Creationist Logic

Help me out, dear readers. I can't for the life of me figure out the logic behind the latest posting at Uncommon Descent: If you make a prediction and it doesn’t happen ….

I'm serious. Although I often make fun of the IDiots, I usually try hard to understand the points they are trying to make so I can expose them as nonsensical. But this one has me completely stumped. On the surface the author seems to be saying that "Darwinism" made a prediction "based on core principles" that wasn't fulfilled. This is bad for "Darwinism."

What is that prediction?

The author ("News") starts with a quotation from The Myth of Junk DNA.

In 2010, University of California Distinguished Professor of Ecology & Evolutionary Biology John C. Avise published a book titled Inside the Human Genome: A Case for Non-Intelligent Design, in which he wrote that "noncoding repetitive sequences–'junk DNA'–comprise the vast bulk (at least 50%, and probably much more) of the human genome." Avise argued that pseudogenes, in particular, are evidence against intelligent design. For example, "pseudogenes hardly seem like genomic features that would be designed by a wise engineer. Most of them lie scattered along the chromosomes like useless molecular cadavers." To be sure, "several instances are known or suspected in which a pseudogene formerly assumed to be genomic ‘ junk’ was later deemed to have a functional role in cells. But such cases are almost certainly exceptions rather than the rule. And in any event, such examples hardly provide solid evidence for intelligent design; instead, they seem to point toward the kind of idiosyncratic tinkering for which nonsentient evolutionary processes are notorious."

Jonathan Wells, The Myth of Junk DNA (Seattle: Discovery Institute Press, 2011), pp. 26-27

This is a pretty accurate representation of what John Avise actually says except that it juxtaposes two separate facts. It's true that repetitive DNA sequences—mostly defective transposons—make up about half our genome. Then there's pseudogenes. They are found in the other half and they make up about 1% of the human genome.

Avise, and many others, point out that the presence of pseudogenes is inconsistent with good design and therefore poses a problem for Intelligent Design Creationism.¹ I note that the IDiots have consistently refused to address this problem. Instead, they try and convince their followers that pseudogenes don't exist.

Here's what Avise says in his book Inside the Human Genome: A Case for Non-intelligent design (p. 115). You can see that Wells accurately represented the actual argument that he (Avise) was making.

At face value, pseudogenes hardly seem like genomic features that would be designed by a wise engineer. Most of them lie scattered among the chromosome like useless molecular cadavers. This sentiment does not preclude the possibility that an occasional pseudogene is resuscitated such that it contributes positively to cellular operations, several instances are known or suspected in which a pseudogene formerly assumed to be genomic "junk" was later deemed to have a functional role in cells. But such cases are almost certainly exceptions and not the rule. And in any event, such examples hardly provide solid evidence for intelligent design; instead, they seem to point toward the kind of idiosyncratic genetic tinkering for which nonsentient evolutionary evolutionary processes are notorious.

It's important to make sure you understand the argument that Avise and others are making. When looking at the big picture the presence of thousands of pseudogenes in the human genome is a challenge for those who argue for Intelligent Design Creationism. The fact that a handful of these regions were misidentified as pseudgenes and now turn out to have a function cannot be taken as evidence that all of the 20,000 known pseudogenes have a function.

So, how does Wells deal with this challenge to his belief? On the next page of his book (p. 27) he says ...

But Is It True?
The arguments by Dawkins, Miller, Shermer, Collins, Kitcher, Coyne and Avise rest on the premise that most non-coding DNA is junk, wihout any significnat biological function. Yet a virtual flood of recent evidence shows that they are mistaken. Much of the DNA they claim to be "junk" actually performs important functions in living cells.

The following chapters cite hundreds of scientific articles (many of them freely accessible on the Internet) that testify to those functions—and those articles are only a small sample of a large and growing body of literature on the subject. This does not mean that the authors of those articles are critics of evolution or supporters of intelligent design. Indeed, most of them interpret the evidence within an evolutionary framework. But many of them explicitly point out that the evidence refutes the myth of junk DNA.

This is a classic "bait-and-switch." The argument from Avise and the others is mostly about the presence of pseudogenes. There is solid evidence that many pseudogenes are completely non-functional. There is evidence that non-functional pseudogenes have been inherited from common ancestors, strongly suggesting that the genes were inactivated in ancient ancestors and passed down to modern species as the evolved.

This argument is NOT about "most noncoding DNA." It's about that 1% of the genome that contains known pseudogenes. Unless that point is addressed directly (it isn't) then Wells is guilty of ignoring one of the main arguments of his critics.

But that's not the point of this posting. I'm concerned about the point that "News" makes in the recent posting on Uncommon Descent. He/she says ...

Darwinism predicts something, based on its core principles, and it doesn’t happen. And there are no consequences? Only on planet Darwin. Where all correct predictions originate in Darwin’s theory and are grandfathered as such by his loyal heirs. All incorrect predictions are “proved” to have originated elsewhere, no matter where they actually originated.

