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Friday, December 22, 2006
Skeptical Climatologists
Kevin Vranes of No Se Nada writes about impressions he got from a recent meeting of geophysicists [So what happened at AGU last week?]. Apparently, some climatologists are worried that they may have oversold climate change and supressed legtimate skepticism over some of the details.
This is a very important issue in science. It does not mean that warnings about climate change are totally wrong or misguided. What it means is that contrary opinions within the scientific community aren't getting attention for fear of diluting the important message that the public needs to hear.
It's an issue in other disciplines as well, such as evolutionary biology. Skepticism, which is the essence of science, doesn't play very well in the public arena. Scientists who are skeptical about some aspects of evolutionary biology are sometimes considered to be traitors to the cause of defeating creationism. I imagine that the same sort of thing might be happening in the field of climate change.
Varsity Centre Bubble Now Inflated
The new Varsity Centre bubble has now been inflated over the University of Toronto football field on Bloor Street. Students have been looking forward to this event for some time: it means they can now play Ultimate Frisbee all winter.
The press release talks exclusively about athletics but we all know the real reason for creating such a large, heated enclosure. In Canada, the gyms and arenas are stuffed with desks and chairs at this time of year and used for exams.
Rumor has it that the bubble is energy efficient. It recycles a lot of the hot air generated on campus.
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Thursday, December 21, 2006
Mammalian Gene Families: Humans and Chimps Differ by 6%
The first issue of PLoS ONE has just been published. PloS ONE publishes peer-reviewed, open-access, articles that are freely available on the internet. The journal is supported by the Public Library of Science (PloS), a non-profit organization. |
Demuth, J.P., De Bie, T., Stajich, J.E., Cristianini, N., and Hahn, M.W. (2006) The Evolution of Mammalian Gene FamiliesDemuth et al. examined gene families in five species whose genomes have been sequenced (human, chimpanzee, mouse, rat, dog). Gene families are normally defined as groups of related genes having more than one copy in a genome. For example, the globin gene family consists of multiple copies of related globin genes such as myoglobin, α-globin, β-globin, and others. The authors appear to use a different definition, which counts orthologous genes in different species as a gene family. Thus, their paper discusses "gene families" that have single genes in different species.
By scanning the available genome sequences, Demuth et al. were able to cluster all genes into 15,389 groups called "gene families." Of these, 3,114 were single genes confined to a single species. These were presumed to be annotation artifacts and were discarded. Not all of the remaining groups were present in all five species. A total of 2,285 additional groups were confined to distinct lineages on the mammalian tree indicating that they had been "created" after divergence from the common ancestor. This leaves 9,990 groups that were probably present in the ancestor of dog, human, chimp, mouse, and rat.
The question is, how many of these gene families show gain or loss of numbers during mammalian evolution? The answer is 5,622 or 56.3% (5622/9,990). The data is shown in Figure 1 (below). The red section of the pie chart represents groups that have experienced a reduction in the number of members of a gene family (or loss of the entire group) in a particular lineage. The green section represents a gain in the number of genes in a family.
Figure 1. Distribution of gene gain and loss among mammalian lineages. |
Creative Commons Attribution License |
If we focus on the human/chimp comparison, it turns out that the human genome contains 1,418 genes that do not have orthologs in the chimpanzee genome. What this means is that if we look at the identical sections of human and chimp chromosomes one of them will have a gene that the other one does not have at that position. It turns out that the human genome has 689 genes not present in the chimp and the chimp has 729 genes not present in humans. If there are 22,000 genes in the genome, then this total of 1,418 differences represents 6.4% of the genes.
It's important to note that this does not mean that entirely new genes are created or destroyed. What it means is that there have been duplication events such that a gene has been duplicated in one of the lineages. For example, let's say that the region of the chromosome containing the α-globin genes was duplicated in the chimpanzee lineage. This would count as a gain in chimps relative to humans.
There are several problems with the analysis. One of the most severe is the lack of complete coverage of the chimp genome and the relatively poor annotation compared to the human genome. Only 94% of the chimp genome is available while the human genome is about 99% complete and much more accurate. This means that there will be a number of genes in humans that won't appear in chimps. It's unlikely that these problems lead to errors of more than 2-fold.
The authors are clearly aware of the fact that most of these changes in gene number have no effect on the organism. They are accidental changes due to random genetic drift. They are also aware of the fact that some of the duplications and losses are variants that are segregating in the human and chimp populations. In other words, they are not fixed differences.
Nevertheless, Demuth et al. point out that some of the gains and losses of genes could be responsible for the phenotypic differences between chimpanzees and humans. They caution us that the traditional 1% difference in the sequences of orthologous genes may not be the whole story.
