The main goal of Intelligent Design Creationism is to cast doubt on modern science, especially evolutionary biology. Most of the IDiot books are devoted to attacks on evolution. The underlying assumption is that if modern science is discredited then "god-did-it" becomes a viable alternative.
The latest book by Stephen Myer is no exception. The theme is that evolutionary biologists cannot explain the Cambrian Explosion; therefore, God must have created all the animals in the space of a few million years back in the Cambrian Era (about 530 million years ago).
Most of the book is about the lack of transitional fossils that document the slow transition from primitive worm-like creatures to modern phyla such as arthropods and chordates. Others have dealt with this and I'm not going to comment because it's outside of my area of expertise.1
There is strong evidence from molecular evolution that the major animal phyla share common ancestors and that these common ancestors predate the Cambrian by millions of years. In other words, there's a "long fuse" of evolution leading up to the Cambrian Explosion. Meyer refers to this as the "deep-divergence" assumption.
There are many versions of these trees. The one shown here is from Erwin et al. (2011). It's the one shown in the book The Cambrain Explosion by Douglas Erwin and James Valentine. It isn't necessarily correct in all details but that's not the point.
The point is that molecular phylogenies demonstrate conclusively that the major groups of animals share common ancestors AND that the overall pattern does not conform to a massive radiation around 530 million years ago. Also, it's very clear that the pattern is consistent with evolution and not with God creating all the animals at once.
Stephen Meyer has to address this evidence because it casts doubt on his main theme (God did it). I suppose I don't need to tell you what he says ... it's typical creationist denial. He claims that the evidence doesn't exist. Here are his reasons ...
- There are no fossils to support the earliest branches in the molecular phylogenies.
- There are many different molecular trees and they don't all agree with each other in terms of branching order and timing.
- Evolutionary biologists cherry-pick the data by only picking molecules that give reasonable trees.
- The trees rely on questionable assumptions; namely, that the molecular clock ticks at a constant rate and that there is a universal tree.
- The molecules being compared must be homologous but this is what is being tested so the argument is circular.
The conclusion is ....
Comparative genetic analyses do not establish a single deep-divergence point, and thus do not compensate for the lack of fossil evidence for key Cambrian ancestors—such as the ur-bilateran or the ur-metazoan ancestor. The results of different studies diverge too dramatically to be conclusive, or even meaningful; the methods of inferring divergence points are fraught with subjectivity; and the whole enterprise depends on a question-begging logic. Many leading Cambrian paleontologists, and even some leading evolutionary biologists, now express skepticism about both the results and the significance of deep-divergence studies.
I'm hoping to find time to go over each of Meyer's objections since they reveal a lot about IDiot misconceptions of evolution (and science) and a lot about how they employ strawmen, lies, quote-mining, and distortions in order to discredit an entire field (molecular evolution).2
1. Most IDiots are experts in everything. I'm not as smart as they are.
2. It always amazes me to discover that IDiots like Stephen Meyer think they know more than thousands of expert biologists who do this sort of stuff for a living.
Erwin, D.H., Laflamme, M., Tweedt, S.M., Sperling, E.A., Pisani, D. and Peterson, K.J. (2011) The Cambrian conundrum: early divergence and later ecological success in the early history of animals. Science 334:1091-1097. [doi: 10.1126/science.1206375]
My son was born in this building 35 years ago. It will look very different when the destruction/construction is complete (Women's College Hospital).
From the Onion: Poll: Majority Of Americans Approve Of Sending Congress To Syria
WASHINGTON—As President Obama continues to push for a plan of limited military intervention in Syria, a new poll of Americans has found that though the nation remains wary over the prospect of becoming involved in another Middle Eastern war, the vast majority of U.S. citizens strongly approve of sending Congress to Syria.
The New York Times/CBS News poll showed that though just 1 in 4 Americans believe that the United States has a responsibility to intervene in the Syrian conflict, more than 90 percent of the public is convinced that putting all 535 representatives of the United States Congress on the ground in Syria—including Senate pro tempore Patrick Leahy, House Speaker John Boehner, House Majority Leader Eric Cantor, and House Minority Leader Nancy Pelosi, and, in fact, all current members of the House and Senate—is the best course of action at this time.
Citing overwhelming support from the international community—including that of the Arab League, Turkey, and France, as well as Great Britain, Iraq, Iran, Russia, Japan, Mexico, China, and Canada, all of whom are reported to be unilaterally in favor of sending the U.S. Congress to Syria—the majority of survey respondents said they believe the United States should refocus its entire approach to Syria’s civil war on the ground deployment of U.S. senators and representatives, regardless of whether the Assad regime used chemical weapons or not.
