I don't have a lot of time today (I leave for Boston tomorrow) but I can't let this pass.
The complete draft genome of the African coelacanth, Latimeria chalumnae has just been published in Nature (Amemiya et al. 2013). Ceolacanths have long been regarded as "living fossils," a term that persists even though the data have been disputed ever since the first fish were identified 75 years ago. I couldn't believe what I was reading when I saw the press release from the Broad Institute in Boston [Coelacanth genome surfaces]. The author, Haley Bridger of Broad Communications, says ...
An international team of researchers has decoded the genome of a creature whose evolutionary history is both enigmatic and illuminating: the African coelacanth. A sea-cave dwelling, five-foot long fish with limb-like fins, the coelacanth was once thought to be extinct. A living coelacanth was discovered off the African coast in 1938, and since then, questions about these ancient-looking fish – popularly known as “living fossils” – have loomed large. Coelacanths today closely resemble the fossilized skeletons of their more than 300-million-year-old ancestors. Its genome confirms what many researchers had long suspected: genes in coelacanths are evolving more slowly than in other organisms.
“We found that the genes overall are evolving significantly slower than in every other fish and land vertebrate that we looked at,” said Jessica Alföldi, a research scientist at the Broad Institute and co-first author of a paper on the coelacanth genome, which appears in Nature this week. “This is the first time that we’ve had a big enough gene set to really see that.”
Researchers hypothesize that this slow rate of change may be because coelacanths simply have not needed to change: they live primarily off of the Eastern African coast (a second coelacanth species lives off the coast of Indonesia), at ocean depths where relatively little has changed over the millennia.
This can't be right, I said to myself. Let's check out the actual paper.
Unfortunately, it was right. Here's the figure and here's what the authors say in the results section of the paper.
The morphological resemblance of the modern coelacanth to its fossil ancestors has resulted in it being nicknamed ‘the living fossil.’ This invites the question of whether the genome of the coelacanth is as slowly evolving as its outward appearance suggests. Earlier work showed that a few gene families, such as Hox and protocadherins, have comparatively slower protein-coding evolution in coelacanth than in other vertebrate lineages. To address the question, we compared several features of the coelacanth genome to those of other vertebrate genomes.
Protein-coding gene evolution was examined using the phylogenomics data set described above (251 concatenated proteins) (Fig. 1). Pair-wise distances between taxa were calculated from the branch lengths of the tree using the two-cluster test proposed previously to test for equality of average substitution rates. Then, for each of the following species and species clusters (coelacanth, lungfish, chicken and mammals), we ascertained their respective mean distance to an outgroup consisting of three cartilaginous fishes (elephant shark, little skate and spotted catshark). Finally, we tested whether there was any significant difference in the distance to the outgroup of cartilaginous fish for every pair of species and species clusters, using a Z statistic. When these distances to the outgroup of cartilaginous fish were compared, we found that the coelacanth proteins that were tested were significantly more slowly evolving (0.890 substitutions per site) than the lungfish (1.05 substitutions per site), chicken (1.09 substitutions per site) and mammalian (1.21 substitutions per site) orthologues (P < 10−6 in all cases) (Supplementary Data 5). In addition, as can be seen in Fig. 1, the substitution rate in coelacanth is approximately half that in tetrapods since the two lineages diverged. A Tajima’s relative rate test confirmed the coelacanth’s significantly slower rate of protein evolution (P < 10−20)
The authors make it clear in the discussion that they think of molecular evolution of amino acid sequences only in terms of adaptation.
Since its discovery, the coelacanth has been referred to as a ‘living fossil’, owing to its morphological similarities to its fossil ancestors. However, questions have remained as to whether it is indeed evolving slowly, as morphological stasis does not necessarily imply genomic stasis. In this study, we have confirmed that the protein-coding genes of L. chalumnae show a decreased substitution rate compared to those of other sequenced vertebrates, even though its genome as a whole does not show evidence of low genome plasticity. The reason for this lower substitution rate is still unknown, although a static habitat and a lack of predation over evolutionary timescales could be contributing factors to a lower need for adaptation. A closer examination of gene families that show either unusually high or low levels of directional selection indicative of adaptation in the coelacanth may provide information on which selective pressures acted, and which pressures did not act, to shape this evolutionary relict.
