| Evolution: Human beings evolved from less advanced life forms over millions of years | Creation: God created human beings in their present form within the last 10,000 years | Not sure | |
| British Columbia | 65% | 21% | 15% |
| Alberta | 58% | 28% | 14% |
| Manitoba/Saskatchewan | 56% | 33% | 11% |
| Ontario | 51% | 26% | 23% |
| Quebec | 71% | 9% | 20% |
| Atlantic | 53% | 26% | 21% |
| Canada | 59% | 22% | 19% |
| United States* | 53% | 66% | 3% |
*USA Today/Gallup Poll (separate questions)
The latest version of Tangled Bank has been posted on Greg Laden's blog.
In a follow-up to previous studies, Gregory W. Graffin and William B. Provine surveyed prominent evolutionary biologists to find out what they thought about religion. The results are summarized in the latest issue of American Scientst [Evolution, Religion and Free Will]. (Click on the figure to see a larger version where you can read the fine print.)Our study was the first poll to focus solely on eminent evolutionists and their views of religion. As a dissertation project, one of us (Graffin) prepared and sent a detailed questionnaire on evolution and religion to 271 professional evolutionary scientists elected to membership in 28 honorific national academies around the world, and 149 (55 percent) answered the questionnaire. All of them listed evolution (specifically organismic), phylogenetics, population biology/genetics, paleontology/paleoecology/paleobiology, systematics, organismal adaptation or fitness as at least one of their research interests. Graffin also interviewed 12 prestigious evolutionists from the sample group on the relation between modern evolutionary biology and religion.
A primary complaint of scientists who answered the earlier polls was that the concept of God was limited to a "personal God." Leuba considered an impersonal God as equivalent to pure naturalism and classified advocates of deism as nonbelievers. We designed the current study to distinguish theism from deism—that is to day a "personal God" (theism) versus an "impersonal God" who created the universe, all forces and matter, but does not intervene in daily events (deism). An evolutionist can be considered religious, in our poll, if he calls himself a deist. ...
Perhaps the most revealing question in the poll asked the respondent to choose the letter that most closely represented where her views belonged on a ternary diagram. The great majority of the evolutionists polled (78 percent) chose A, billing themselves as pure naturalists. Only two out of 149 described themselves as full theists (F), two as more theist than naturalist (D) and three as theistic naturalists (B). Taken together, the advocacy of any degree of theism is the lowest percentage measured in any poll of biologists' beliefs so far (4.7 percent).
No evolutionary scientists in this study chose pure deism (I), but the deistic side of the diagram is heavy compared to the theistic side. Eleven respondents chose C, and 10 chose other regions on the right side of the diagram (E, H or J). Most evolutionary scientists who billed themselves as believers in God were deists (21) rather than theists (7).
When asked directly whether they believe in God, almost 80% said no. I wonder how many of them think of themselves as atheists as opposed to agnostics?We anticipated a much higher percentage for option B and a low percentage for A, but got just the opposite result. One of us (Provine) has been thinking about human free will for almost 40 years, has read most of the philosophical literature on the subject and polls his undergraduate evolution class (200-plus students) each year on belief in free will. Year after year, 90 percent or more favor the idea of human free will for a very specific reason: They think that if people make choices, they have free will. The professional debate about free will has moved far from this position, because what counts is whether the choice is free or determined, not whether human beings make choices. People and animals both certainly choose constantly. Comments from the evolutionists suggest that they were equating human choice and human free will. In other words, although eminent, our respondents had not thought about free will much beyond the students in introductory evolution classes. Evolutionary biology is increasingly applied to psychology. Belief in free will adds nothing to the science of human behavior.There's one other surprise. 72% think that religion is part of evolution—it's an adaptation. One can only wonder what these evolutionary biologists think of themselves. Are they able to overcome their deterministic predisposition to God or are they mutants who lack the gene(s)? Maybe it explains why they believe in free will?