An Example of High School Biochemistry
I don't know exactly what to make of this. It is not exactly correct, but it's not exactly wrong, either. I wonder what grade produced it?
Wednesday, December 20, 2006
Grading Exams
I've written about the difficulties of grading exams and about the fact that it's almost impossible to get the perfect distribution. We have our tricks. Now, Daniel J. Solove of Concurring Opinions has let the cat out of the bag by revealing one of our most garded secrets—the staircase technique. He spills the beans in A Guide to Grading Exams.
You'd think there ought to be a movement to drum him out of the teacher's union, but no, instead his article is advertised in The 98th Carnival of Education. What is this world coming to?
The Carl Sagan memorial blog-a-thon
Carl Sagan died ten years ago today. My contribution to the Carl Sagan memorial blog-a-thon is a quotation from page 297 of The Demon-Haunted World.
Have I ever heard a skeptic wax superior and contemptuous? Certainly. I've even sometimes heard, to my retrospective dismay, that unpleasant tone in my own voice. There are human imperfections on both sides of this issue. Even when it's applied sensitively, scientific skepticism may come across as arrogant, dogmatic, heartless, and dismissive of the feeling and deeply held beliefs of others. And, it must be said, some scientists and dedicated skeptics apply this tool as a blunt instrument, with little finesse. Sometimes it looks as if the skeptical conclusion came first, that contentions were dismissed before, not after, the evidence was examined. All of us cherish our beliefs. They are, to a degree, self-defining. When someone comes along who challenges our beliefs as insufficiently well-based—or who, like Socrates, merely asks embarrassing questions that we haven't thought of, or demonstrates that we've swept key underlying assumptions under the rug—it becomes much more than a search for knowledge. It becomes a personal attack.Sagan combined skepticism with finesse. That was part of his charm.
The Blasphemy Challenge
The IDiots are making a fuss about The Blasphemy Challenge. If you don't know why the IDiots have their knickers in a knot then watch this video from YouTube .
Dissent Isn't Welcome on Uncommon Descent!
DaveScot says,
Larry, why do Darwinists insist on calling ID creationism?I don't know. Why don't you ask a Darwinist?
If you want to ask me why I call your creed Intelligent Design Creationism then feel free to come on over here and ask. I don't ban IDiots. In fact, most science bloggers don't ban IDiots because the IDiots supply much of the comic relief on science blogs.
You’ll need to answer on your own blog because you’re no longer welcome on this one.
Libya Reverts to the Stone Age
Several bloggers are all over the this story [Six innocent people sentenced to death.] It concerns five foreign nurses and a doctor who went to Libya in 1999 to help look after sick children. Many of the children became infected with HIV and developed AIDS. Genetic testing has shown that the virus was present before the team of nurses and doctors arrived at the hospital but, in spite of the scientific evidence, the Tripoli Six have been convicted of spreading the disease and sentenced to death.
There has been rejoicing in the street in Libya as citizens demonstrate their support for an ignorant court.
Denyse O'Leary Never Learns
Since first meeting Denyse O'Leary a few months ago, we've had several interactions where I attempted to explain why "Darwinism" is not an appropriate synonym for modern evolutionary biology. From time to time she actually seems to get it. She's even agreed to try and be more honest about referring to evolution instead of harping on "Darwinism" as the number one bogey man.
Alas, it didn't last long. Denyse has posted a long diatribe based on some unsubstantiated claim that a professional society is "hassling" a scientist who dares to question Darwin. She says,
Darwinism is their perpetually virgin theory that can never be impugned. Have you noticed how absolute are the claims they make for it? You’d have as much luck discussing science-related questions about Darwin’s theory with them as discussing Mary’s state of grace with Mickey and Ladislaw.Once again, you're dead wrong Denyse. Lots of us question classic "Darwinism," as did Stephen Jay Gould, the former President of the American Association for the Advancement of Science (AAAS, a professional society). Modern evolutionary theory has moved well beyond what Darwin knew in the nineteenth century. Science is constantly changing—it does not rely on the literal reading of ancient texts. When will you ever learn?
Nobel Laureates: Hans Krebs
The Nobel Prize in Medicine 1953.
"for his discovery of the citric acid cycle"
Hans Krebs (1900-1981) received the Nobel Prize for working out the pathway for oxidation of the two carbon acetyl group on acetyl-CoA via a series of tricarboxylic intermediates. The cyclic pathway is now known as the Krebs cycle, the citric acid cycle, or the tricarboxylic acid cycle (TCA cycle).