What are these predictions of "Darwinism"? It's surely not pseudogenes since no evolutionary theory that I know of predicted pseudogenes. Bacteria don't have many pseudogenes and that's perfectly consistent with evolutionary theory. Plant genomes have lots of pseudogenes and that's perfectly consistent with evolutionary theory. Yeast has a few pseudogenes but not nearly as many as plants and that's perfectly consistent with modern evolutionary theory.

Is "News" referring to junk DNA in general? That's not a prediction of "Darwinism" or any evolutionary theory that I know of. The fact that bacteria have very little junk DNA has never been taken as a fact that overthrows modern evolutionary theory. I'm unaware of any evolutionary biologist who predicted back in the 1960s that most of the mammalian genome would be junk and that this prediction was a requirement of modern evolutionary theory. The arguments of Avise et al. are not based on the "premise" that most of our genome is junk, they're based on the evidence that pseudogenes exist.

No prediction was made so no prediction has been refuted. The point that "News" is making seems illogical.

Unless I'm missing something obvious.

What about the predictions of the IDiots? Casey Luskin explains it [Intelligent Design and the Death of the "Junk-DNA" Neo-Darwinian Paradigm].

Proponents of intelligent design have long maintained that Neo-Darwinism's widely held assumption that our cells contain much genetic "junk" is both dangerous to the progress of science and wrong. As I explain here, design theorists recognize that "Intelligent agents typically create functional things," and thus Jonathan Wells has suggested, "From an ID perspective, however, it is extremely unlikely that an organism would expend its resources on preserving and transmitting so much ‘junk'." [4] Design theorists have thus been predicting the death of the junk-DNA paradigm for many years: ...

and in Another Intelligent Design Prediction Fulfilled: Function for a Pseudogene ...

Darwinists have long made an argument from ignorance, where our lack of present knowledge of the function for a given biological structure is taken as evidence that there is no function and the structure is merely a vestige of evolutionary history. Darwinists have commonly made this mistake with many types of "junk" DNA, now known to have function. In contrast, intelligent agents design objects for a purpose, and therefore intelligent design predicts that biological structures will have function.²

Here's another prediction, according to Barry Arrington on Uncommon Descent [FAQ4 is Open for Comment].

ID does not make scientifically fruitful predictions.

This claim is simply false. To cite just one example, the non-functionality of “junk DNA” was predicted by Susumu Ohno (1972), Richard Dawkins (1976), Crick and Orgel (1980), Pagel and Johnstone (1992), and Ken Miller (1994), based on evolutionary presuppositions. In contrast, on teleological grounds, Michael Denton (1986, 1998), Michael Behe (1996), John West (1998), William Dembski (1998), Richard Hirsch (2000), and Jonathan Wells (2004) predicted that “junk DNA” would be found to be functional.

The Intelligent Design predictions are being confirmed and the Darwinist predictions are being falsified. For instance, ENCODE’s June 2007 results show substantial functionality across the genome in such “junk DNA” regions, including pseudogenes.

Thus, it is a matter of simple fact that scientists working in the ID paradigm carry out and publish research, and they have made significant and successful ID-based predictions.

It seems like it's the IDiots that have hitched their star to a prediction about junk DNA. If any genome turns out to have a substantial amount of junk DNA then Intelligent Design Creationism is refuted. As it turns out, many genomes do have a lot of junk DNA in spite of what Jonathan Wells would have you believe. Thus, Intelligent Design Creationism is no longer a credible scientific hypothesis.

But you knew that already, didn't you?

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1. Most scientists actually argue a more specific point; namely, that the conservation of specific pseudogenes in different species is an especially serious problem for Intelligent Design Creationists.

2. It's interesting that Casey Luskin seems to know something about the motivations of the intelligent designer because when scientists point out that the genome doesn't look like it was designed this is not taken as an argument against the IDiot position. Instead it's taken as illegitimate science as pointed out by Wells in his book (p. 103), "Do arguments based on speculations about a creator or designer have a legitimate place in science? Not according to Canadian biologist Steven Scadding, who once wrote that although he accepted evolutionary theory, he objected to defending it on the grounds that a creator would or would not do certain things. 'Whatever the validity of this theological claim,' Scadding concluded, 'it certainly cannot be defended as a scientific statement, and thus should be given no place is a scientific discussion of evolution."

Junk Poll Results

Here are the results of the most recent poll on junk DNA. Below it is the result from several years ago. I realize that the questions are different but the shift toward favoring junk DNA is still a surprise. I'd like to think it's because more and more Sandwalk readers are becoming aware of the science behind junk DNA but it could be just that more "junkers" are reading my blog.

Is there anyone out there who changed their minds over the past few years? Is The Myth of Junk DNA going to convert everyone to rejecting junk DNA? I'll have to do another poll in six months to see if the Intelligent Design Creationists are having an impact.

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Zoë and Window Shopping

Don't you just hate it when bloggers post cute pictures of their children, grandchildren, cats, or molluscs?

