BTW, you guys did great on last week's molecule but not so good on the supplemental questions in the comments. Does everyone now know the 21st, 22nd, and 23rd amino acids?
Monday, November 27, 2006
Monday's Molecule #3
Name this molecule. Comments will be blocked for 24 hours. Comments are now unblocked.
BTW, you guys did great on last week's molecule but not so good on the supplemental questions in the comments. Does everyone now know the 21st, 22nd, and 23rd amino acids?
BTW, you guys did great on last week's molecule but not so good on the supplemental questions in the comments. Does everyone now know the 21st, 22nd, and 23rd amino acids?
Sunday, November 26, 2006
Imagine No Religion
In The God Delusion, Richard Dawkins refers to John Lennon who asked us to imagine no religion. For those of you who never knew John Lennon, here he is singing Imagine. No, John, you're not the only one. (Thanks to The Scientific Indian for finding the video on Google Videos.)
The Three Domain Hypothesis (part 3)
The scientific dispute over The Three Domain Hypothesis is based on the validity of RNA trees, the importance of protein trees that disagree with the rRNA tree, the evidence for fusions, and the frequency of Lateral Gene Transfer (LGT). But, as usual, there’s more to it than just science. The side with the best advocates has a huge advantage in fights like this.
Let's set the stage by quoting from the article by William Martin.
One of the key problems in deep phylogeny is choosing the right gene. Pace argues in favor of ribosomal RNA—not a surprise since he has invested over 20 years in this molecule. Ideally, what kind of gene do we want to examine in order to determine the deepest branches in the tree of life? According to Pace there are three criteria ....
There’s no question about #1. Ribosomal RNA genes are fond in all species. There are very few other genes that meet this criterion. Almost all other candidates are absent in at least a few species. Ribosomal RNA satisfies #3 as well. Even the small subunit is large enough.
What about #2? Which genes have “resisted” lateral gene transfer? You can’t just declare by fiat that ribosomal RNA genes haven’t been transferred. It’s a debatable question as we’ll see later on.
I would add three other criteria.
Ribosomal RNA does not encode protein. That’s a serious problem that Pace never addresses.
Ribosomal RNA genes are well conserved but not as highly conserved as some others. This is why rRNA can be used to distinguish closely related species whereas the sequences of other genes are identical unless the species diverged more than 10-20 million years ago. Part of the problem with using rRNA sequences in deep phylogeny is that they are too divergent.
Having declared that ribosomal RNA genes are the best choice, Pace then goes on to show us the “true”universal tree of life. As you can see, it is divided into three distinct clusters separated by long branches. The clades represent Bacteria, Archaea, and Eukaryotes; the Three Domains. The prokarotes (Bacteria and Archaea) seem to associate and the eukaryotes seem to be more distantly related.
But first impressions can be misleading. Pace puts the root on the branch leading to bacteria and not on the long branch leading to Eukaryotes. This root is based entirely on two old 1989 papers, which he references. Both of these papers have been refuted, but that’s not something you would learn from reading Pace’s article. (There are other, more recent, experiments that root the tree on the bacterial branch and these should have been used. The fact that they weren’t reflects Pace’s degree of critical thinking on this problem. )
To many of us, the large scale structure of the tree of life just doesn’t look right. The long branches leading from the trifurcation point to Bacteria and Eukaryotes smack of artifact. The branching within each of the domains looks too simple. It’s part of the reason why there’s skepticism about the rRNA tree, as we’ll see.
The rest of the article is a passionate defense of the importance of bacteria. I agree with him, for the most part, and so do lots of evolutionary biologists. Bacteria are much more important than eukaryotes! :-)
Pace contributes very little to the debate since he is not willing to entertain any doubts about the Three Domain Hypothesis. For that we have to look at some other papers.
Microbobial Phylogeny and Evolution: Concepts and Controversies Jan Sapp, ed., Oxford University Press, Oxford UK (2005)
Jan Sapp The Bacterium’s Place in Nature
Norman Pace The Large-Scale Structure of the Tree of Life.