On the other hand, I admit to deep disappointment in the intellectual substance of Collins’ arguments, which I unpack in the multipart review at Access Research Network.Hmmm ... I don't know of very many radical materialist atheists who fall for evolutionary psychology. I wonder who she could be talking about? Maybe it's PZ?
Note to all, especially Collins fans: C. S. Lewis is not a security blanket, and the debate over the origin of free will, morality, altruism, and consciousness has moved on from his day. Today's atheist is not usually a genial, classical God-denier; he is a radical materialist who honestly believes that we are all just robots replicating our selfish genes. And he cannot wait to get his gospel onto the curriculum of publicly funded schools, as "evolutionary psychology," forcing everyone's nose into his nonsense.
The Nobel Prize in Physiology or Medicine 1993."for their discoveries of split genes"
Richard J. Roberts (1943 - ) and Phillip A. Sharp (1944 - ) received the Nobel Prize in Physiology or Medicine for their discovery of interrupted genes and splicing in eukaryotes [see RNA Splicing: Introns and Exons and Monday's Molecule #31]. Your Majesties, Your Royal Highnesses, Ladies and Gentlemen,
Why do children resemble their parents? This question has probably always fascinated humans, but not until the advent of natural science have we arrived at an increasingly satisfactory answer.
In the middle of the last century, the Austrian monk Gregor Mendel conducted his famous breeding experiments with the garden pea. He concluded that every trait of an individual plant is determined by a set of two genes, one obtained from each parental plant. To Mendel a gene was an abstract concept, which he used to interpret his breeding experiments. He had no idea of the physical properties of genes.
Only in the mid-1940s could it be established that in terms of chemistry, genetic material is composed of the nucleic acid DNA. About ten years later the double helical structure of DNA was revealed. Ever since then, progress within the field of molecular biology has been very rapid, and several Nobel prizes have been awarded in this area of research.
Initially, genetic material was studied mainly in simple organisms, particularly in bacteria and bacterial viruses. It was shown that a gene occurs in the form of a single continuous segment of the long, thread-like DNA, and it was generally assumed that the genes in all organisms looked this way. Therefore, it was a scientific sensation when this year's Nobel Laureates, Richard Roberts and Phillip Sharp, in 1977, independently of each other, observed that a gene in higher organisms could be present in the genetic material as several distinct and separate segments. Such a gene resembles a mosaic. Both Roberts and Sharp analyzed an upper respiratory virus, which is particularly suitable for studies of the genetic material in complex organisms. It soon became apparent that most genes in higher organisms, including ourselves, exhibited this mosaic structure.
Roberts' and Sharp's discovery opened up a new perspective on evolution, that is, on how simple organisms develop into more complex ones. Earlier it was believed that genes evolve mainly through the accumulation of small discrete changes in the genetic material. But their mosaic gene structure also permits higher organisms to restructure genes in another, more efficient way. This is because during the course of evolution, gene segments - the individual pieces of the mosaic - are regrouped in the genetic material, which creates new mosaic patterns and hence new genes. This reshuffling process presumably explains the rapid evolution of higher organisms.
Roberts and Sharp also predicted that a specific genetic mechanism is required to enable split genes to direct the synthesis of proteins and thereby to determine the properties of the cell. Researchers had known for many years that a gene contains detailed instructions on how to build a protein. This instruction is first copied from DNA to another type of nucleic acid, known as messenger RNA. Subsequently, the RNA instruction is read, and the protein is synthesized. What Roberts and Sharp were now stating was that the messenger RNA in higher organisms has to be edited. The required process, called splicing, resembles the work that a film editor performs: the unedited film is scrutinized, the superfluous parts are cut out and the remaining ones are joined to form the completed film. Messenger RNA treated in this manner contains only those parts that match the gene segments. It later turned out that the same parts of the original messenger RNA are not always saved during the editing- there are choices. This implies that splicing can regulate the function of the genetic material in a previously unknown way.