This extraordinary claim flies in the face of everything we know about molecular evolution. Preliminary data from some of these same authors was criticized by Casane and Laurenti1 (2013) earlier this year. I'll quote what they said and leave it up to Sandwalk readers to draw their own conclusions.
Transposing the concept of ‘living fossil’ to the genomic level has led to the hypothesis of genetic stasis (or at least to the idea of a reduced molecular evolutionary rate) that is in sharp contrast with the principles of evolutionary genetics. Genomes change continuously under the combined effects of various mutational processes, that produce new variants, and genetic drift and selection, that eliminates or fixes them in populations. In other terms, the only possibility for genomes to replicate without change implies at least one of the two following conditions: (i) new variants do not appear (i.e. no mutations), and (ii) new variants are systematically eliminated by selection (i.e. no genetic drift and very powerful selection against new variants). Of course we can consider a less extreme case, i.e. a reduced evolutionary rate of the genome, but this still implies a lower mutation rate and/or stronger selection against new variants than observed in other species.
The coelacanth data make no sense. You should be very skeptical.
You should also wonder about the kind of people that Nature asks to review their papers. Reviewers may not be inclined to challenge the data but they should challenge the conclusions and they should ask the authors to address the fact that their interpretation is inconsistent with the modern evolutionary theory.
One other thing, if you look through the names of the authors, you will see several people who should know better than to attach their name to a paper like this. What's going on?
[Photo Credit: This is a photo of a model of a related species Latimeria chalumnae from the Oxford University Museum. (Wikipedia)]
Amemiya, C.T. et al. (2013) The African coelacanth genome provides insights into tetrapod evolution. Nature 496:311–316. [doi: 10.1038/nature12027]
Casane, D. and Laurenti, P. (2013) Why coelacanths are not ‘living fossils.’ BioEssays 35:332-338. [doi: 10.1002/bies.201200145]
Ryan Gregory asked what he should do with his old conference name tags (on Facebook).
You hang them on your office door, of course. What else would you do with them?
Sometimes I wonder about those young professors. You have to help them with every little problem that comes up. Being a mentor is such a drag.
This National Ask An Atheist Day in the USA. It's sponsored by the Secular Student Alliance and supported by the Center for Inquiry.
Canadians can participate as well. Ask me anything ...
The phrase "to have your cake and eat it too" means that you can't have it both ways or "shouldn't try to have two incompatible things" [You can't have your cake and eat it].
The Intelligent Design Creationists are giving us a good example of just what this means. They have a new book coming out called "Darwin's Doubt." It's to be published by the religious arm of HarperCollins. The book will be available in a few months in the USA so the IDiots are ramping up the hype in preparation. We are told that this book, just like several previous books from the Discovery Institute, will definitively refute evolution and demonstrate the truth of Intelligent Design Creationism.
Here's how casey Luskin put it a few days ago [Three (or Four) Reasons Everyone Should Read Darwin's Doubt].
When published, Darwin's Doubt will be the single most up-to-date rebuttal to neo-Darwinian theory from the ID-paradigm. In this regard, one exciting element of Darwin's Doubt is that Meyer reviews much of the peer-reviewed research that's been published by the ID research community over the last few years, and highlights how ID proponents are doing relevant research answering key questions that show Darwinian evolution isn't up to the task of generating new functional information.
Here's how the strategy works. The IDiots are arguing the merits of Meyer's new book on the leading creationist blogs. They are generating lots of publicity and convincing their followers that the book is going to be a devastating rebuttal of "Darwinism." None of their followers have read the book but that doesn't matter. They won't have to.
How are scientist supposed to respond? None of us have read the book so we can't (yet) show that it is just more of the same old propaganda that we've seen before. What we can say is that we are very skeptical of the claims being made and we think it is disingenuous to promote those claims when we can't examine the "evidence." We can confidently speculate about what Stephen Meyer is going to say because he has a history and because he gives away some of his arguments in the publicity surrounding the book. The IDiots only sing one note and there's a very high probability that this isn't going to change.