Sounds like a good idea but shouldn't Barack Obama and John Kerry go with them?
There are several required steps in constructing phylogenetic trees from sequence data. The first step is to align the sequences so you can make direct comparisons. It used to be the case that multiple sequence alignments had to be checked manually because none of the available computer programs were as good as an experienced scientist. That hasn't changed. What's changed is that the data sets have become so large and complicated that nobody wants to even look at the sequence alignments to see if they can be improved.
Drew et al. (2013) suggest that sequence alignments should be made available.
Until recently, uploading sequences to GenBank (or EMBL) was generally considered sufficient to ensure reproducibility of phylogenetic studies using DNA sequence data. Increasingly, however, the systematics community is realizing that archiving raw DNA sequences is not adequate, and that the underlying alignments of DNA sequences as well as the resulting phylogenetic trees are pivotal for reproducibility, comparative purposes, meta-analyses, and ultimately synthesis. Indeed, there has been a growing clamor for journals to adopt and enforce more rigorous data archiving practices across diverse disciplines [4]–[8]. As a result, about 35 evolutionary journals [5],[9] have adopted policies to encourage or require authors to upload alignments, phylogenetic trees, and other files requisite for study reproducibility [5] to TreeBASE (http://treebase.org/) and/or other public repositories such as Dryad (http://datadryad.org). Unfortunately, enforcement of such data deposition policies is generally lax, and most journals in systematics and evolution still do not require DNA sequence alignment or tree deposition. As a result, the alignments and trees underlying most published papers in systematics/phylogenetics and evolutionary biology remain inaccessible to the scientific community at large [8],[10].
I sympathize with the goal but I doubt that it can be achieved. I strongly suspect that many scientists don't even bother to produce sequence alignments. They just feed the electronic data directly into their tree-making algorithm.
I wonder how many anomalies could be resolved if they just looked at the alignments? Would they even know if bad sequence data was being used for one or two species in their alignment?
Drew, B.T., Gazis, R., Cabezas, P., Swithers, K.S., Deng, J., Rodriguez, R., Katz, L.A., Crandall, K.A., Hibbett, D.S., and Soltis, D.E. (2013) Lost Branches on the Tree of Life. PLoS Biol 11(9): e1001636. [doi: 10.1371/journal.pbio.1001636]
David Klinghoffer wonders why I'm not criticizing Stephen Myer's new book Darwin's Doubt [see On Darwin's Doubt, Still Waiting to Hear from Big Shots in the Darwin Brigade].
Where is Jerry Coyne in this debate? Where is Dawkins? Even PZ Myers? Or Lawrence Moran, who promised "I'm planning to read [Darwin's Doubt] as soon as I can get a hold of a copy -- probably sometime in August in Canada." (I'm still puzzled by that one. The book was published in June in Canada as well.) It would seem noble for the generals to go into battle alongside the ordinary foot soldiers, putting themselves at risk as well, instead of hanging back at a safe distance.
I preordered the book three months ago and received my copy from Amazon.ca on August 1st. I've been busy with other things for most of the month so I've only turned my attention to the book in the past few days.
David Klinghoffer probably thinks that reviewing another creationist book is my highest priority. That's not the case. In fact, I never promised to review it and after reading it, I never will. There are plenty of others who know more about the subject and some of them are taking the book apart, chapter by chapter [Slaying Meyer’s Hopeless Monster]. If you want details, you can do no better than Darwin’s Doubt – A Review on Skeptic Ink.
For those of you who want a brief summary, I can do no better that point you to the tree of eukaryotes on the left (Keeling et al., 2005). It summarizes tons of molecular data showing the relationships of various eukaryotes. The tree is based on solid molecular evidence that Darwin never knew existed and that evidence is direct conformation of evolution, properly defined. It represents the fixation of nearly neutral alleles by random genetic drift. Of course, you have to read very carefully to find any mention of modern evolutionary theory in Meyer's book—he prefers to focus his attack on mutation + natural selection.