Woflgang Ludwig and Karl-Heinz Schleifer The Molecular Phylogeny of Bacteria Based on Conserved Genes.
Carl Woese Evolving Biological Organization.
W. Ford Doolittle If the Tree of Life Fell, Would it Make a Sound?.
William Martin Woe Is the Tree of Life.
Radhey Gupta Molecular Sequences and the Early History of Life.
C. G. Kurland Paradigm Lost.
Let's set the stage by quoting from the article by William Martin.
Thus, it seems to me that there is a schisma abrew in cell evolution, with the rRNA tree and proponents of its infallibility on the one side and other forms of evidence, proponents of LGT, or proponents of a symbiotic origin of eukaryotes on the other. The former camp is well organized behind a unified view (be it right or wrong, still a view) and is arguing that we already have the answers to microbial evolution. The latter camp is not organized into castes of recognized leadership and followers, meaning that (if we are lucky) concepts and their merits, not position or power, will determine the outcome of the battle as to what ideas might or might not be worthwhile entertaining as a working hypothesis for the purpose of further scientific endeavour.The article by Norman Pace represents the side that already has the answers. He is a strong proponent of the Three Domain Hypothesis. These days, the main thrust of his argument is that we should all jump on the bandwagon or risk being left behind. I heard him speak in San Francisco last April and he sounded more like a preacher than a scientist. His article in Nature, ”Time for a Change”, is an example of the way the Three Domain Hypothesis proponents have been arguing for 20 years.
One of the key problems in deep phylogeny is choosing the right gene. Pace argues in favor of ribosomal RNA—not a surprise since he has invested over 20 years in this molecule. Ideally, what kind of gene do we want to examine in order to determine the deepest branches in the tree of life? According to Pace there are three criteria ....
1. The gene must be universal.Only ribosomal RNA meets all three criteria, says Pace.
2. The gene must have resisted lateral gene transfer.
3. The gene must be large enough to provide useful phylogenetic information.
There’s no question about #1. Ribosomal RNA genes are fond in all species. There are very few other genes that meet this criterion. Almost all other candidates are absent in at least a few species. Ribosomal RNA satisfies #3 as well. Even the small subunit is large enough.
What about #2? Which genes have “resisted” lateral gene transfer? You can’t just declare by fiat that ribosomal RNA genes haven’t been transferred. It’s a debatable question as we’ll see later on.
I would add three other criteria.
4. The gene must be unique, or if it isn’t, paralogues must be easily recognized.Ribosomal RNA doesn’t do so well when we add these criteria. Most bacterial genomes have multiple copies of ribosomal RNA genes. They are usually 99% similar but there are known examples of more divergent paralogues. This is not likely to be a serious problem for deep phylogeny, but it has caused problems at the species level.
5. The gene must encode a protein because it’s much more accurate to analyze amino acid sequences than nucleic acid sequences. (And easier to align.)
6. The gene must be highly conserved in order to retain significant sequence similarity at the deepest levels.
Ribosomal RNA does not encode protein. That’s a serious problem that Pace never addresses.
Ribosomal RNA genes are well conserved but not as highly conserved as some others. This is why rRNA can be used to distinguish closely related species whereas the sequences of other genes are identical unless the species diverged more than 10-20 million years ago. Part of the problem with using rRNA sequences in deep phylogeny is that they are too divergent.