That's exactly what Jerry Coyne said in his post: A (formerly) reputable publisher sells out to creationists. He puts it very nicely—and undoubtedly accurately— when he says, "But creationist Stephen Meyer, from the Discovery Institute, has apparently wrapped up the story. He’s hit upon the real reason for the Cambrian explosion: it’s intelligent design! Yes, baby Jesus made the phyla!"
Does anyone with an IQ over 50 think Coyne's prediction is wrong?
You know what's coming because we've seen it all before with the pre-publication hype for "The Myth of Junk DNA." "Science of Human Origins," and "Signature in the Cell." This time it's David Klinghoffer who is the designated whiner [Current Trends in Darwinian Book-Reviewing].
With a pub date of June 18, naturally no books are available. (Though you can preorder at a nice discount, for now, better than Amazon, over at DarwinsDoubt.com.) Nevertheless, at Why Evolution Is True, University of Chicago biologist Jerry Coyne assumes he knows what will be in the book. His absurd summary: "Yes, baby Jesus made the phyla!"
...
Darwinists have a curious way of responding to serious scientific and intellectual challenges to their beliefs. And it's getting more curious, isn't it? It's sort of evolving. If they had answers to ID's challenges, surely they would wait till they read the book, then accurately characterize what it says, and then tell us why Steve Meyer is wrong. But so far, and wasting no time, they have signaled in this strange prophylactic manner their unwillingness to do so.
The solution is obvious to everyone but the IDiots. Don't make outlandish claims about what's in a book until it's published and everyone can check for themselves. It you speculate about what the book is going to say then don't be surprised if others do as well.
You can't have your cake and eat it too.
I'm replying to a post by andyjones (More and more) Function, the evolution-free gospel of ENCODE. That was the fourth post in an exchange between me and him. In response to his latest post, I'm working my way through five issues that Intelligent Design Creationists need to understand. So far, we've covered four of them.
Educating an Intelligent Design Creationist: Introduction
Educating an Intelligent Design Creationist: Pervasive Transcription
Educating an Intelligent Design Creationist: Rare Transcripts
Educating an Intelligent Design Creationist: The Specificity of DNA Binding Proteins
Educating an Intelligent Design Creationist: The Meaning of Darwinism
Intelligent Design Creationists have difficulty understanding the arguments for junk DNA and the evidence that supports those arguments. We try to explain the genetic load argument but it doesn't seem to penetrate. We try to explain that half of our genome is composed of defective transposons and viruses—often fragments of the intact genes. This doesn't phase them. And no matter how many times we describe the "C-value Paradox" and why junk DNA resolves the paradox, that evidence is ignored. We patiently describe the megabase pair deletions of the mouse genome and why this is evidence of junk. We teach them about copy number variation in the human genome and why DNA fingerprinting works. We show them examples of deletions and insertions in the genomes of different individuals telling them that these seem to have no effect as far as we know. We take time to explain modern evolutionary theory and why it is consistent with junk DNA. Finally, we describe our detailed textbook understanding of transcription and DNA binding proteins and they don't listen.
Andyjones says,
The fact that some very good scientists have not found functions for all of the genome does not negate the many functions they have found so far, for many classes of genetic element, including those commonly classed as ‘junk’. And they are still working. Part of the problem is this: if a layperson were to take apart a microchip, would he be able to discern the function of all the parts at the first attempt? Probably not. The problem is not lack of intelligence, but an early lack of understanding of the principles by which the thing is built. As soon as he understands a particular design principle, suddenly huge areas of the chip will be comprehensible to him. I humbly suggest that we have a number of such minor revolutions ahead of us in molecular biology. We are making great strides, but we do not yet understand all the principles of the transcriptome never mind the whole interactome. Perhaps there is more to learn about binding sites for RNAP? Or take pseudogenes: they have already been found to function in some cases as regulators, through their RNA transcripts interacting with real gene RNA transcripts. Then, alternative splicing is only partly understood. Who knows what other mechanisms operate at the RNA level? If you can’t imagine the function yet, it can be pretty hard to find it. But if one asserts there is no function (for example for rare transcripts) like Larry does, it will be even harder to find it.