I've drawn a little red circle around the part of this tree that Stephen Meyer discusses in Darwin's Doubt. It's the evolution of animals and, in particular the early fossil evidence of multicellular animals. Most of these appear rather suddenly in the fossil record during the Cambrian (about 530 million years ago). Scientists have long been puzzled about this rapid evolution of complex animals and there are many hypotheses that attempt to account for it. In fact, there's a recent book by Douglas Erwin and James Valentine that summarizes the science behind The Cambrian Explosion. It all seems quite reasonable to me.1 I don't know exactly why complex animals evolved so rapidly but I don't see any reason to doubt the facts of evolution and I don't see any reason to propose that God must have been responsible for this little bit of the tree of life.
Myer does and that's what his book is all about.
1. I don't agree with everything in that book.
Keeling, P.J., Burger, G., Durnford, D.G., Lang, B.F., Lee, R.W., Pearlman, R.E., Roger, A.J. & Gray, M.W. (2005) The tree of eukaryotes. Trends in ecology & evolution 20:670-676. [doi: 10.1016/j.tree.2005.09.005]
After two devastating world wars, the nations of the world got together in San Francisco in 1945 to form the United Nations. The goal was to prevent further wars by pledging to resolve conflicts peaceably or, if that were not possible, to act collectively to reign in rogue nations. The fundamental idea was that no one nation could decide on its own to act as judge, jury, and executioner when it comes to making war. This applies especially to powerful nations whose self righteous attitudes often led them to believe that they could ignore the views of other nations.
The goals of the United Nations have not always been achieved. We have plenty of examples of nations acting unilaterally by going to war and many examples of groups of nations that ignored the United Nations. In spite of these examples, most nations still profess allegiance to the principles that led to the founding of the United nations.
Here's Chapter 1 of the Charter of the United Nations.
Article 1
The Purposes of the United Nations are:
- To maintain international peace and security, and to that end: to take effective collective measures for the prevention and removal of threats to the peace, and for the suppression of acts of aggression or other breaches of the peace, and to bring about by peaceful means, and in conformity with the principles of justice and international law, adjustment or settlement of international disputes or situations which might lead to a breach of the peace;
- To develop friendly relations among nations based on respect for the principle of equal rights and self-determination of peoples, and to take other appropriate measures to strengthen universal peace;
- To achieve international co-operation in solving international problems of an economic, social, cultural, or humanitarian character, and in promoting and encouraging respect for human rights and for fundamental freedoms for all without distinction as to race, sex, language, or religion; and
- To be a centre for harmonizing the actions of nations in the attainment of these common ends.
Article 2
The Organization and its Members, in pursuit of the Purposes stated in Article 1, shall act in accordance with the following Principles.
- The Organization is based on the principle of the sovereign equality of all its Members.
- All Members, in order to ensure to all of them the rights and benefits resulting from membership, shall fulfill in good faith the obligations assumed by them in accordance with the present Charter.
- All Members shall settle their international disputes by peaceful means in such a manner that international peace and security, and justice, are not endangered.
- All Members shall refrain in their international relations from the threat or use of force against the territorial integrity or political independence of any state, or in any other manner inconsistent with the Purposes of the United Nations.
- All Members shall give the United Nations every assistance in any action it takes in accordance with the present Charter, and shall refrain from giving assistance to any state against which the United Nations is taking preventive or enforcement action.
- The Organization shall ensure that states which are not Members of the United Nations act in accordance with these Principles so far as may be necessary for the maintenance of international peace and security.
- Nothing contained in the present Charter shall authorize the United Nations to intervene in matters which are essentially within the domestic jurisdiction of any state or shall require the Members to submit such matters to settlement under the present Charter; but this principle shall not prejudice the application of enforcement measures under Chapter Vll.
Today we are dealing with the possibility that the most powerful nation in the world will attack a much weaker nation in spite of the opposition of many other nations, especially important permanent members of the Security Council. No peaceful resolutions are being explored and very few politicians in that powerful nation are expressing concern that they are ignoring the United Nations. All the rhetoric from that nation seems to be based on the idea that their leaders are judge, jury, and executioner when it comes to policing weaker, more vulnerable, nations. Most of those politicians do not see a problem with bombing another nation in order to punish it for a wrongdoing. Violence and war are viable options and, in this case, the first choice.
To those of us who live in other countries, that is not the kind of behavior one would like to see in the most powerful nation in the world.
I think it's about time that the United States of American quit the United Nations since it clearly has no intention of living up to its commitment to peaceful resolution of conflicts and collective action in cooperation with other nations.
The latest issue of Carnival of Evolution is hosted by Adam Benton, an undergraduate at the University of Liverpool. He's studying evolutionary anthropology. Adam blogs at Evoanth. Read: Carnival of Evolution: Eclectic September edition.