Tough. Here's my granddaughter, Zoë, window shopping in Barcelona (Spain) a few weeks ago. The window looked so inviting she decided to check out the shop.

She's only 16 months old and already enjoys shopping!

(Zoë took her parents to Barcelona to meet up with Ms. Sandwalk and our nephew for a week of zoo's, Cava, and Gaudí. You can read all about it on leslie jane moran.)

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Omnisaurus Games

My number one son¹, Gordon Moran, is a texture artist working for a video game company in Vancouver. He has hooked up with his programmer friend Kevin Forbes to found Omnisaurus Games. They are working on an iPhone/iPad game and the unique thing about this is that you can follow their progress on their blog. Did you ever wonder what goes into to making a fabulous app?

Omnisaurus Games is an independent game developer currently developing games for the iPhone, iPad, and iPod Touch. Founded May 2011 in Vancouver, Canada by Kevin Forbes and Gordon Moran, we stress open game development, meaning we share every aspect of our development cycle with you the players. Follow our game development journey through our blog, twitter, facebook, or rss feed. Watch our game grow from the conceptual phase, all the way through the entire development cycle. We regularly post our work in progress builds so that you can test them out online and most importantly give us your feedback and great ideas. After all, we’re making these games for you, so shouldn’t you have a say in how they’re made? Most importantly, keep in touch. We’d love to hear anything you have to say about our games, any games, or life in general. We’ll try really hard to implement the best and most popular ideas into our games and reward the most helpful suggestions and ideas with free copies of our game when it launches. We look forward to hearing from you!

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1. Note for the irony deficient - whenever someone says this it usually means they only have one son/daughter. Note that I did not say "number one child" 'cause that would have gotten me in trouble.

A Visit from Rick

It was late in the day when I heard a knock on my office door. I opened it to discover a strange man I hadn't seen in many years he introduced me to his wife and son. Rick Nicholson is a former graduate student in my lab. He got his Ph.D. 25 years ago ("The HSP70 Multi-Gene Family in Saccharomyces cerevisiae.") Rick was the first person to clone and sequence the yeast BiP gene.

Rick went from Toronto to Strasbourg (France) to work in Pierre Chambon's lab and from there he went to Australia. He is currently Professor at the Hunter Medical Research Institute in Newcastle, NSW where he works on peptide hormones expressed during pregnancy in humans.

I've reached the age where it's a real thrill to remember the "olden days" and how much better they were than today. Over dinner, Rick and I agreed that graduate students and young professors were much better 25 years ago than they are today.¹

We tried to remember everyone who was in the the lab during the early 1980's. Fortunately there was a list in Rick's thesis (undergraduates. graduate students, post-docs): Sean Blaine, Kim Bird, Eric Degan, Monica Fuchs, David Lowe, Marc Perry, Andrea Townsend, Sharon Shtang, Scott Young and Kee Wan. I know where most of them are but I haven't seen some of them for decades. That's sad.

Rick and his family are on their way to Strasbourg to celebrate Pierre Chambon's 80th birthday. When I reach 80 I'll have to throw a big party so I can invite all my former colleagues and students.

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1. I recently had dinner with my former Ph.D. supervisor and we reached the same conclusion only it was for 40 years ago. Isn't that strange?

Carnival of Evolution #36

This month's Carnival of Evolution (36th version) is hosted by Greg Laden at Greg Laden's Blog ["If You Love Evolution, Tweet About It!" COE # 36].

Here are the subtitles ...

• Hard Core Theory, Genetics, Mutations
• Kin Selection (or not)
• Ecology and evolution
• Microbes with ESP
• Applied Evolution
• Fish Physiology
• Crayfish Sex
• Human Evolution
• Darwinia
• Time and Deep Time
• Elephants
• Basic Concepts and Pedagogy
• Brains
• Extinction
• Blog The Controversy

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Gil Dodgen Explains the Salem Conjecture

The Salem Conjecture is the work of Bruce Salem. He suggested in the mid 1990s on talk.origins that of those creationists who claim professional expertise in evolution, a substantial percentage are engineers.

Bruce explained that most engineers are NOT creationists. It's only those who think they have special insight into biology who tend to be creationists.

This conjecture seems to hold but nobody knows why. It's one of the great mysteries of the world, right up there with why so many people hang toilet paper incorrectly and why it's only men who need to change after they get married.

Finally, after 15 years, Gil Dodgen offers an explanation for why engineers have such special insight into evolution [Who are the Real Freethinkers, Darwinists or ID Folks?].

The only thing I can think of is that the average Darwinist has no experience in designing any complex, functionally integrated system. The workings of the simplest cell make my AI program and the hardware on which it runs look like tinker toys.....

Self-replication does nothing to mitigate the probabilistic hurdles the Darwinian mechanism must overcome. How could this not be obvious to anyone with any experience in software or any other rigorous engineering discipline, and who has a basic understanding of combinatorial mathematics?

Oops, I forgot, most of these people have no experience in any rigorous engineering discipline. And those who do, and still believe in the Darwinian fantasy, have obviously undergone the atrophy and crippling of their basic reasoning powers — the product of many years of Darwinian indoctrination and suppression of free thought.