Roberts' and Sharp's discovery also helps us understand how diseases arise. One example is a form of anemia called thalassemia, which is due to inherited defects in the genetic material. Several of these defects cause errors in the editing process during splicing; thus, an abnormal messenger RNA is formed and subsequently also a protein that functions poorly or not at all.
The discovery of split genes was revolutionary, triggering an explosion of new scientific contributions. Today this discovery is of fundamental importance for research in biology as well as in medicine.
Dr. Richard Roberts and Dr. Phillip Sharp,
Your discovery of split genes led to the prediction of a new genetic process, that of RNA splicing. The discovery also changed our view of how genes in higher organisms develop during evolution. On behalf of the Nobel Assembly of the Karolinska Institute I wish to convey to you our warmest congratulations, and I now ask you to step forward to receive the Nobel Prize from the hands of His Majesty the King.
Since last October emergency vehicles in Toronto have been displaying a decal in support of our troops in Afghanistan. The decals were placed on the vehicles at the request of firefighters and paramedics, whose unions are strong supporters of the soldiers. The original deal was that the decals would stay on for one year and then be removed when the vehicles came in for routine maintenance this Fall. Some councilors believe the decision to remove the decals is a black mark on the city.It should also come as no surprise that some councilors want to stick to the original agreement and remove the decals in September.
"I was stunned this morning to hear on the radio that some official at the city had ordered emergency services, particularly ambulances, to take off the decal that supports our troops in Afghanistan," city councilor Brian Aston told CTV News on Tuesday.
"These decals are on there and it makes a very strong statement. To take them off, Toronto is the largest city, would just be an outrage. It would be a black eye on the reputation of our city," Ashton said.
Coun. Janet Davis said just as many councillors want to see the decals removed as those who support their presence on emergency vehicles.I'm one of those who believe that the "Support the Troops" ribbon is a political statement. I don't know very many people who are opposed to the war but have this sticker on their car. On the surface it seems like a no-brainer to offer support to our troops while opposing the mission. But, in fact, the term "no-brainer" is quite appropriate in this case. By blindly advertising support for the military you obscure the true difficulty in making rational decisions about how to deploy our army. It's no secret that most people who "support our troops" are also conservatives who are in favour of the war.
Mayor David Miller said while emergency crews should continue to support Canadian troops, the one-year time limit for the decals was enough time.
"It's controversial on both sides. There are people who see it as support for the troops and there are people who see it as support for war," Miller said.
Note that all the coding regions in the exons (hatched) are contiguous in the mature mRNA. The relationship between the exons and the structure of the protein is shown on the right where the color of each segment of the protein corresponds to the color of the exons in the upper figure. There is no correlation between the exons and any protein domains or motifs. (It used to be thought that exons corresponded to domains in the protein.)
In the first step of the splicing reaction, the various components of the spliceosome bind to the 5′ splice site, the 3′ splice site, and the branch site. Then the three complexes interact with each other to draw together the ends of the intron and position them near the branch site. This forms the spliceosome.
Meanwhile, the 5′ end of the transcript is still bound to the spliceosome. This is important because it's about to be joined to the next exon and the reaction wouldn't work if the 5′ end were released following the first cleavage reaction.
The two reactions are known as transesterification reactions because they require the breaking of one strand of RNA and formation of a new ester linkage. The details are not very important. What's important is to recognize that splicing depends on the correct interaction between the components of the spliceosome and the 5′ and 3′ splice site sequences (and the branch site).
Back in January we had a discussion about the definition of a gene [What is a gene?]. At that time I presented my personal preference for the best definition of a gene.A gene is a DNA sequence that is transcribed to produce a functional product.This is a definition that's widely shared among biochemists and molecular biologists but there are competing definitions.