Having declared that ribosomal RNA genes are the best choice, Pace then goes on to show us the “true”universal tree of life. As you can see, it is divided into three distinct clusters separated by long branches. The clades represent Bacteria, Archaea, and Eukaryotes; the Three Domains. The prokarotes (Bacteria and Archaea) seem to associate and the eukaryotes seem to be more distantly related. But first impressions can be misleading. Pace puts the root on the branch leading to bacteria and not on the long branch leading to Eukaryotes. This root is based entirely on two old 1989 papers, which he references. Both of these papers have been refuted, but that’s not something you would learn from reading Pace’s article. (There are other, more recent, experiments that root the tree on the bacterial branch and these should have been used. The fact that they weren’t reflects Pace’s degree of critical thinking on this problem. )
To many of us, the large scale structure of the tree of life just doesn’t look right. The long branches leading from the trifurcation point to Bacteria and Eukaryotes smack of artifact. The branching within each of the domains looks too simple. It’s part of the reason why there’s skepticism about the rRNA tree, as we’ll see.
The rest of the article is a passionate defense of the importance of bacteria. I agree with him, for the most part, and so do lots of evolutionary biologists. Bacteria are much more important than eukaryotes! :-)
Pace contributes very little to the debate since he is not willing to entertain any doubts about the Three Domain Hypothesis. For that we have to look at some other papers.
Microbobial Phylogeny and Evolution: Concepts and Controversies Jan Sapp, ed., Oxford University Press, Oxford UK (2005)
Jan Sapp The Bacterium’s Place in Nature
Norman Pace The Large-Scale Structure of the Tree of Life.
Woflgang Ludwig and Karl-Heinz Schleifer The Molecular Phylogeny of Bacteria Based on Conserved Genes.
Carl Woese Evolving Biological Organization.
W. Ford Doolittle If the Tree of Life Fell, Would it Make a Sound?.
William Martin Woe Is the Tree of Life.
Radhey Gupta Molecular Sequences and the Early History of Life.
C. G. Kurland Paradigm Lost.
ORFans
Over on talk.origins there's a discussion about ORFans. It was started by referring to an article from The Christian Post that reported on a talk given by Paul Nelson. According to Nelson, the presence of ORFan genes in bacterial genomes represents a serious change to evolution.
Ernest Major posted a nice analysis of the paper with references to the many eplanations of the origin of ORFans. I'd like to add a bit more to his description of the "problem."
Here's the primary reference ...
ORF stands for "open reading frame" a term that refers to a stretch of codons for amino acids. It means that this ORF probably identifies a protein encoding gene. In order to be meaningful, the ORF should; (a) begin with a start codon, (b) end with a termination codon, and (c) contain a minimum number of codons (typically more than 100).
In this age of genomics and bioinformatics, there are computer programs that scan both strands of DNA to identify ORF's. These are putative genes. When the first genomes were sequenced there were a lot of putative genes that matched sequences already in the database. In other words, the computer programs identified ORF's that showed significant sequence similarity to individual genes that had already been cloned and sequenced by other labs. These genomic ORF's represented genes that were homologous to known genes.
Yin and Fischer are interested in the ORF's that aren't homologous to known genes. They concentrate on bacterial (prokaryote) genomes since the coverage is more extensive. As more and more genomes were sequenced the number of new genes represented by these non-homologous ORF's declined, as expected. Today, for every new genome that's added to the database, almost 80% of the genes have been previously identified.
The surprise is that there are so many unique ORF's in every genome. These are putative genes that have no known homologues. They are ORFans. In order to determine the number of ORFans, Yin and Fischer analyzed the complete genomes of 277 bacteria. For each and every gene they ran a search against all other genes in the database. The result was the histogram shown below.
The figure shows the distribution of all 818,906 ORF's in 277 sequenced prokaryote genomes. (A typical genome has about 3000 genes.) The bottom axis represents the frequency of each of the putative genes in the database. The tall bar at the extreme left-hand side shows the number of ORF's that are only found in a single species. These are the ORFans. There are almost 80,000 of them; or, about 280 per genome. This is what the paper is all about.
There are some putative genes that are only present in one or two related species. These are represented by the bars at U=0.01, 0.02 etc. Some of these are also counted as ORFans since they are only present in closely related species.