Krebs had previously been known for his excellent work on the urea cycle in the 1920's and 30's. However, the citric acid cycle was controversial from the beginning. (See Monday's Molecule #6.) By the time he received the Nobel Prize, most biochemists were convinced but there were some hold-outs, making this one of the more controversial awards.
The modern citric acid cycle differs very little from the one published by Krebs over fifty years ago. The main difference is that today we recognize cis-aconitate as an intermediate in the reaction catalyzed by aconitase and not as a separate intermediate in the pathway.
Tuesday, December 19, 2006
It's Official! Pharyngula Is Best Science Blog!
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Monday, December 18, 2006
Michael Denton and Molecular Clocks
It's easy to construct a phylogenetic tree using cytochrome c sequences (left). The tree shows us that bacteria and eukaryotes form two separate branches just as predicted by evolution. Within the eukaryote branch, we see that plants, fungi, and animals form distinct groups. Again, this is exactly what evolution predicted.
One of the remarkable things about these trees is that the branches have similar lengths. Beginning at the base of the tree, the distance to plants, animals, fungi, and bacteria is about the same. It differs by a factor of two, at most, for any species. This is evidence of a molecular clock—a roughly constant rate of evolutionary change for every lineage over a period of hundreds of millions of years. (Cytochrome c is not the ideal sequence for showing this since it's pretty small as far as proteins go. Substitutions of only a few amino acids can make a big difference to branch lengths. Larger proteins show more regular molecular clocks.)
We know why there's a molecular clock. It's because the vast majority of changes in the amino acid sequences of proteins are due to fixation of neutral, or nearly neutral, mutations by random genetic drift. As with any stochastic process, the law of large numbers produces a predictable pattern. In this case, a relatively constant rate of change over hundreds of millions of years.
As it turns out, the overall rate of fixation of neutral alleles should be close to the mutation rate. This is a conclusion derived from population genetics models and those models are well supported by evidence. Since mutation rates are similar, if not identical, between species this rate becomes roughly constant in each lineage. The branch lengths in the cytochrome c tree reflect this indirectly since they result from a combination of fixation times and mutation rates. Furthermore, they are amino acid sequences so a lot of the underlying mutations at the nucleotide level are hidden.
Michael Denton knows of this population genetics explanation since he mentions it on page 289 of Nature's Destiny: How the Laws of Biology Reveal Purpose in the Universe.
Random genetic drift is a perfectly reasonable explanation of the molecular clock but Denton rejects that explanation. He says that,
The second reason for skepticism is that for most of the history of life the "generation time" of different organisms isn't that much different. Large terrestrial mammals, for example, have only been around for about 15% of the time since single-celled life began.
Molecular biologists and population geneticists have thought about these things. They conclude that the evidence favors the idea that phylogenetic trees are due to fixation of nearly neutral alleles by random genetic drift. This explains the molecular clock.
Denton doesn't buy it. He thinks the molecular clock proves Intelligent Design Creationism.
One of the remarkable things about these trees is that the branches have similar lengths. Beginning at the base of the tree, the distance to plants, animals, fungi, and bacteria is about the same. It differs by a factor of two, at most, for any species. This is evidence of a molecular clock—a roughly constant rate of evolutionary change for every lineage over a period of hundreds of millions of years. (Cytochrome c is not the ideal sequence for showing this since it's pretty small as far as proteins go. Substitutions of only a few amino acids can make a big difference to branch lengths. Larger proteins show more regular molecular clocks.)
We know why there's a molecular clock. It's because the vast majority of changes in the amino acid sequences of proteins are due to fixation of neutral, or nearly neutral, mutations by random genetic drift. As with any stochastic process, the law of large numbers produces a predictable pattern. In this case, a relatively constant rate of change over hundreds of millions of years.
As it turns out, the overall rate of fixation of neutral alleles should be close to the mutation rate. This is a conclusion derived from population genetics models and those models are well supported by evidence. Since mutation rates are similar, if not identical, between species this rate becomes roughly constant in each lineage. The branch lengths in the cytochrome c tree reflect this indirectly since they result from a combination of fixation times and mutation rates. Furthermore, they are amino acid sequences so a lot of the underlying mutations at the nucleotide level are hidden.
Michael Denton knows of this population genetics explanation since he mentions it on page 289 of Nature's Destiny: How the Laws of Biology Reveal Purpose in the Universe.
Comparisons of these two rates, the rate of mutation and the evolutionary substitution rate, have revealed the very surprising fact that the two rates are the same. This remarkable finding that the difference between the DNA sequences of different species have been generated by mutation and that other factors such as natural selection could only have played a relatively minor role.Denton knows that the data supports such an idea because he brings up cytochrome c on the next page.