Who are the real freethinkers, Darwinists or ID folks? The Darwinian world is Orwellian.

Well, I'm glad that's settled. Now, I wish he'd turn his attention to some of the other serious mysteries that call out for an engineer's special insight. Maybe he can tell us the correct way to hang toilet paper?

(BTW, the posting just went up a few hours ago and there aren't any comments yet. I expect a flood of comments criticizing Gil for being rude to the scientists Darwinists. We all know that the IDiots are very sensitive about such behavior. They pride themselves on being polite and respectful toward their evolutionary biology Darwinist opponents.)

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Junk DNA Poll

If you haven't answered the junk DNA poll question in the margin then now's the time! There's only one week left.

The results so far are surprising—very different from my previous poll on this topic. It looks like one side is wining.

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The Central Dogma Strawman

Whenever you're trying to promote a new idea it's nice to have a scapegoat to beat up on. You're going to get a lot more attention if you can demonstrate that your latest results overthrow some key scientific concept that everyone took for granted. If you can't find a real "key concept" then the next best thing is to make one up.

For the past several decades that strawman target has been The Central Dogma of Molecular Biology. The Central Dogma is supposed to represent the key concept of molecular biology yet it gets "overthrown" on a regular basis every six months. Isn't that strange?

The latest example comes from a Nature review of a recent Science paper. The Science paper presents evidence that many mRNA sequences differ from the sequences in the exons that encode them (Li et al., 2011). RNA editing has been known for decades and every few years it is trotted out again as proof that the Central Dogma is wrong. The recent Li et al. (2011) paper doesn't present evidence for a new phenomenon but it does suggest that RNA editing may be much more common than previously suspected.

Here's what Nature staff writer Erika Check Hayden says about this paper ("Cells may stray from 'central dogma'" Hayden, 2011a).

All science students learn the 'central dogma' of molecular biology: that the sequence of bases encoded in DNA determines the sequence of amino acids that makes up the corresponding proteins. But now researchers suggest that human cells may complicate this tidy picture by making many proteins that do not match their underlying DNA sequences.

Now if that really was what the Central Dogma actually said then it would have disappeared thirty years ago.

The real Central Dogma of Molecular Biology is ...

... once (sequential) information has passed into protein it cannot get out again (F.H.C. Crick, 1958)

The central dogma of molecular biology deals with the detailed residue-by-residue transfer of sequential information. It states that such information cannot be transferred from protein to either protein or nucleic acid. (F.H.C. Crick, 1970)

I've explained why this is the correct version in an old blog posting from 2007: Basic Concepts: The Central Dogma of Molecular Biology. A very similar definition can be found on the Wikipedia site: Central Dogma of Molecular Biology. The key point is that once information flows into protein it can't flow back to nucleic acid. The standard misconception of the Central Dogma is actually the normal information flow pathway or what Crick called the "Sequence Hypothesis." It's a generality that was never meant to be an inviolate rule like the actual Central Dogma.

Hayden has another article in this week's print version of Nature (Hayden, 2011b). The second article emphasizes the controversy surrounding the Li et al. (2011) paper—lots of people are skeptical—but she doesn't back off the implications.

If verified, the findings would require a rewrite of the 'central dogma' of molecular biology, which posits that the RNA transcripts that carry genetic information to the ribosome, where they are used as templates for protein assembly, are generally faithful matches to the original DNA.

There are two remarkable things about such a statement. First, RNA editing has been an established fact for almost thirty years so if the Central Dogma needed rewriting it would have been done a long time ago. Second, Hayden was informed in the comments to her first article that there was a problem with her definition of the Central Dogma. Maybe she didn't have time to change the second version that was about to be published.

To be fair, this isn't just a problem with science writers who don't do their homework. Hayden is right when she says that most science students learn an incorrect version of the Central Dogma of Molecular Biology. It's true that most textbooks promote the information flow pathway as the Central Dogma and they fail to point out that the real version only precludes reverse translation. I don't understand why so many textbook writers and teachers continue to teach something they know to be false as the "Central Dogma" of molecular biology.

Is it because they don't know about the exceptions?

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Crick, F.H.C. (1958) On protein synthesis. Symp. Soc. Exp. Biol. XII:138-163.

Crick, F. (1970) Central Dogma of Molecular Biology. Nature 227, 561-563. [PDF file]

Hayden, E.C. (2011a) Cells may stray from 'central dogma.' Nature Published online 19 May 2011 [doi:10.1038/news.2011.304.

Hayden, E.C. (2011a) Evidence of altered RNA stirs debate. Nature 473:432. [doi:10.1038/473432a]

Li, M., Wang, I.X., Li, Y., Bruzel, A., Richards, A.L., Toung, J.M., and Cheung, V.G. (2011) Widespread RNA and DNA Sequence Differences in the Human Transcriptome. Science. 2011 May 19. [Epub ahead of print] [Science]

The Black Knight

It's been fun battling the IDiots over junk DNA but it's time for a break. For no particular reason I thought of this video.