This is a common theme among the Intelligent Design Creationists and, in fairness, among many molecular biologists. They think that junk DNA is simply an expression of ignorance. They ignore everything we tell them. They think that just because they don't understand something then nobody else does either.
In spite of what our opponents say, we actually have a pretty good understanding of the principles behind how a genome is built. Population genetics tells us that it ain't designed.
When I assert that rare transcripts probably have no function I'm not just talking through my hat and I'm not the only biochemist who says that. When I say that one million little bits and pieces of Alu SINES are very unlikely to have a function, that's not just idle speculation. When the ENCODE workers try to tell me that most of the genome is a huge web of 636,336 regulatory sequences, I can test this claim against the vast amount of information that we already know about genomes and transcriptional regulation and declare that this makes no sense. These are not arguments from ignorance.
Opponents of junk DNA are never going to be credible unless they tell us why the genetic load argument is invalid. They need to explain how their ideas comport with the data on genome size (The Onion Test). They need to explain why the average gene needs 5000 regulatory sites. They need to come up with a reasonable explanation for lack of sequence conservation. They need to tell us why the vast majority of defective transposons evolved a function.
Opponents of junk DNA need to address the arguments and evidence for junk DNA and stop pretending that those arguments don't exist.
I've been thinking a lot about fundamental concepts in biochemistry. One of them has to be energy—where do cells and organisms get the energy to grow and divide?
Most of the metabolism section of biochemistry courses in North America are taught from an anthropomorphic, fuel metabolism perspective. That's understandable since the purpose of such courses is mostly to prepare students for the MCAT exam. (Medical school entrance exam.) I prefer an evolutionary approach to teaching biochemistry but that's not very popular these days.
By the time the course is over, students will have learned that humans get their energy from food, especially glucose. The next step is to ask where the glucose comes from. The simple answer is that food (i.e. glucose) comes from plants. The next question is where do plants get the energy to make glucose? The answer is, of course, sunlight. This should lead to an explanation of photosynthesis but that rarely happens in introductory biochemistry courses.
This description leads to the classic "food chain" as shown in the figure (above) from FT Exploring Science and Technology [The Flow of Energy Through Plants and Animals]. This is conceptually sound biochemistry as far as it goes. As long as students understand how sunlight can be used to make ATP and how ATP can be used to make macromolecules (including glucose), then they will understand that humans ultimately get their energy from sunlight. I would be happy if all biochemistry students could explain this food chain at the molecular level.
But in order to make sure that students really understand this process, I go one step further. I explain that there are many species of bacteria that are chemoautotrophs. Chemoautotrophs are incapable of photosynthesis yet they are able to grow and divide in the absence of any organic compounds. Their carbon source is CO2, just like photosynthetic organisms. These bacteria have a basic metabolism that teaches us what primitive life forms must have been like. Knowing how they get their energy helps students understand evolution.
Where do chemoautotrophs get their energy? I'm interested in knowing how many readers have taken biochemistry and are able to answer that question. Please let me know in the comments before you read the answer in these posts [Carbon Dioxide Fixation in the Dark Ocean] [Core Concepts: Pathways and Transformations of Energy and Matter] [Ubiquinone and the Proton Pump].
The last Monday's Molecule was the pyrrolysine, 23rd amino acid. The winner was Michael Florea [Monday's Molecule #201].
Today's molecule is an enzyme. Homologous enzymes are found in all species. They play an essential role in metabolism. The green part binds the substrate and the subsequent reaction reduces a bound FAD prosthetic group (yellow). Electrons are then passed to an FAD molecule in the purple part in the orientation shown on the left. Notice that the yellow FAD molecules are close together. (The two purple parts on the left should be joined but the connection can't be resolved in the structure.) This electron transfer results in a shift in conformation to the conformation of the purple structure shown on the right. Note that the FAD molecule has shifted to a less exposed position. The purple protein then dissociates and carries electrons to an membrane-bound enzyme that transfers electrons to ubiquinol (QH2). Name the green protein and the purple protein.
This week I'm trying a new format in order to avoid moderating comments. Email your answers to me at: Monday's Molecule #202. I'll hold off posting your answers for 24 hours. The first one with the correct answer wins. I will only post mostly correct answers to avoid embarrassment. The winner will be treated to a free lunch.