By comparing sequences a curious pattern was observed. For example, in the case of cytochromes, all the higher organism cytochromes (yeasts, plants, insects, mammals, birds, etc.) exhibit an almost equal degree of sequence divergence from the bacterial cytochrome in Rhodospirillum. This means that all their cytochrome genes have changed to about the same degree—in other words, have evolved at a uniform rate.The uniform rate of change is what impresses Michael Denton. As I mentioned above, Denton knows that adaptation (selection) is ruled out as an explanation. Unlike many other IDiots, Denton knows that pan-adaptationism (often called Darwinism) is not the prevailing view in evolutionary biology.
Random genetic drift is a perfectly reasonable explanation of the molecular clock but Denton rejects that explanation. He says that,
Explanations of uniform rates of evolution in protein genes in terms of genetic drift of neutral mutations fare no better. The rate of genetic drift in a population is determined by the mutation rate. This is not controversial. Although mutation rates for many organisms are somewhat similar per generation time—10^-6/gene/generation—the problem is that generation times are vastly different, so that the rate of mutation per year in, say, yeast, may be 100,000 times greater than a tree or a mammal such as man or elephant, organisms that have long generation times. (p. 291)The generation time argument is a bit bogus for several reasons. First, mutation rates are based on changes per cell division (replication) and not generation time. Thus, in mammals such a mouse, there are about 50 cell divisions between zygote and gamete and the organism reproduces in about 100 days. Thus, there is, on average, one mutation-causing replication event every two days. This is no more than the average "generation time" of single-celled organisms such as yeast or bacteria. (Bacteria divide once every few days, at most, contrary to what most people believe.)
The second reason for skepticism is that for most of the history of life the "generation time" of different organisms isn't that much different. Large terrestrial mammals, for example, have only been around for about 15% of the time since single-celled life began.
Molecular biologists and population geneticists have thought about these things. They conclude that the evidence favors the idea that phylogenetic trees are due to fixation of nearly neutral alleles by random genetic drift. This explains the molecular clock.
Denton doesn't buy it. He thinks the molecular clock proves Intelligent Design Creationism.
These twin discoveries—that the mutation rate equals the evolutionary substitution rate, and that the rate of change in many genes is regulated by a clock which seems to tick simultaneously in all branches of the tree of life—may represent the first evidence, albeit indirect, that the mutational processes that are changing the DNA sequences of living things over time are indeed directed by some as yet unknown mechanism, or more likely mechanisms. Of course, these discoveries do not prove directed evolution, but it is far easier to imagine them as the outcome of some sort of direction than the outcome of purely random processes. (p. 292)In other words, Michael Denton can't imagine how stochastic evolutionary processes might work, so God did it. Another argument from ignorance, albeit an ignorance that's on a much higher level than the ignorance usually on display on creationist websites and blogs. (Michael Denton is by far, the most knowledgeable IDiot when it comes to understanding evolution and molecular biology. Perhaps it's why he's out of favor with the true IDiots.)
Junk DNA Disproves Intelligent Design Creationism
Micheal Denton explains it in Nature's Destiny on page 289.
If it is true that a vast amount of DNA in higher organisms is in fact junk, then this would indeed pose a very serous challenge to the idea of directed evolution or any teleological model of evolution. Junk DNA and directed evolution are in the end incompatible concepts. Only if the junk DNA contained information specifying for future evolutionary events, when it would not in a strict sense be junk in any case, could the finding be reconciled with a teleological model of evolution. Indeed, if it were true that the genomes of higher organisms contained vast quantities of junk, then the whole argument of this book would collapse. On any teleological model of evolution, most, perhaps all, the DNA in the genomes of higher organisms should have some functions.Sorry Michael, it is true. The genomes of many complex multicellular organisms have vast quantities of DNA that serves no purpose. It's junk. The whole argument of your book just collapsed, as did any argument for intelligent design.
The fact of junk DNA disproves intelligent design and discredits strict Darwinism as well. The IDiots lose twice. Their strawman version of evolutionary biology is wrong and so is design by God.
FLASH! Dembski Will be Paid for his Expert Advice in Dover
I'm not making this up. Denyse O'Leary announces that the Thomas More Law Center will pay Bill Dembski for over 100 hours of expert advice on the Kitzmiller case in Dover PA.
Discerning readers might recall that this is the case where the IDiots were blown out of the water. Not a single one of their points was accepted by the judge. I wonder what the going rate is for IDiotic experts?
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