Step right up ladies and gentlemen, here for one month only under the big top is the one, the only, the carnival of evolution. For your delectable delight we have a range of articles, covering everything from bacterial evolution to Neanderthal hearing to T. rex‘s eating habits.
As someone who spends a lot of time focusing on human evolution it can be rather easy to get tunnel vision and miss all of this excellent writing on non-evoanth subjects. I’ve thoroughly enjoyed being given a taste of the world outside my field. I only wish there were some way to get people to send me these stories every month.
But before I start trying to contract out my science reading, I better get round to the reason we’re all here. So without much further ado: Welcome to the September edition of the Carnival of Evolution!
This month's edition highlights the people who SUBMITTED articles as opposed to those who wrote them. This is a reminder that anyone can submit at article—it's not just authors who submit their own works.
If you want to host a Carnival of Evolution please contact Bjørn Østman. Bjørn is always looking for someone to host the Carnival of Evolution. He would prefer someone who has not hosted before but repeat hosts are more than welcome right now! Bjørn is threatening to name YOU as host even if you don't volunteer! Contact him at the Carnival of Evolution blog. You can send articles directly to him or you can submit your articles at Carnival of Evolution although you now have to register to post a submission. Please alert Bjørn or the upcoming host if you see an article that should be included in next month's. You don't have to be the author to nominate a post.
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This is Orientation Week at the University of Toronto. There are 10,000 beginning first year students who are just leaning what they got themselves into. Classes start next week.
Today is "Clubs Day." It's the day when all the clubs set up booths around Hart House Circle and the students come to sign up for various activities. That's Cameron Proctor, the Vice President of the University of Toronto Secular Alliance [Facebook] at his booth. I saw his list—there were about 50 people signed up. I had to clear away a huge crowd in order to get the picture. 
I didn't count the number of religious clubs but there must have been at least a dozen. Each one had five or six people soliciting new members and each one had more inquisitive students at the tables than UTSA. I don't get it. I figure that half the students are nonblievers but I guess they aren't interested in a club for nonbelievers.
UTSA has a number of programs planned for this Fall and the members meet every second Thursday starting Sept. 28. Maybe I'll see you there?
Last week's molecule was 6-phosphogluconolactone, the first intermediate in the pentose phosphate pathway. The winner was Brian Shewchuck [Monday's Molecule #212].
Today (Wednesday, but who's counting?) we're going to continue with basic metabolism in honor of all students who are just being introduced to the wonders of introductory biochemistry. Give the common name and identify the pathway. Explain briefly why this pathway is important.
Email your answers to me at: Monday's Molecule #213. I'll hold off posting your answers for 24 hours. The first one with the correct answer wins. I will only post the names of people with 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.)
We were at a wedding in Orillia (Ontario) on the weekend with my son and his wife. On the way home we took the long route and stopped at the Creemore Union Cemetery in Creemore, Ontario. The town is known mainly for its beer (Creemore Springs Brewery) but we were looking for ancestors.
James Hood was born on April 6, 1775 in Kelso, Scotland but his family moved to the Glascow area a few years later. His father was a Calton weaver and so was James. The recession following the end of the Napoleonic Wars meant that the weavers could no longer make a decent living and the British government encouraged them to emigrate to Canada by offering free passage and free land.
James and his family arrived in Canada on the "Prompt" in 1820. They settled originally in the area around Perth, Ontario. My wife, Leslie (neé Rodger) descends from James' son William whose family remained in Perth. James Hood and many of his other children moved to the Creemore area in 1830 and that's where he died on July 30, 1859.
James Hood is my wife's great, great, great, great, grandfather (and the great5 grandfather of Gordon and Jane). He is also the great, great, great grandfather of Mitt Romney [see A Mormon Tale].
Richard Lenski has joined a number of other biologists and blogged about classic "must-read" papers. His first example is Luria and Delbrück (1943)—the Fluctuation Test. It's an excellent description and there's a personal touch.
John Dennehy [The Fluctuation Test and Jonathan Eisen [Luria and Delbrück] also picked the same paper. That means it must really be a "must-read"! (I agree.)
Given that the early history of molecular biology is no longer being taught, I imagine that there are quite a few of you who have never heard of Max Delbrück (1906-1981) or Salvador Luria (1912-1991) in spite of the fact they are Nobel prize winners. Here's some of my posts on them ....