As you can see, there's a broad peak of genes found in about 60% (U=0.6) of all sequenced prokaryote genomes. These represent the standard genes of metabolism. Hardly any genes are present in every single species (U=1.0). This is because the database may be incomplete, the genes may have diverged too far to be detectable, or the species is really missing that gene.
Where did the unique genes (ORFans) come from? If they are real, it seems unlikely that they sprung into existence in a single lineage. They were most likely "borrowed" from a distantly related species by a process known as lateral gene transfer. However, as more and more genomes from diverse species are added to the database it becomes worrisome that the source of these genes isn't identified.
What about viruses? It has long been known that viral genes can be incorporated into bacterial genomes so this seems like a good possibility. Yin and Fischer screened all 818,906 ORF's against the viral database to test this hypothesis. They found that only 2.8% of bacterial ORFans have detectable homologues in the viral genomes. Thus, the transfer of viral genes to bacterial genomes doesn't seem to account for all of the ORFans.
The authors discuss the problems with their experiment and urge us not to reject the viral origin hypothesis just yet. There are only 280 bacteriophage in the viral genome databse and this represents a very tiny percentage of all bacteriophage. (There may be 100 million different phage.) There are still lots of places for ORFan homologues to hide.
I think there's another problem; one that the authors are not taking seriously. It's quite possible that many of the ORFans aren't real genes at all. The computer programs that detect these ORF's are notorious for their false positives. There may be ORFan "genes" that are never transcribed or there may be ORFan "genes" that are transcribed and translated but the protein product doesn't do anything. It's an accident of evolution. In addressing this problem the authors make the common mistake of pointing to those cases where known ORFans have proven to be functional genes, while ingoring that fact most haven't. Just because some of them are real genes doesn't mean that all of them are. If most ORFans are artifacts then it's not surprising that they aren't found in other species.
Ernest Major posted a nice analysis of the paper with references to the many eplanations of the origin of ORFans. I'd like to add a bit more to his description of the "problem."
Here's the primary reference ...
Yin, Y. and Fischer, D. (2006) On the origin of microbial ORFans: quantifying the strength of the evidence for viral lateral transfer. BMC Evolutionary Biology 2006, 6:63
[Get your free copy here]Open Access Charter
ORF stands for "open reading frame" a term that refers to a stretch of codons for amino acids. It means that this ORF probably identifies a protein encoding gene. In order to be meaningful, the ORF should; (a) begin with a start codon, (b) end with a termination codon, and (c) contain a minimum number of codons (typically more than 100).
In this age of genomics and bioinformatics, there are computer programs that scan both strands of DNA to identify ORF's. These are putative genes. When the first genomes were sequenced there were a lot of putative genes that matched sequences already in the database. In other words, the computer programs identified ORF's that showed significant sequence similarity to individual genes that had already been cloned and sequenced by other labs. These genomic ORF's represented genes that were homologous to known genes.
Yin and Fischer are interested in the ORF's that aren't homologous to known genes. They concentrate on bacterial (prokaryote) genomes since the coverage is more extensive. As more and more genomes were sequenced the number of new genes represented by these non-homologous ORF's declined, as expected. Today, for every new genome that's added to the database, almost 80% of the genes have been previously identified.
The surprise is that there are so many unique ORF's in every genome. These are putative genes that have no known homologues. They are ORFans. In order to determine the number of ORFans, Yin and Fischer analyzed the complete genomes of 277 bacteria. For each and every gene they ran a search against all other genes in the database. The result was the histogram shown below.
The figure shows the distribution of all 818,906 ORF's in 277 sequenced prokaryote genomes. (A typical genome has about 3000 genes.) The bottom axis represents the frequency of each of the putative genes in the database. The tall bar at the extreme left-hand side shows the number of ORF's that are only found in a single species. These are the ORFans. There are almost 80,000 of them; or, about 280 per genome. This is what the paper is all about.There are some putative genes that are only present in one or two related species. These are represented by the bars at U=0.01, 0.02 etc. Some of these are also counted as ORFans since they are only present in closely related species.