The ENCODE consortium recently completed its characterization of 1% of the human genome by various high-throughput experimental and computational techniques designed to characterize functional elements (The ENCODE Project Consortium 2007). This project represents a major milestone in the characterization of the human genome, and the current findings show a striking picture of complex molecular activity. While the landmark human genome sequencing surprised many with the small number (relative to simpler organisms) of protein-coding genes that sequence annotators could identify (~21,000, according to the latest estimate [see www.ensembl.org]), ENCODE highlighted the number and complexity of the RNA transcripts that the genome produces. In this regard, ENCODE has changed our view of "what is a gene" considerably more than the sequencing of the Haemophilus influenza and human genomes did (Fleischmann et al. 1995; Lander et al. 2001; Venter et al. 2001). The discrepancy between our previous protein-centric view of the gene and one that is revealed by the extensive transcriptional activity of the genome prompts us to reconsider now what a gene is.Keep in mind that I personally reject the premise and I don't think I'm alone. As far as I'm concerned, the "extensive transcriptional activity" could be artifact and I haven't had a "protein-centric" view of a gene since I learned about tRNA and ribosomal RNA genes as an undergraduate in 1967. Even if the ENCODE results are correct my preferred definition of a gene is not threatened. So, what's the fuss all about?
Gerstein et al. are worried because many definitions of a gene include regulatory sequences. Their results suggest that many genes have multiple large regions that control transcription and these may be located at some distance from the transcription start site. This isn't a problem if regulatory sequences are not part of the gene, as in the definition quoted above (a gene is a transcribed region). As a mater of fact, the fuzziness of control regions is one reason why most modern definitions of a gene don't include them.Overlapping Genes
According to Gerstein et al.SplicingAs genes, mRNAs, and eventually complete genomes were sequenced, the simple operon model turned out to be applicable only to genes of prokaryotes and their phages. Eukaryotes were different in many respects, including genetic organization and information flow. The model of genes as hereditary units that are nonoverlapping and continuous was shown to be incorrect by the precise mapping of the coding sequences of genes. In fact, some genes have been found to overlap one another, sharing the same DNA sequence in a different reading frame or on the opposite strand. The discontinuous structure of genes potentially allows one gene to be completely contained inside another one’s intron, or one gene to overlap with another on the same strand without sharing any exons or regulatory elements.We've known about overlapping genes ever since the sequences of the first bacterial operons and the first phage genomes were published. We've known about all the other problems for 20 years. There's nothing new here. No definition of a gene is perfect—all of them have exceptions that are difficult to squeeze into a one-size-fits-all definition of a gene. The problem with the ENCODE data is not that they've just discovered overlapping genes, it's that their data suggests that overlapping genes in the human genome are more the rule than the exception. We need more information before accepting this conclusion and redefining the concept of a gene based on analysis of the human genome.
Splicing was discovered in 1977 (Berget et al. 1977; Chow et al. 1977; Gelinas and Roberts 1977). It soon became clear that the gene was not a simple unit of heredity or function, but rather a series of exons, coding for, in some cases, discrete protein domains, and separated by long noncoding stretches called introns. With alternative splicing, one genetic locus could code for multiple different mRNA transcripts. This discovery complicated the concept of the gene radically.
Perhaps back in 1978 the discovery of splicing prompted a re-evaluation of the concept of a gene. That was almost 30 years ago and we've moved on. Now, many of us think of a gene as a region of DNA that's transcribed and this includes exons and introns. In fact, the modern definition doesn't have anything to do with proteins.Trans-splicing
Alternative splicing does present a problem if you want a rigorous definition with no fuzziness. But biology isn't like that. It's messy and you can't get rid of fuzziness. I think of a gene as the region of DNA that includes the longest transcript. Genes can produce multiple protein products by alternative splicing. (The fact that the definition above says "a" functional product shouldn't mislead anyone. That was not meant to exclude multiple products.)
The real problem here is that the ENCODE project predicts that alternative splicing is abundant and complex. They claim to have discovered many examples of splice variants that include exons from adjacent genes as shown in the figure from their paper. Each of the lines below the genome represents a different kind of transcript. You can see that there are many transcripts that include exons from "gene 1" and "gene 2" and another that include exons from "gene 1" and "gene 4." The combinations and permutations are extraordinarily complex.