There could be two winners. If the first correct answer isn't from an undergraduate student then I'll select a second winner from those undergraduates who post the correct answer. You will need to identify yourself as an undergraduate in order to win. (Put "undergraduate" at the bottom of your email message.)
Lately there's been a flurry of activity in the American press about the value (or lack of value) of science. There have also been attempts by various organizations to enhance science education.1 Most defenders of science and science education will eventually end up trying to explain how science directly benefits the economy, usually in the form of return on investment. In other words, we need to do science because eventually the result will be used by somebody to make a profit.
I posted an example of this a few days ago [Zack Kopplin Defends Science].
I think this is a dangerous strategy. There are several ways of responding to the "what's in it for me" question without bringing up indirect economic benefit. These strategies are common when defending public support for the arts, for example. They're also used when defending research in the humanities.
Phill Plait of Bad Astronomy hits the nail on the head as far as I'm concerned [Wall Street Journal Editorial Board Member Gets Schooled on Science Funding]. His defense of science should be the primary talking point whenever anyone questions the value of learning about the natural world. Here's what Phil Plait says in response to Zack Kopplin's "return on investment" defense of science when Stephen Moore asks why the government is funding research on sex in snails.
How’s that for return on investment?
And that’s just a pedestrian, look-at-what’s-directly-in-front-of-you kind of thinking. We research the Universe around us because we are curious, inquisitive, intelligent animals. We don’t know what snail mating habits might teach us. That’s why we study it. Maybe it’ll lead into insight on how animals behave, or a new chemical secreted during the process, or to insight on the environment where snails live. Maybe none of that.
But that’s not the damn point. We study science because we want to learn about the real world. If we wanted to stick our heads in the sand, as people like Moore would have us do, he wouldn’t even have the venue he has to say ridiculous things like he just did.
Science is about exploration and discovery, and making sure we don’t fool ourselves. It’s among the noblest of all human endeavors, and something we should be both pursuing to our fullest abilities as well as defending from those who would drag it down.
Right on, Phil! Science leads to knowledge and knowledge is always better than ignorance. That's reason enough to fund science research and reason enough to support science education.
As sure as night follows day, there are going to be comments from people who advocate the "return on investment" strategy for defending science research. The argument frequently boils down to the fact that most politicians don't care about knowledge. All they want to see is how science can help business or improve the health and physical well-being of our citizens. Because these politicians are ignorant of the real value of knowledge, we must cow-tow to their ignorance and defend science on their turf.
That's what's happening in Canada with our Conservative government. In my field (biochemistry & molecular biology), many of my colleagues think we have to justify our research by showing how it will improve health. The current buzzword is "translational research." If you don't engage in the kind of research that Conservatives want, then you won't get funded.
Unfortunately, that may be true in today's climate. That doesn't mean we have to fool ourselves into thinking that that "translational research" be our primary goal. We recognize that the ignorance of our Conservative government is a problem, not a virtue. It's a problem that has to be fixed ... in the long term. Our goal should be to educate the next generation of politicians so we don't have to be embarrassed by them in the future. Let's at least have some people like Phil Plait who will speak out for basic curiosity-motivated research. We'll never succeed in convincing politicians and the general public of the value of knowledge if we don't even try.
Let's make sure we start with our students. Let's at least ensure that when we have them in our clutches as undergraduates we make sure that they understand science and the importance of knowledge. If we don't do that then we have nobody to blame but ourselves when future societies demand that science generate a return on investment.
Looking at my own university, it's obvious that we are not doing a very good job in our courses. I fear for the future of science.
1. In the USA "science" often gets lumped in with "technology," "engineering," and "mathematics"(=STEM) as though they had the same goals.
Regis College is a Jesuit College at the University of Toronto. One of their main jobs is to train students for the priesthood in the Roman Catholic Church.
Earlier this year it offered a course on "Responding to 21st-Century Atheism." This attracted the attention of Huffington Post who published a story about it on January 27, 2013 [Regis College, Catholic Institution, Offers Course On Atheism]. This provoked some traffic in the blogosphere [e.g. Jesuit college teaches atheism!].