As you can see, there's a broad peak of genes found in about 60% (U=0.6) of all sequenced prokaryote genomes. These represent the standard genes of metabolism. Hardly any genes are present in every single species (U=1.0). This is because the database may be incomplete, the genes may have diverged too far to be detectable, or the species is really missing that gene.
Where did the unique genes (ORFans) come from? If they are real, it seems unlikely that they sprung into existence in a single lineage. They were most likely "borrowed" from a distantly related species by a process known as lateral gene transfer. However, as more and more genomes from diverse species are added to the database it becomes worrisome that the source of these genes isn't identified.
What about viruses? It has long been known that viral genes can be incorporated into bacterial genomes so this seems like a good possibility. Yin and Fischer screened all 818,906 ORF's against the viral database to test this hypothesis. They found that only 2.8% of bacterial ORFans have detectable homologues in the viral genomes. Thus, the transfer of viral genes to bacterial genomes doesn't seem to account for all of the ORFans.
The authors discuss the problems with their experiment and urge us not to reject the viral origin hypothesis just yet. There are only 280 bacteriophage in the viral genome databse and this represents a very tiny percentage of all bacteriophage. (There may be 100 million different phage.) There are still lots of places for ORFan homologues to hide.
I think there's another problem; one that the authors are not taking seriously. It's quite possible that many of the ORFans aren't real genes at all. The computer programs that detect these ORF's are notorious for their false positives. There may be ORFan "genes" that are never transcribed or there may be ORFan "genes" that are transcribed and translated but the protein product doesn't do anything. It's an accident of evolution. In addressing this problem the authors make the common mistake of pointing to those cases where known ORFans have proven to be functional genes, while ingoring that fact most haven't. Just because some of them are real genes doesn't mean that all of them are. If most ORFans are artifacts then it's not surprising that they aren't found in other species.
Saturday, November 25, 2006
A Teapot in Space
Freecell
Andrew Brown over at Helmintholog points us to Freecell fanatic about a man who has played all 32,000 games three times, and is working his way through the fourth round. You probably don't want to know which games can be won by never using the free cells, but I bet you want to know the one and only game that can't be won at all! Here it is!!!
Dissection of larval CNS in Drosophila melanogaster
Have you ever wanted to know how to remove the central nervous system (CNS) from a fruit fly larva? Of course you have.
Now you can see an expert in action thanks to The Journal of Visualized Experiments. Nathaniel Hafer in Paul Schedl's lab at Princeton shows you how to do it.
Watch the CNS form during development of the embryo in this video from YouTube. (The CNS is the black thing at the bottom.)
Now you can see an expert in action thanks to The Journal of Visualized Experiments. Nathaniel Hafer in Paul Schedl's lab at Princeton shows you how to do it.
Watch the CNS form during development of the embryo in this video from YouTube. (The CNS is the black thing at the bottom.)
Calico Cats
There's been a discussion on talk.origins about calico cats—do they have to be female? The color pattern is an interesting combination of sex-linked genetics and epigenetics. Epigenetics is the inheritance of characteristics other than nuleotide sequence. In this case, it's inheritance of an inactivated X-chromosome.I used calico cats as an example in the Moran/Scrimgeour et al. textbook (1994) published by Neil Patterson/Prentice Hall. Here's an excerpt from that book.One X Chromosome Is Inactivated in Mammalian Females by Condensation into Heterochromatin
The DNA within polytene chromosome bands is condensed but nevertheless accessible to transcription factors. However, there are forms of chromatin known as heterochromatin, that are much more highly condensed. Constitutive heterochromatin refers to chromosomes or parts of chromosomes that are heterochromatic in all cells of a given species. Examples of constitutive heterochromatin can be found in every multicellular eukaryote and can take the form of entire chromosomes or parts of chromosomes. For example, some maize cells contain multiple copies of a small, heterochromatic chromosome called chromosome B. In addition, between one-fourth and one-third of all DNA in Drosophila is found in heterochromatic regions near the centromeres.