If this represents the true picture of gene expression in the human genome, then it would require a radical rethinking of what we know about molecular biology and evolution. On the other hand, if it's mostly artifact then there's no revolution under way. The issue has been fought out in the scientific literature over the past 20 years and it hasn't been resolved to anyone's satisfaction. As far as I'm concerned the data overwhelmingly suggests that very little of that complexity is real. Alternative splicing exists but not the kind of alternative splicing shown in the figure. In my opinion, that kind of complexity is mostly an artifact due to spurious transcription and splicing errors.
Trans-splicing refers to a phenomenon where the transcript from one part of the genome is attached to the transcript from another part of the genome. The phenomenon has been known for over 20 years—it's especially common in C. elegans. It's another exception to the rule. No simple definition of a gene can handle it.Parasitic and mobile genes
This refers mostly to transposons. Gerstein et al say, "Transposons have altered our view of the gene by demonstrating that a gene is not fixed in its location." This isn't true. Nobody has claimed that the location of genes is fixed.The large amount of "junk DNA" under selection
If a large amount of what we now think of as junk DNA turns out to be transcribed to produce functional RNA (or proteins) then that will be a genuine surprise to some of us. It won't change the definition of a gene as far as I can see.The paper goes on for many more pages but the essential points are covered above. What's the bottom line? The new definition of an ENCODE gene is:
There are three aspects to the definition that we will list below, before providing the succinct definition:On the surface this doesn't seem to be much different from the definition of a gene as a transcribed region but there are subtle differences. The authors describe how their new definition works using a hypothetical example.This can be concisely summarized as:
- A gene is a genomic sequence (DNA or RNA) directly encoding functional product molecules, either RNA or protein.
- In the case that there are several functional products sharing overlapping regions, one takes the union of all overlapping genomic sequences coding for them.
- This union must be coherent—i.e., done separately for final protein and RNA products—but does not require that all products necessarily share a common subsequence.
The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products.
How the proposed definition of the gene can be applied to a sample case. A genomic region produces three primary transcripts. After alternative splicing, products of two of these encode five protein products, while the third encodes for a noncoding RNA (ncRNA) product. The protein products are encoded by three clusters of DNA sequence segments (A, B, and C; D; and E). In the case of the three-segment cluster (A, B, C), each DNA sequence segment is shared by at least two of the products. Two primary transcripts share a 5' untranslated region, but their translated regions D and E do not overlap. There is also one noncoding RNA product, and because its sequence is of RNA, not protein, the fact that it shares its genomic sequences (X and Y) with the protein-coding genomic segments A and E does not make it a co-product of these protein-coding genes. In summary, there are four genes in this region, and they are the sets of sequences shown inside the orange dashed lines: Gene 1 consists of the sequence segments A, B, and C; gene 2 consists of D; gene 3 of E; and gene 4 of X and Y. In the diagram, for clarity, the exonic and protein sequences A and E have been lined up vertically, so the dashed lines for the spliced transcripts and functional products indicate connectivity between the proteins sequences (ovals) and RNA sequences (boxes). (Solid boxes on transcripts) Untranslated sequences, (open boxes) translated sequences.This isn't much different from my preferred definition except that I would have called the region containing exons C and D a single gene with two different protein products. Gerstein et al (2007) split it into two different genes.
Gerstein, M.B., Bruce, C., Rozowsky, J.S., Zheng, D., Du, J., Korbel, J.O., Emanuelsson, O., Zhang, Z.D., Weissman, S. and Snyder, M. (2007) What is a gene, post-ENCODE? History and updated definition. Genome Res. 17:669-681.