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IDiots vs the Truth

I don't expect the IDiots to agree with me. I don't expect them to be happy about what I say. But I do expect them to tell the truth, or at least make the attempt.

Over at Evolution News & Views David Klinghoffer posted the following under: At Forbes, John Farrell Joins in "Ayala'ing" of Jonathan Wells.

Thus we have several posts from University of Toronto biochemist Larry Moran, criticizing Myth while being totally open about not having read it first. Moran wrote no fewer than four posts on the book in this fashion, claiming as an excuse that Myth would not be published in Canada until May 31. (In fact, the book was available for purchase from Amazon since early May.)

The four postings are:

1. Junk & Jonathan: Part 1—Getting the History Correct—a posting in which I addressed an interview of Jonathan Wells conducted by Denise O'Leary.
2. Junk & Jonathan: Part 2— What Did Biologists Really Say About Junk DNA?—a posting in which I addressed an interview of Jonathan Wells conducted by Denise O'Leary.
3. Junk & Jonathan: Part 3—The Preface—a discussion of the preface that was posted online.
4. See the IDiots Gloat over Jonathan Wells—a blog posting about what David Klinghoffer had to say about me and the book.

Only one of these postings was about the contents of the book and that one was about the preface, which I had read. In all these postings I was careful to say that I had not read the book but it was on order. I was waiting for it to arrive.

My order was placed weeks ago on amazon.ca. Their website said that the book would not be released until May 31. Fortunately amazon.ca was able to ship it to me last week and I was happy to get it.

Now that I've read the book it will be interesting to see if David Klinghoffer has any comments about my review.

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Junk & Jonathan: Part 8—Chapter 5

This is part 8 of my review of The Myth of Junk DNA. For a list of other postings on this topic see the link to Genomes & Junk DNA in the "theme box" below or in the sidebar under "Themes."

Pseudogenes are the classic example of junk DNA and, as pointed out by many evolutionary biologists, they represent a difficult challenge for Intelligent Design Creationists. It's especially difficult to explain pseudogenes that are located in the same place in different species.

Chapter 5: Pseudogenes—Not so Pseudo After All

Chapter 5 is Pseudogenes—Not so Pseudo After All. This is the chapter where Jonathan Wells takes the standard creationist approach to the problem of pseudogenes—he denies that they exist!

Wells begins the chapter by reminding us that several evolutionary biologists have challenged the IDiots to come up with an explanation for pseudogenes, especially those that are found in closely related species. The usual suspects are quoted: Ken Miller, Douglas Futuyma, Jerry Coyne, Richard Dawkins, and John Avise. All of these challenges are based on solid evidence that most pseudogenes are actually pseudogenes (non-functional, degenerate copies of functional genes). But Wells says, "Yet there is growing evidence that many pseudogenes are not functionless, after all."

Types of Pseudogenes

There are three kinds of pseudogenes [Pseudogenes]. The first category contains genes that used to be functional in our ancestors but currently are non-functional. The best example is the human GULOP pseudogene that used to encode a key enzyme in the pathway for synthesis of vitamin C [Human GULOP Pseudogene]. This gene is active in most animals but it has become a pseudogene in primates and, independently, in a few other animals.


UPDATE: see: Creationists questioning pseudogenes: the GULO pseudogene

The second category includes genes that arise from a gene duplication event followed by inactivation of one of the copies. These pseudogenes tend to be located near their active siblings and they retain most of the features of the original gene except they can't produce an active product. Many of them are transcribed, especially if they have only recently become pseudogenes.

The third category is called "processed" pseudogenes. They arise when a mature mRNA molecule is copied into DNA by reverse transcriptase and the resulting DNA is integrated into the genome. Processed pseudogenes will usually not have any introns and when they integrate they will not be near a promoter. Many of them are truncated because the copying process was not complete. Processed pseudogenes were never able to produce their original functional product (protein or RNA) and they accumulate mutations at the rate expected from fixation of neutral alleles by random genetic drift.

The first two categories of pseudogene will also accumulate mutations once they become inactive. It's a characteristic of pseudogenes that the older they are the more mutations they have. Thus a pseudogene that is only found in chimpanzees and humans will have fewer mutations than one found in monkeys and apes and even fewer that one found in both rodents and primates.

The human genome contains about 20,000 pseudogenes, about the same as the number of genes. Many of these pseudogenes belong to the same family so not every gene has a corresponding pseudogene. About 6,000 of these pseudogenes arose from duplication events and 14,000 are processed. (The first category is rare.)

The pseudogenes in the "duplicated" category tend to be associated with large families of related genes. For example, in the human genome there are 414 pseudogenes in the olfactory receptor gene family [Olfactory Receptor Genes, The Evolution of Gene Families]. It's difficult to imagine how any substantial number of these genes could have a function.

