [DOI: 10.1128/JB.01779-08]
How to Prevent Evolution in Mosquitos
A paper in PLoS Biology discusses How to Make Evolution-Proof Insecticides for Malaria Control. The idea is to develop drugs that only kill mosquitoes after they've reproduced. That way the population can't evolve resistance to the drug.What's interesting about this paper is the response of two different bloggers. On adaptationist, Jerry Coyne's blog, guest writer Matthew Cobb thinks it's a great idea [Of mosquitoes and the menopause]. In fact he links his discussion of the paper to the well-known adaptationist explanation of menopause.
The pluralist, Ryan Gregory, is much more skeptical, pointing out that evolution is smarter than you are ["Evolution-proof"?].
Grab your popcorn and enjoy the fight. My money's on Gregory.
Monday's Molecule #116: Winners
UPDATE:The photographs of the mouse embryos are from a paper by Kothary et al. (1989). This was a study where a lacZ (β-galactosidase) gene under the control of a strong, ubiquitously competent promoter was introduced into mouse zygotes. When the gene was induced (right) the presence of β-galactosidase was detected by a blue color assay. The foreign gene is induced in almost every tissue.
These sorts of experiments in construction of transgenic mice were later extended by the work of Nobel Lauteates Mario Capecchi, Martin Evans, and Oliver Smithies who developed techniques for using embryonic stem cells.
Several people guessed the Nobel Laureates but only two people provided an explanation of the "molecule." Dima Klenchin, who is ineligible, was the only one to pick up on the hint and find the 1989 paper.
The winner is Shumona De of Dalhousie University.
If you look closely you'll realize that these mouse embryos aren't really "molecules" in any meaningful sense of the word "molecule." That doesn't matter 'cause I still want you to identify what's going on here. This is the first time that I've resorted to using photographs from my previous life—shows you how desperate I'm getting!The images are supposed to remind you of the work of some Nobel Laureates. See if you can guess who they are.
The first person to identify the photographs and the Nobel Laureates wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.
There are eight ineligible candidates for this week's reward: David Schuller of Cornell University, Adam Santoro of the University of Toronto, Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Peter Horwich from Dalhousie University, and Devin Trudeau from the University of Toronto.
Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.
THEME:
Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.
Correct responses will be posted tomorrow.
Kothary, R., Clapoff, S., Darling, S., Perry, M.D., Moran, L.A., Rossant, J. (1989) Inducible expression of an hsp68-lacZ hybrid gene in transgenic mice. Development. 105:707-14. [PDF]
Applying to NSERC? Everyone gets a grant!
According to a study done by Richard Gordon and Bryan J. Poulin, Cost of the NSERC Science Grant Peer Review System Exceeds the Cost of Giving Every Qualified Researcher a Baseline Grant. (NSERC is Canada's funding agency for non-medical science research.)
Using Natural Science and Engineering Research Council Canada (NSERC) statistics, we show that the $40,000 (Canadian) cost of preparation for a grant application and rejection by peer review in 2007 exceeded that of giving every qualified investigator a direct baseline discovery grant of $30,000 (average grant). This means the Canadian Federal Government could institute direct grants for 100% of qualified applicants for the same money. We anticipate that the net result would be more and better research since more research would be conducted at the critical idea or discovery stage. Control of quality is assured through university hiring, promotion and tenure proceedings, journal reviews of submitted work, and the patent process, whose collective scrutiny far exceeds that of grant peer review. The greater efficiency in use of grant funds and increased innovation with baseline funding would provide a means of achieving the goals of the recent Canadian Value for Money and Accountability Review. We suggest that developing countries could leapfrog ahead by adopting from the start science grant systems that encourage innovation.This sounds like a good idea to me. Thanks to Bora Zivkovic of A Blog Around the Clock for finding the paper.
Royal Protocol
Ever country has a protocol officer and part of their job is to specify how one is supposed to treat the Head of State. In America, for example, you must always refer to the President as Mr. President and unelected cabinet ministers are addressed as Mr./Madam Secretary [Office of the Chief of Protocol].Visiting Heads of State are expected to conform to American protocol and when the President visits another country he is expected to conform to their rules of protocol. That's how international diplomacy works. It's a system that has evolved over several centuries to try and makes things easier when two different countries communicate. The idea is for countries to respect each other.
Postdiluvian at The Unexamined Life doesn't think that Americans need to respect the protocols and traditions of a foreign country [Is it OK to hug the Queen?]. Now, as it turns out, Michelle's hug was a breach of protocol but not that big a deal, even in England. It would be comparable to someone forgetting to say "Mr. President" when addressing Barack Obama.
That doesn't justify this kind of response ....