Condensation of chromatin is an effective mechanism of repressing eukaryotic gene expression and is best exemplified by the process of X-chromosome inactivation in mammalian females. The sex of a mammal is determined by the presence or absence of the male-specific Y chromosome. In humans, males normally have one X and one Y chromosome per somatic cell, whereas females normally have two X chromosomes per somatic cell. The X chromosome is quite large and contains a number of genes, most of which play no role in sex differences. Proper human development requires that only one X chromosome be fully active in each somatic cell of an adult. Thus, one of the X chromosomes in females is inactivated by condensation into heterochromatin (Figure 27.53). Such condensed chromosomes are known as sex-chromosome bodies or Barr bodies. X-chromosome inactivation is one example of the genetic phenomenon known as dosage compensation because it involves regulating the dosage of genes.
In human females, X-chromsome inactivation occurs very early in embryonic development, at about the 20-cell stage. Condensation of an X chromosome into heterochromatin appears to begin at a unique point, the xist gene, and proceed bidirectionally along the DNA. Inactivation is associated with extensive methylation of DNA. Once a specific X chromosome has been inactivated in a particular cell of the 20-cell embryo, the same X chromosome remains inactivated in all daughter cells descended from that presursor cell (Figure 27_54). In each human cell, either the maternal of paternal X chromosome can be inactivated.
The frequencies of maternal and paternal X chromosome inactivation vary among mammals. In female marsupials, for example, the paternal X chromosome appears to be preferentially inactivated. This observation indicates that the maternal and paternal chromosomes are not identical and can be distinguished in the developing embryo. However, in most other mammals, including humans, the X chromosome that is condensed appears to be selected more or less at random. As a result, some of the cells in the mature organism contain an active maternal X chromsome, and some contain an active paternal chromosome. Consequently, the organism is a mosaic composed of cells expressing different genetic information.
Sometime cells containing an active maternal X chromosome can be physically distinguished from those containing an active paternal X chromosome. An example of such a visible mosaic is the calico cat, which has patches of orange and black fur. Calico cats are always female if they have normal X chromosomes. The patchiness results from random inactivation of X chromosomes in female cats in which the X chromosome inherited from one parent carries the gene [allele] for orange fur and the X chromosome inherited from the other parent carries the gene [allele] for black fur. (The white fur on the underside is due to expression of an autosomal gene.)
Genetic mosaicism due to X-chromosome inactivation also occurs in human females. For example, the gene for glucose-6-phosphate dehydrogenease is located on the X chromosome. If each chromosome carries a different allele, patches of cells will contain either one isoform or the other, depending on which X chromosome is inactivated. The theory of X-chromosome inactivation was developed in large part by Mary Lyon, and the process is sometimes known as Lyonization.
[Calico_cat_Phoebe is from Free Software Foundation.]
Go, Leafs, Go!!!
Tonight is hockey night in Canada. We get to watch Don Cherry on TV.Last night, the Leafs punished the Washington Capitals 7-1. This puts them solidly in third place in the Northeast Division of the Eastern Conference. They're only 8 points behind the division leader (Buffalo) with over 55 games left!
Tonight, the Leafs play Boston at the Air Canada Centre. Some of you might recall that Boston barely squeaked out an overtime victory last time they played. Boston is home to Boston University, MIT, and some other schools.This is the year the Leafs are going to win the Stanley Cup. Yes Siree, Bob, you can count on it! There'll be dancing in the streets next June.
Poking with Needles, Running with Scissors
noctiluca has posted an interesting article on talk.origins, "The Humpty Dumpty argument - the wit and wisdom of Jonathan Wells." noctiluca quotes Jonathan Wells from a Lee Strobel DVD called"The Case for the Creator." (If you go to the site you can actually watch clips showing the IDiots in action!)
The talk.origins article closes with, "My wife didn't know if I was laughing or crying." Thanks noctilura, for sharing that with us. :-)
We tell little children not to run with scissors. We should not forget to warn them against poking at things with needles.