The Velvet Underground of Molecular Biology
Nobel Laureates Max Delbrück, Alfred D. Hershey, Salvador E. Luria
Sarah C.P. Williams is a science writer. She published an article in PNAS last February: Epigenetics. Here's the opening paragraphs ...
Despite the fact that every cell in a human body contains the same genetic material, not every cell looks or behaves the same. Long nerve cells stretch out the entire length of an arm or a leg; cells in the retina of the eye can sense light; immune cells patrol the body for invaders to destroy. How does each cell retain its unique properties when, in its DNA-containing nucleus, it has the same master set of genes as every other cell? The answer is in the epigenetic regulation of the genes: the control system that dictates which of many genes a cell uses and which it ignores. The same mechanism could also explain why identical twins—who have identical genes—can develop different diseases, traits, or personalities.
Epigenetic regulation consists of chemical flags, or markers, on genes that are copied along with the genes when the DNA is replicated. Without altering the sequence of DNA’s molecular building blocks, epigenetic changes can alter the way a cell interacts with DNA. These changes can block a cell’s access to a gene, turning it off for good.
Statements like that make me cringe. Not only is she ignoring decades of work on the real explanation of differential gene expression, she is also proposing an explanation that can't possibly live up to the claim she is making.
PNAS should be embarrassed.
Fortunately, I'm not the only one who was upset. Mark Ptashne had the same reaction as several hundred other scientists but he took the time to write up his objections and get them published in the April issue of PNAS [Epigenetics: Core Misconcept]. I'll quote his opening paragraph and then let you follow the link and get educated about real science.
Indeed understanding this problem has been an overarching goal of research in molecular, developmental, and, increasingly, evolutionary biology. And over the past 50 years a compelling answer has emerged from studies in a wide array of organisms. Curiously, the article ignores this body of knowledge, and substitutes for it misguided musings presented as facts.
There was a time when every molecular biology student knew how gene expression was controlled. They knew about the pioneering work in bacteria and 'phage and the exquisite details that were worked out in the '60s, '70s, and '80s. That information has been lost in recent generations. Our current crop of graduate students couldn't tell you how gene expression is controlled in bacteriophage λ.
If you are one of those students then I urge you to read Ptashne's book A Genetic Switch before it goes out of print. If the current trends continue, that information is soon going to pass out of the collective memory of molecular biologists just as it has been forgotten (or never learned) by science writers.
A few days ago, Jonathan McLatchie published an article on evolution News & Views (sic) where he claimed that humans embryos synthesize the enzyme that makes vitamin C [A Simple Proposed Model For Function of the Human Vitamin C GULO Pseudogene]. This is important for creationists because the gene for that enzyme is a classic pseudogene—a formerly active gene that has lost it's function.
Intelligent Design Creationists don't like pseudogenes because they are junk and their intelligent designer would not fill up the human genome with junk. Hence, pseudogenes must have some function that has yet to be discovered.
Cornelius Hunter is gloating over another study that disputes the notion of junk DNA [More Functions For “Junk” DNA, and More Functions For “Junk” DNA]. His article sounded interesting so I followed the link to the press release.
There was something about the press release that sounded suspicious and that prompted me to seek out the original published paper. Here it is with the abstract ...
Wong, J.J.-L., Ritchie, W., Ebner, O.A., Selbach, M., Wong, J.W., Huang, Y., Gao, D., Pinello, N., Gonzalez, M. and Baidya, K. (2013) Orchestrated Intron Retention Regulates Normal Granulocyte Differentiation. Cell 154:583-595. [PDF] [doi: 10.1016/j.cell.2013.06.052]
Intron retention (IR) is widely recognized as a consequence of mis-splicing that leads to failed excision of intronic sequences from pre-messenger RNAs. Our bioinformatic analyses of transcriptomic and proteomic data of normal white blood cell differentiation reveal IR as a physiological mechanism of gene expression control. IR regulates the expression of 86 functionally related genes, including those that determine the nuclear shape that is unique to granulocytes. Retention of introns in specific genes is associated with downregulation of splicing factors and higher GC content. IR, conserved between human and mouse, led to reduced mRNA and protein levels by triggering the nonsense-mediated decay (NMD) pathway. In contrast to the prevalent view that NMD is limited to mRNAs encoding aberrant proteins, our data establish that IR coupled with NMD is a conserved mechanism in normal granulopoiesis. Physiological IR may provide an energetically favorable level of dynamic gene expression control prior to sustained gene translation.