I thought this was pretty interesting so when Regis College announced a one-day workshop I signed up and sent in my $50. Yesterday I spent more than seven hours at Regis College: six hours of lectures and an hour to eat my peanut butter sandwiches.
Join Professors Scott Lewis, S.J., Gordon Rixon, S.J., and Jeremy Wilkins from the faculty of Regis College as they explore responses to the challenges presented by contemporary atheism. This one day seminar will discuss the role of Scripture, tradition, and theology to address the questions about human living posed by today's culture and climate of disbelief.
Saturday, April 13, 2013 from 9:00 am to 4:00 pm. Cost $50.00
I mentioned a few days ago that Stephen Meyer's new book Darwin's Doubt is about to be released [see Two Books on the Cambrian Explosion]. I'm planning to read it as soon as I can get a hold of a copy—probably sometime in August in Canada.
You are all going to have to read this book because, according to Casey Luskin, it is "going to be another landmark for the ID movement" [Three (or Four) Reasons Everyone Should Read Darwin's Doubt]. Luskin has read it. Here are his three reasons why the book is important and worth reading.
- Arguments for intelligent design in the Cambrian explosion have certainly been made before. But Darwin's Doubt will be by far the most in-depth and mature development of those arguments to date, addressing in detail many ideas and rebuttals and theories advanced by evolutionary scientists, and showing why the theory of intelligent design best explains the explosion of biodiversity in the Cambrian animals.
- When published, Darwin's Doubt will be the single most up-to-date rebuttal to neo-Darwinian theory from the ID-paradigm. In this regard, one exciting element of Darwin's Doubt is that Meyer reviews much of the peer-reviewed research that's been published by the ID research community over the last few years, and highlights how ID proponents are doing relevant research answering key questions that show Darwinian evolution isn't up to the task of generating new functional information.
- As many ENV readers already know, we now live in a "post-Darwinian" world, where more and more evolutionary biologists are realizing that neo-Darwinism is failing, so they scramble to propose new materialistic evolutionary models to replace the modern synthesis. (These models include, or have included, self-organization, evo-devo, punc eq, neo-Lamarckism, natural genetic engineering, neutral evolution, and others.) In this regard, Darwin's Doubt does something that's never been done before: it surveys the landscape of these "post-neo-Darwinian evolutionary models," and shows why they too fail as explanations for the origin of animal body plans and biological complexity.
I know that it's a bit annoying to have to read all this hype when the book won't be available for several months. The Intelligent Design Creationists want you to know that any criticism of what they are saying about the book is unethical unless you've read it yourself. However, it's not the least bit unethical for them to make outlandish claims about what's in the book months before we can verify whether those claims are correct.
This is creationist ethics. It's not supposed to make sense.
Intelligent Design Creationists love to refer to their opponents as "Darwinists." We all know why they do it. It's a rhetorical device designed to belittle those who accept evolution. The term makes it look like evolutionary biologists worship a man who died 130 years ago and it implies that we still believe in nineteenth century science. The term "Darwinist" also makes it easy to associate modern scientists with social Darwinism. That's a common strategy employed by creationists of all stripes. I get it. It has nothing to do with scientific debates about evolution.
But sometimes rhetoric gets in the way of understanding. There seem to be a few (very few) Intelligent Design Creationists who genuinely want to understand the issues—even if their motive is still to push a scientific view of creationism. They pop up from time to time on the Intelligent Design Creationist websites. Andyjones seems to be one of them. (I'm giving him the benefit of the doubt.)
I'm replying to a post by andyjones (More and more) Function, the evolution-free gospel of ENCODE. This was the fourth post in a series and I'm working my way through five issues that Intelligent Design Creationists need to understand. The first two were "Pervasive Transcription" and "Rare Transcripts."
Educating an Intelligent Design Creationist: Introduction
Educating an Intelligent Design Creationist: Pervasive Transcription
Educating an Intelligent Design Creationist: Rare Transcripts
The Specificity of DNA Binding Proteins
It is absolutely essential that you understand the basic biochemistry of DNA binding proteins if you want to interpret the ENCODE results and the controversy surrounding junk DNA. You might think this is a given since almost everyone involved in the discussion has had some exposure to biochemistry in undergraduate courses. Unfortunately, most of these courses don't teach that stuff anymore1 so we've raised a generation of scientists who were never exposed to the facts.