As expected, the processed pseudogenes are scattered thoughout the genome because they insert at random. Roughly 2,000 of them are found in introns and this is further evidence that introns are mostly junk. Of course, if a processed pseudogene plunks down in an intron sequence it will be transcribed. Processed pseudogenes tend to come from functional genes that are abundantly expressed in the germ line. That's because the processed pseudogene has to be integrated into germ line DNA in order to be passed on to the progeny. Most of these genes are standard housekeeping genes. For example, there are 1300 pseudogenes derived from ribosomal protein genes.

Jonathan Wells describes the three categories but doesn't explain any of the other things I just mentioned.

Transcribed Pseudogenes

The first important section of his chapter is "Transcribed Pseudogenes." He quotes a number of papers showing that some pseudogenes are transcribed in humans, cows, and plants. In humans he claims that about one-fifth of pseudogenes are transcirbed at some time or another. This is probably an upper limit since most workers suggest that only 10% are transcribed.

I'm sure that some pseudogenes are transcibed. Many of the pseudogenes derived from gene duplication events will still be transcribed from active promoters even though they may not produce a functional product. Many of the processed pseudogenes will be transcribed because they are found within a gene (introns) or have fortuitously integrated near a promoter.

'Pseudogenes' That Encode Proteins

The key question is whether any pseudogenes produce a functional product and that's addressed in the next section: "'Pseudogenes' That Encode Proteins." Wells describes five studies where presumed pseudogenes were found to be genes after all (three in humans and two in fruit flies). Interesting but irrelevant. These genes are not junk. What about the other 20,000 real pseudogenes? Here's what Wells says at this point in the chapter ...

To be sure, only a relatively small proportion of known pseudogenes have been shown to encode proteins. But there is growing evidence that RNAs transcribed from pseudogenes perform essential functions in the cell

Here's where we get to the most important part of the chapter. It's in a section called "RNA Interference."

RNA Interference

RNA interference arises when one RNA molecule interferes with the expression of another. The easiest example to understand is when part of a gene is transcribed in the opposite direction producing what's called "antisense" RNA. This antisense RNA will hybridize to the functional mRNA and either block translation or induce degradation. In either case, less protein is made.

If a pseudogene is transcribed in the opposite direction then its antisense RNA could interfere with the expression of the normal gene. Wells gives us three examples of this phenomenon: one famous one from snails (1999), one from mouse oocytes (2008), and one from rice (2009). I don't know whether all these results have been confirmed but even if they have it doesn't amount to much. All kinds of strange things happen in biology and the fact that a few pseudogenes might have acquired a regulatory function isn't shocking. What about the other 20,000 pseudogenes?

Pseudogene Enhancement of Gene Expression

Theme

Genomes
& Junk DNAWell, there's always the possibility that pseudogenes could enhance gene expression. The next section is "Pseudogene Enhancement of Gene Expression." Jonathan Wells begins this section with a description of the results on the mouse Mkrn-1-p1 pseudogene. The authors of this famous 2003 Nature paper claim that transcripts from the pseudogene protect the functional mRNA by shielding it from degradation. The title of their paper is "An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene" (Hirotsune et al., 2003).

Wells devotes three paragraphs to this important paper. There's only one slight problem. This work has been discredited in a 2006 PNAS paper with the title "The putatively functional Mkrn-1-p1 pseudogene is neither expressed nor imprinted nor does it regulate its source in trans." (Gray et., 2006) Oops!

Wells knows about this 2006 paper because he discusses it in Chapter 8 when he attacks the defenders of junk DNA. In chapter 5 he adds the following remark in parentheses, "Other biologists later challenged the Makorin-1 pseudogene results, which remain controversial." I think this is the only time when he mentions any legitimate scientific controversy.

There are three other examples of pseudogenes that might have an enhancement function: one from plants and two from humans. I don't know if these studies have been confirmed but even if they have they don't have much of an impact on the possible functions of the remaining 20,000 pseudogenes.

Sequence Conservation

The only significant evidence of widespread functionality of pseudogenes comes from two studies on sequence conservation. Wells covers this in a one-page section on "Sequence Conservation." The studies purport to show that pseudogene sequences are much more conserved than expected if they are really junk DNA. These studies have not been reproduced, as far as I know, and they fly in the face of much evidence to the contrary—evidence that Wells forgets to mention.

The first paper is a review by Balakirev and Ayala (2003). They review the possible functions of some pseudogenes in Drosophila and mammals. Some of them show evidence of sequence conservation. They conclude that most pseudogenes are probably functional. A study published that same year looked at all the known pseudogenes in the human genome and concluded that 95% of them evolved as though they had no function (i.e. they were not conserved) (Torrents et al., 2003)

The second paper that Wells mentions is Khachane and Harrison (2009). They identify 68 human pseudogenes whose sequences appear to be conserved in at least two other mammals. These are good candidates for functional genes.

The strange thing about this argument is that Wells doesn't believe in common descent so the evidence of sequence conservation really shouldn't have any meaning for him. Nevertheless, he says ...