The ENCODE Project Consortium (2007) Nature 447:799-816. [PDF]
Alan R. Templeton has long been a critic of those who would over-interpret the genetic data on human origins. He's not alone. There are a surprisingly large number of biologists who refuse to jump on the "Out-of-Africa" bandwagon. This group does not get the same amount of publicity as the advocates of a recent (<100,000 years) wave of migration out of Africa. I think it's because skepticism of a new theory is seen as sour grapes. That, plus the fact that it's hard to publish criticisms of work that's already in the scientific literature. Starting with "mitochondrial Eve" in 1987, genetics has played an increasingly important role in studies of the last two million years of human evolution. It initially appeared that genetic data resolved the basic models of recent human evolution in favor of the "out-of-Africa replacement" hypothesis in which anatomically modern humans evolved in Africa about 150,000 years ago, started to spread throughout the world about 100,000 years ago, and subsequently drove to complete genetic extinction (replacement) all other human populations in Eurasia. Unfortunately, many of the genetic studies on recent human evolution have suffered from scientific flaws, including misrepresenting the models of recent human evolution, focusing upon hypothesis compatibility rather than hypothesis testing, committing the ecological fallacy, and failing to consider a broader array of alternative hypotheses. Once these flaws are corrected, there is actually little genetic support for the out-of-Africa replacement hypothesis. Indeed, when genetic data are used in a hypothesis-testing framework, the out-of-Africa replacement hypothesis is strongly rejected. The model of recent human evolution that emerges from a statistical hypothesis-testing framework does not correspond to any of the traditional models of human evolution, but it is compatible with fossil and archaeological data. These studies also reveal that any one gene or DNA region captures only a small part of human evolutionary history, so multilocus studies are essential. As more and more loci became available, genetics will undoubtedly offer additional insights and resolutions of human evolution.
The May issue of Evolution contains an article by Hoekstra and Coyne on Evolutionary-Developmental Biology or Evo-Devo. There are many evolutionary biologists who have serious doubts about the claims of evo-devo but these doubts don't often make it into the scientific literature because it's very hard to publish critiques. The Hoekstra and Coyne (2007) article is a welcome contribution to the debate.An important tenet of evolutionary developmental biology (“evo devo”) is that adaptive mutations affecting morphology are more likely to occur in the cis-regulatory regions than in the protein-coding regions of genes. This argument rests on two claims: (1) the modular nature of cis-regulatory elements largely frees them from deleterious pleiotropic effects, and (2) a growing body of empirical evidence appears to support the predominant role of gene regulatory change in adaptation, especially morphological adaptation. Here we discuss and critique these assertions. We first show that there is no theoretical or empirical basis for the evo devo contention that adaptations involving morphology evolve by genetic mechanisms different from those involving physiology and other traits. In addition, some forms of protein evolution can avoid the negative consequences of pleiotropy, most notably via gene duplication. In light of evo devo claims, we then examine the substantial data on the genetic basis of adaptation from both genome-wide surveys and single-locus studies. Genomic studies lend little support to the cis-regulatory theory: many of these have detected adaptation in protein-coding regions, including transcription factors, whereas few have examined regulatory regions. Turning to single-locus studies, we note that the most widely cited examples of adaptive cis-regulatory mutations focus on trait loss rather than gain, and none have yet pinpointed an evolved regulatory site. In contrast, there are many studies that have both identified structural mutations and functionally verified their contribution to adaptation and speciation. Neither the theoretical arguments nor the data from nature, then, support the claim for a predominance of cis-regulatory mutations in evolution. Although this claim may be true, it is at best premature. Adaptation and speciation probably proceed through a combination of cis-regulatory and structural mutations, with a substantial contribution of the latter.
Hoekstra, Hopi, E. and Coyne, Jerry, A. (2007) THE LOCUS OF EVOLUTION: EVO DEVO AND THE GENETICS OF ADAPTATION. Evolution 65:995–1016.
Today's molecule is complicated but it makes a lot of sense if you know your basic biochemistry. We don't need a long complicated name this time. It's sufficient to simply describe what you're looking at and why it's significant. You have to identify the key residue to get credit for the answer.