The Next Generation Science Standards are a set of recommendations for teaching science to public school children in the USA. The standards were made up by representatives from the National Research Council and 26 states. The standards have been extensively reviewed and many drafts were posted on the web.
You can look at the final version at DCI Arrangements of the Next Generation Science Standards.
Let's look at the High School Section on Biological Evolution : Unity and Diversity. Let me know what you think.
HS-LS4 Biological Evolution: Unity and Diversity
Students who demonstrate understanding can:
HS-LS4-1. Communicate scientific information that common ancestry and biological evolution are supported by multiple lines of empirical evidence. [Clarification Statement: Emphasis is on a conceptual understanding of the role each line of evidence has relating to common ancestry and biological evolution. Examples of evidence could include similarities in DNA sequences, anatomical structures, and order of appearance of structures in embryological development.}
HS-LS4-2. Construct an explanation based on evidence that the process of evolution primarily results from four factors: (1) the potential for a species to increase in number, (2) the heritable genetic variation of individuals in a species due to mutation and sexual reproduction, (3) competition for limited resources, and (4) the proliferation of those organisms that are better able to survive and reproduce in the environment. [Clarification Statement: Emphasis is on using evidence to explain the influence each of the four factors has on number of organisms, behaviors, morphology, or physiology in terms of ability to compete for limited resources and subsequent survival of individuals and adaptation of species. Examples of evidence could include mathematical models such as simple distribution graphs and proportional reasoning.] [Assessment Boundary: Assessment does not include other mechanisms of evolution, such as genetic drift, gene flow through migration, and co-evolution.]
HS-LS4-3. Apply concepts of statistics and probability to support explanations that organisms with an advantageous heritable trait tend to increase in proportion to organisms lacking this trait. [Clarification Statement: Emphasis is on analyzing shifts in numerical distribution of traits and using these shifts as evidence to support explanations.] [Assessment Boundary: Assessment is limited to basic statistical and graphical analysis. Assessment does not include allele frequency calculations.]
HS-LS4-4. Construct an explanation based on evidence for how natural selection leads to adaptation of populations. [Clarification Statement: Emphasis is on using data to provide evidence for how specific biotic and abiotic differences in ecosystems ( such as ranges of seasonal temperature, long-term climate change, acidity, light, geographic barriers, or evolution of other organisms) contribute to a change in gene frequency over time, leading to adaptation of populations.]
HS-LS4-5. Evaluate the evidence supporting claims that changes in environmental conditions may result in: (1) increases in the number of individuals of some species, (2) the emergence of new species over time , and (3) the extinction of other species. [Clarification Statement: Emphasis is on determining cause and effect relationships for how changes to the environment such as deforestation, fishing, application of fertilizers, drought, flood, and the rate of change of the environment affect distribution or disappearance of traits in species.]
HS-LS4-6. Create or revise a simulation to test a solution to mitigate adverse impacts of human activity on biodiversity. * [Clarification Statement: Emphasis is on designing solutions for a proposed problem related to threatened or endangered species, or to genetic variation of organisms for multiple species.]
I'm replying to a post by andyjones (More and more) Function, the evolution-free gospel of ENCODE. This was the fourth post in a series and I'm working my way through five issues that Intelligent Design Creationists need to understand.
Educating an Intelligent Design Creationist: Introduction
Educating an Intelligent Design Creationist: Pervasive Transcription
Andyjones says he didn't know that many of the unusual transcript are very rare. That's a shame because it's one of the very important things you need to know in order to have an intelligent opinion about junk DNA. Here's a question from andyjones ...
The second point is interesting, but I have to ask the question: given the fact that we don’t know everything about the genome, isn’t it precisely those parts that are rarely transcribed that would give most difficulty when it comes to determining their functions?