How odd! As we saw in Chapter 2, Kenneth Miller, Richard Dawkins, Douglas Futuyma, Michael Shermer, Jerry Coyne and John Avise argue that pseudogenes confirm Darwinism because they are non-functional. But if we assume that Darwinism is true and then compare the DNA of unrelated organisms, sequence similarities imply that many of their pseudogenes are functional. So nonfunction supposedly implies Darwinism, but Darwinism plus sequence conservation implies function. When it comes to conserved pseudogenes, it seems, Darwinism saws off the very branch on which it sits.

For the record, if the majority of pseudogenes really are more conserved than expected from random mutations and fixation by random genetic drift then this would, indeed, be evidence that something is going on. Maybe they do have a function we don't know about. I don't think the evidence points in this direction at all—in fact much of the evidence contradicts it. Balakirov and Ayala (2003) are just speculating. I prefer the evidence of Torrents et al. (2003) suggesting that only a small number of potential pseudogenes have a function. This is consistent with the results of Khachane and Harrison (2009).

[If all 1,000 presumed pseudogenes turned out to be real genes then this moves about 0.06% of the genome from the junk category to the functional category. This isn't enough to save the IDiots.]

The Vitamin C Pseudogene

Finally, there's a section I haven't covered. It's titled "The Vitamin C Pseudogene." Wells has to address this particular pseudogene because it's the one that comes up most often when evolutionary biologists (e.g. Ken Miller and Jerry Coyne) criticize Intelligent Design Creationism. Here's what Wells says,

The evidence is not as straightforward as Miller and Coyne make it out to be, however, and their argument is ultimately circular. In any case, common ancestry and intelligent design are two different issues, and the vitamin C story would take us on a detour from the issue of junk DNA that's the focus of this book, so the details are omitted here and included in an appendix.

Which brings us to the Appendix: "The Vitamin C Pseudogene."

The main argument of scientists like Ken Miller and Jerry Coyne is not that the GULOP pseudogene exists. It's that the GULOP gene and its pseudogene are at the same location in the genomes of all mammals. In the primate lineage this gene is non-functional due to a number of mutations that make it impossible to produce a functional protein. Some of the same deactivating mutations are found in related species such as humans and chimpanzees. This suggests strongly that the non-functional pseudogene was inherited from a common ancestor. How do Intelligent Design Creationists deal with this evidence?

How does Wells respond?

... intelligent design and common ancestry are two different issues. Major ID proponents pointed this out before Miller wrote his book....Although some ID proponents (including me) question universal common ancestry on empirical grounds (as do some evolutionary biologists), intelligent design is not necessarily inconsistent with common ancestry.

I'm not sure what this means. Does it mean that people like Wells are completely bamboozled by this data since they can't refute either the evidence of common descent or the evidence of bad design? Other IDiots, like Michael Behe, only have to explain the bad design?

Jerry Coyne has published a similar argument but Wells attacks him on two fronts. First, he claims that human and chimpanzee Y chromosomes differ by 60 million nucleotide substitutions. If they really have a common ancestor then one would expect much greater sequence similarity. According to Wells, "If similarities in the vitamin C pseudogene are evidence for common ancestry, then differences in the Y chromosome are presumably evidence against it."

The Y chromosome paper is Hughes et al. (2010). Their results show that in orthologous regions of the Y chromosomes the human and chimp sequences are 98.3% identical. However, the chimp and human chromosomes differ in other regions because of large inserts and deletions. This is still evidence of common ancestry.

As usual, Wells is wanting to have his cake and eat it too.

The second attack is based on a number of quibbles. Coyne said that all primates need vitamin C in their diets but Wells points out that prosimians are primates and they can make vitamin C. Furthermore, according to Wells the requirement for vitamin C has only been established in nine species of monkeys. There are 251 other species and we don't know if they need vitamin C. Not only that, Coyne claimed that all primates have the same single nucleotide deletion in their GULOP pseudogene but Wells is quick to point out that only five primate sequences have been published.

Put that in your pipe and smoke it, Jerry Coyne! I assume that Wells is completely incapable of answering the challenge that's been issued and that's why he resorts to red herrings.

Continuing with this shotgun approach we quickly encounter several other arguments that are designed to distract from the main topic.

• "Miller and Coyne rely on speculations about the motives of the designer or creator that have no legitimate place in natural science." (I hope you turned off your irony meter before reading that.)
• Miller and Coyne have not provided any evidence to justify their claim that the GLO pseudogene is completely nonfunctional.
• (Turn off your irony meter!) Their argument is circular. The similarities in sequence between chimp and human pseudogenes could be due to natural selection. "To break the circle, Miller and Coyne would either have to establish the recent ancestry of humans and chimps on other grounds (but why then bother invoking the vitamin C pseudogene at all?), or they would first have to establish that the vitamin C pseudogene has no function whatsoever (but this is impossible). So their argument not only fails to refute ID, but it also fails to establish that humans and chimps are descended from a common ancestor."