It comes down to this: no matter how many molecules you can produce with early earth conditions, plausible conditions, you're still nowhere near producing a living cell.You can't make this stuff up. And you wonder why we call them IDiots?
And here's how I know: If I take a sterile test tube and I put in it a little bit of fluid with just the right salts, just the right balance of acidity and alkalinity, just the right temperature - the perfect solution for a living cell, and I put in it one living cell, this cell is alive, it has everything it needs for life. Now I take a sterile needle and I poke that cell, and all its stuff leaks out into this test tube, you have in this nice little test tube all the molecules you need for a living cell, not just the pieces of the molecules but the molecules themselves, and you can't make a living cell out of them.
You can't put Humpty Dumpty back together again. So what makes you think that a few amino acids dissolved in the ocean are going to give you a living cell? It's totally unrealistic.
The talk.origins article closes with, "My wife didn't know if I was laughing or crying." Thanks noctilura, for sharing that with us. :-)
We tell little children not to run with scissors. We should not forget to warn them against poking at things with needles.
Friday, November 24, 2006
Biochemistry Major
How many universities have a biochemistry major? My students want to know if most universites have such a program. We know that it's common in Canadian universities. What about the rest of the world?
Teaching the Science of Evolution under the Threat of Alternative Views
I posted a version of this over at Stranger Fruit but after doing so I thought it might be of interest to others ...
After years of keeping quiet, I was prompted to enter this debate after attending a meeting organized by the American Society for Biochemistry and Molecular Biology [ASBMB]. The title of the symposium was "Teaching the Science of Evolution under the Threat of Alternative Views". You can see the video by following the link.
Now, it seemed to me entirely inappropriate to emphasize Miller's religion when introducing him at a scientific conference. It seemed inappropriate to invite Rev. Ted Peters to give one of the talks. It seemed inappropriate for Eugenie Scott to praise Miller but take a swipe at Dawkins.
For me that was the tipping point. Now, I know it sounds childish to say "they started it" but it's important to keep it in mind. Atheists have kept their mouths shut for years but the attack on atheistic views—and the praise of religious scientists—have escalated in recent years.
I was getting tired of being told that atheists were not welcome but religious scientists were.
The important talk is the one by Rev. Ted Peters, an ordained pastor of the Evangelical Lutheran church. He makes the case for Theistic Evolution. Keep in mind that this talk was given at a scientific meeting and most of the audience were scientists. A good many of them were atheists.
Listen to Eugenie Scott's talk as well. I like the bit about "We are not Darwinists." At the end of her talk she presents the case for appeasement: Dawkins bad, Peters good.
After years of keeping quiet, I was prompted to enter this debate after attending a meeting organized by the American Society for Biochemistry and Molecular Biology [ASBMB]. The title of the symposium was "Teaching the Science of Evolution under the Threat of Alternative Views". You can see the video by following the link.
Now, it seemed to me entirely inappropriate to emphasize Miller's religion when introducing him at a scientific conference. It seemed inappropriate to invite Rev. Ted Peters to give one of the talks. It seemed inappropriate for Eugenie Scott to praise Miller but take a swipe at Dawkins.
For me that was the tipping point. Now, I know it sounds childish to say "they started it" but it's important to keep it in mind. Atheists have kept their mouths shut for years but the attack on atheistic views—and the praise of religious scientists—have escalated in recent years.
I was getting tired of being told that atheists were not welcome but religious scientists were.
The important talk is the one by Rev. Ted Peters, an ordained pastor of the Evangelical Lutheran church. He makes the case for Theistic Evolution. Keep in mind that this talk was given at a scientific meeting and most of the audience were scientists. A good many of them were atheists.
Listen to Eugenie Scott's talk as well. I like the bit about "We are not Darwinists." At the end of her talk she presents the case for appeasement: Dawkins bad, Peters good.
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