The simple answer to your question is "yes" but that doesn't mean we don't have clues. The best explanation depends on how rare the transcripts are and on whether there's another, equally reasonable, explanation that accounts for their existence. What we can say right now is that the presence of these rare transcripts is consistent with junk DNA. We can also say that there's no reasonable functional explanation for huge numbers of transcripts that are present at less that one copy per cell. Think about that for a minute. It means that right now there are only two scientifically reasonable explanations: (1) junk DNA/RNA, and (2) we don't know if they have a function. It is scientifically incorrect to say that these transcribed regions are functional and therefore junk DNA is refuted.1
I just signed up for the SMBE Conference in Chicago in July. There's lots of cool talks about evolution but, in the end, I decided I just couldn't miss the session on "Where did 'junk' go?" with Wojciech Makalowski as organizer. Here's the blurb ...
Late Susumu Ohno once said "So much junk DNA in our genome" and the phrase junk DNA was born. For a long time mainstream scientists avoided these parts of the genome. However, over the years the picture slowly started to appear suggesting that the junk DNA hides a genomic treasure. With the completion of the current ENCODE project, junk DNA effectively disappeared because there's no longer useless DNA in the genome. This symposium will discuss the current understanding of these not-so-long-ago obscure areas of the genome, with special attention to transposable elements' activities and their evolutionary consequences. The integral part of the symposium will be general discussion of Ohno’s idea and its place in today's biology.
I'm familiar with Makalowski's way of thinking—it resembles the opinions of many Intelligent Design Creationists even though Makalowski is not a creationist [see Junk DNA: Scientific American Gets It Wrong (again)]. Back in 2007 he said,
Although very catchy, the term "junk DNA" repelled mainstream researchers from studying noncoding genetic material for many years. After all, who would like to dig through genomic garbage?
We know who's been invited to talk.
- Josefa Gonzalez (Institut de Biologia Evolutiva, Barcelona, Spain)
"Adaptation is the key concept in Evolutionary Biology. Understanding adaptation has important scientific and social implications since adaptation underlies processes such as the ability of species to survive in changing environments, resistance to antibiotics and cancer chemotherapies and host-pathogen interactions, among others.
However, adaptation is to date a very poorly understood process largely because the current approaches to the study of adaptation are often exclusively based on a priori candidate genes or on searching for signals of selection at the DNA level giving us an incomplete and biased picture of the adaptive process.
In our lab we aimed at understanding the molecular process of adaptation and its functional consequences. Towards this end, we study recent transposable element (TE)-induced adaptations in Drosophila melanogaster."
- Valer Gotea (National Human Genome Institute, Bethesda, USA)
"... it is not surprising that TEs [transposable elements] have a significant influence on the genome organization and evolution. What once was called junk now is considered a treasure. Although much progress has been achieved in understanding of a role that TEs play in a host genome, we are still far from a full understanding of the delicate evolutionary interplay between a host genome and the invaders"
- Dan Graur (University of Houston, Houston, USA)
"This absurd conclusion was reached through various means, chiefly (1) by employing the seldom used “causal role” definition of biological function and then applying it inconsistently to different biochemical properties, (2) by committing a logical fallacy known as “affirming the consequent,” (3) by failing to appreciate the crucial difference between “junk DNA” and “garbage DNA,” (4) by using analytical methods that yield biased errors and inflate estimates of functionality, (5) by favoring statistical sensitivity over specificity, and (6) by emphasizing statistical significance rather than the magnitude of the effect."
- Dixie Mager (University of British Columbia, Canada)
"The fact that transposable elements (TEs) can influence host gene expression was first recognized more than 50 years ago. However, since that time, TEs have been widely regarded as harmful genetic parasites-selfish elements that are rarely co-opted by the genome to serve a beneficial role. Here, we survey recent findings that relate to TE impact on host genes and remind the reader that TEs, in contrast to other noncoding parts of the genome, are uniquely suited to gene regulatory functions. We review recent studies that demonstrate the role of TEs in establishing and rewiring gene regulatory networks and discuss the overall ubiquity of exaptation. We suggest that although individuals within a population can be harmed by the deleterious effects of new TE insertions, the presence of TE sequences in a genome is of overall benefit to the population."
- Masumi Nozawa (National Genetic Institute, Mishima, Japan)
(I don't know anything about his work. Can anybody help?
I don't have a lot of time today (I leave for Boston tomorrow) but I can't let this pass. 
Unfortunately, it was right. Here's the figure and here's what the authors say in the results section of the paper.