Now here’s the bottom line: you can have your “Queen” as a powerless (and utterly pointless) figurehead if you like. She can even keep her massive wealth that somehow came into her family’s possession over the centuries. But if you ever start this bullshit about “Royal Protocol” again, or whether or not it’s okay for people to touch her, you will be removing yourself from the realm of the Serious and joining the realm of Laughingstock, much like the concept of Monarchy did ages ago.Americans often wonder why they have so much trouble making friends in "foreign" countries. I can't imagine why.
Monday, April 06, 2009
Five Against One
It's sounds so unfair. Four Christians against one lone atheist. If you add in the moderator it's five against one.
But the atheist is Christopher Hitchens so they didn't have a chance.1
Next time they should try half a dozen Christians—and they should look for ones that are smart.2
1. Actually, if you watch the "debate" you'll realize that Hitchens didn't need to do or say anything. Every single one of their arguments for the existence of God has been refuted dozens of times. It's like a kindergarten class in Christian apologetics. Most of the time I wish Hitchens had kept his mouth shut.
2. Assuming that ....
[Hat Tip: Friendly Atheist]
What Is Epigenetics?
Berger et al. (2009) attempt to define epigenetics.
"An epigenetic trait is a stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence."Sounds good to me. Just about anything wold be better than the kitchem sink definition proposed by Eva Jablonka [Epigenetics at SEED].
The main examples are "DNA methylation, histone modifications, histone variants, and nucleosome positioning." These are chromosomal alterations that are passed on to daughter cells following cell division by mitosis or meiosis.
Although the Berger et al. don't mention it, these epigenetic signals are all reversible. I still don't find the term useful. It's far more accurate to refer to each of the individual examples by name and the field is "regulation of gene expression."
Berger, S.L., Kouzarides, T., Shiekhattar, R., and Shilatifard, A. (2009) An operational definition of epigenetics. Genes & Dev. 23:781-783. [DOI: 10.1101/gad.1787609]
[Hat Tip: Hopeful Monster]
Monday's Molecule #116
If you look closely you'll realize that these mouse embryos aren't really "molecules" in any meaningful sense of the word "molecule." That doesn't matter 'cause I still want you to identify what's going on here. This is the first time that I've resorted to using photographs from my previous life—shows you how desperate I'm getting!The images are supposed to remind you of the work of some Nobel Laureates. See if you can guess who they are.
The first person to identify the photographs and the Nobel Laureates wins a free lunch at the Faculty Club. Previous winners are ineligible for one month from the time they first won the prize.
There are eight ineligible candidates for this week's reward: David Schuller of Cornell University, Adam Santoro of the University of Toronto, Dima Klenchin from the university of Wisconsin, Alex Ling from the University of Toronto, Bill Chaney of the University of Nebraska, Elvis Cela from the University of Toronto, Paul Horwich from Dalhousie University, and Devin Trudeau from the University of Toronto.
Dima and Bill have donated their free lunch to a deserving undergraduate so I'm going to continue to award an additional free lunch to the first undergraduate student who can accept it. Please indicate in your email message whether you are an undergraduate and whether you can make it for lunch.
THEME:
Nobel Laureates
Send your guess to Sandwalk (sandwalk (at) bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and names the Nobel Laureate(s). Note that I'm not going to repeat Nobel Prizes so you might want to check the list of previous Sandwalk postings by clicking on the link in the theme box.
Correct responses will be posted tomorrow.
Comments will be blocked for 24 hours.
Sunday, April 05, 2009
Religion Wars: Linux and Mac vs. Rationalism
Greg Linux is disappointed that the Confliker virus didn't do more damage on April 1st [Did Conflicker Flop? Yes. Why? Nobody knows].
I wasn't worried because I checked all five of my computers and not one them were infected. If they had been, it was very easy to get rid of the worm. My Linux machine didn't have the worm either.
That doesn't stop Greg from offering this advice ...
Experts expect that the worm is going to re-awaken at some time in the future and possibly actually do something. In the mean time, you may want to get rid of it if is on your system.Sheesh, those religious nuts sure can be silly.
If you run Windows, the best way to get rid of the computer is to get a Mac or a Linux computer. There are probably other ways to do this but I don't really care. If you are running Linux, this worm can't directly affect you.
The End of Christian America?
The number of Americans who don't identify with a religion has increased from 8% in 1990 to 15% today. This is encouraging but it doesn't quite mean that the battle between rationalism and superstition has been won.Nevertheless, the fact that a national magazine could publish an article like "The End of Christian America" is an indication that the debate is on.
If North American societies become much less religious—like those in Europe—then most of the major problems with creationism will go away. Maybe then we can concentrate on promoting good science education. That's why some of us would rather put our efforts into promoting rationalism over superstition rather than defending specific creationist attacks on schools.
Both approaches are needed but those who advocate the compatibility of science and superstition are not helping.
[Hat Tip: Hemant Mehta who has some interesting comment.]
Subscribe to:
Posts
(
Atom
)