The authors found 86 genes expressed in mouse granulocytes where there were at least some transcripts that retained an intron. This could be due to mistakes in splicing but the authors prefer to think that intron retention is part of a regulatory step. The transcripts that retain an intron are degraded and this reduces the level of protein that would have been made if a properly spliced transcript had produced a functional mRNA.
It's an example of down-regulation, according to the authors. In most cases the intron-retaining transcripts make up only a few percent of the total transcripts but this is presumably enough to make a difference. In 25 of the genes, the aberrant transcripts are more that 25% of the total cytoplasmic transcripts.
There's nothing in the paper that mentions junk DNA.
Contrast this with the press release from Centenary Institute, Sydney Australia. I reproduce it below ...
How 'Junk DNA' Can Control Cell Development
Aug. 2, 2013 — Researchers from the Gene and Stem Cell Therapy Program at Sydney's Centenary Institute have confirmed that, far from being "junk," the 97 per cent of human DNA that does not encode instructions for making proteins can play a significant role in controlling cell development.
And in doing so, the researchers have unravelled a previously unknown mechanism for regulating the activity of genes, increasing our understanding of the way cells develop and opening the way to new possibilities for therapy.
Using the latest gene sequencing techniques and sophisticated computer analysis, a research group led by Professor John Rasko AO and including Centenary's Head of Bioinformatics, Dr William Ritchie, has shown how particular white blood cells use non-coding DNA to regulate the activity of a group of genes that determines their shape and function. The work is published today in the scientific journal Cell.
"This discovery, involving what was previously referred to as "junk," opens up a new level of gene expression control that could also play a role in the development of many other tissue types," Rasko says. "Our observations were quite surprising and they open entirely new avenues for potential treatments in diverse diseases including cancers and leukemias."
The researchers reached their conclusions through studying introns -- non-coding sequences which are located inside genes.
As part of the normal process of generating proteins from DNA, the code for constructing a particular protein is printed off as a strip of genetic material known as messenger RNA (mRNA). It is this strip of mRNA which carries the instructions for making the protein from the gene in the nucleus to the protein factories or ribosomes in the body of the cell.
But these mRNA strips need to be processed before they can be used as protein blueprints. Typically, any non-coding introns must be cut out to produce the final sequence for a functional protein. Many of the introns also include a short sequence -- known as the stop codon -- which, if left in, stops protein construction altogether. Retention of the intron can also stimulate a cellular mechanism which breaks up the mRNA containing it.
Dr Ritchie was able to develop a computer program to sort out mRNA strips retaining introns from those which did not. Using this technique the lead molecular biologist of the team, Dr Justin Wong, found that mRNA strips from many dozens of genes involved in white blood cell function were prone to intron retention and consequent break down. This was related to the levels of the enzymes needed to chop out the intron. Unless the intron is excised, functional protein products are never produced from these genes. Dr Jeff Holst in the team went a step further to show how this mechanism works in living bone marrow.
So the researchers propose intron retention as an efficient means of controlling the activity of many genes. "In fact, it takes less energy to break up strips of mRNA, than to control gene activity in other ways," says Rasko. "This may well be a previously-overlooked general mechanism for gene regulation with implications for disease causation and possible therapies in the future."
The published paper has nothing to do with junk DNA. Even if intron retention were a common mechanism of gene regulation (it is not), that would only account for about 100 base pairs per gene of additional sequence-dependant information. That's less than 0.1% of the genome.
This is a bad press release because it highlights information that is not in the published paper. The authors bear responsibility for press releases from their own institute that distort their published work. While they may not have written the press release, they presumably are quoted correctly and they should be aware of what's in the press release.
I wonder if they are willing to defend this press release as an accurate representation of their published work?
John Mattick and Jonathan Wells both believe that most of the DNA in our genome is functional. They do not believe that most of it is junk.
John Mattick and Jonathan Wells use the same arguments in defense of their position and they quote one another. Both of them misrepresent the history of the junk DNA debate and both of them use an incorrect version of the Central Dogma of Molecular Biology to make a case for the stupidity of scientists. Neither of them understand the basic biochemistry of DNA binding proteins leading them to misinterpret low level transcription as functional. Jonathan Wells and John Mattick ignore much of the scientific evidence in favor of junk DNA. They don't understand the significance of the so-called "C-Value Paradox" and they don't understand genetic load. Both of them claim that junk DNA is based on ignorance.