I feel a bit sorry for Ken Miller and Jerry Coyne. If this is the best the IDiots can do then why bother trying to argue with them in the first place?

Thus endeth Chapter 5.

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Gray TA, Wilson A, Fortin PJ, Nicholls RD. (2006) The putatively functional Mkrn1-p1 pseudogene is neither expressed nor imprinted, nor does it regulate its source gene in trans. Proc. Natl. Acad. Sci. USA 103:12039-12044. [PDF]

Hirotsune, S., Yoshida, N., Chen, A., Garrett, L., Sugiyama, F., Takahashi, S., Yagami, K., Wynshaw-Boris, A., and Yoshiki, A. (2003) An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene. Nature 423:91-6. [PDF]

Hughes, J.F., Skaletsky, H., Pyntikova, T., Graves, T.A., van Daalen, S.K., Minx, P.J., Fulton, R.S., McGrath, S.D., Locke, D.P., Friedman, C., Trask, B.J., Mardis, E.R., Warren, W.C., Repping, S., Rozen, S., Wilson, R.K., and Page, D.C. (2010) Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content. Nature 463:536-539. [Nature]

Khachane, A.N., and Harrison, P.M. (2009) Assessing the genomic evidence for conserved transcribed pseudogenes under selection. BMC Genomics 15:435-449. [PDF]

Torrents, D., Suyama, M., Zdobnov, E., and Bork, P.. (2003) A genome-wide survey of human pseudogenes. Genome Res. 13:2559-2567. [PDF]

Junk & Jonathan: Part 7—Chapter 4

This is part 7 of my review of The Myth of Junk DNA. For a list of other postings on this topic see the link to Genomes & Junk DNA in the "theme box" below or in the sidebar under "Themes."

The title of Chapter 4 is Introns and the Splicing Code. It opens with a brief description of eukaryotic genes and alternative splicing. Here's a better description of splicing for those who want a quick refresher: RNA Splicing: Introns and Exons. Alternative splicing is when a transcript can be spliced in at least two different ways to produce 2 distinct mRNAs. Each of them will make a different, but related, protein. The process has been known for thirty years and the mechanism is well-understood. It's described very well in a Wikipedia article: Alternative Splicing.

Here's some important background information from Junk in Your Genome: Protein-Encoding Genes.

The minimum size of a eukaryotic intron is less than 50 bp. For a typical mammalian intron, the essential sequences in the introns are: the 5′ splice site (~10 bp); the 3′ splice site (~30 bp): the branch site (~10 bp); and enough additional RNA to form a loop (~30 bp). This gives a total of 80 bp of essential sequence per intron or 20,500 × 7.2 × 80 = 11.8 Mb. Thus, 0.37% of the genome is essential because it contains sequences for processing RNA.

In other words, assuming that introns aren't all junk we can estimate how much of the intron sequence is essential for it's function by taking into account the known regulatory sequences and the amount needed to form a loop.

The rest of an intron sequence may be junk. If it is, then we would expect to see two things.

• Considerable variation is intron size from species to species.
• Frequent examples of transposons, endogenous retroviruses, and even other genes inserting into introns.

This is exactly what we see [Junk in Your Genome: Intron Size and Distribution]. There's no indication that intron sequences are conserved or essential.

Jonathan Wells explains that alternative splicing is important in some genes. He is correct. He then explains that there are sequences in introns that regulate alternative splicing. He's correct about that as well. We've been writing this up in the textbooks and teaching it in introductory biochemistry courses since early in the 1980s. The classic example is the determination of sex in Drosophila—it's largely controlled by alternative splicing and we know a great deal about which proteins bind to which sequences in the introns to promote or repress a given splice site [Sex in the fruit fly Drosophila melanogaster].

Nothing new here. We know about binding sites and we know that most of them are 10 bp or less. Their presence makes no significant difference in our calculations of junk DNA. I get the distinct impression that Wells and the other IDiots don't really understand splicing and alternative splicing.

Here's a series of blog posts I did last year when Richard Sternberg tried to pretend that he knew something about molecular biology and alternative splicing. Later on, Jonathan Wells weighs in to try and help his friend but ends up showing that he too, is in way over his head.

Creationists, Introns, and Fairly Tales

IDiots Do Arithmetic a Second Time - Same Result

Jonathan Wells Weighs in on Alternative Splicing

Having "proven" that something like 0.03% of our genome may not be junk, Wells then goes on to describe other sequences that are found in introns. Some of these are regulatory sequences or enhancers. These aren't common, but they do exist. They're usually located in the 5′ intron and they are often associated with alternative transcription start sites. The total amount of non-junk DNA due to regulatory sequences has already been taken into account in my calculations (Junk in Your Genome: Protein-Encoding Genes) and it doesn't matter whether these regulatory sequences are intergenic or included within an intron.

Theme

Genomes
& Junk DNAWells also notes that many genes for small RNAs are located within introns. These include some of the genes for the splicing machinery, tRNA genes, snoRNA genes etc. He doesn't mention that introns are also loaded with Alu sequences and other transposable elements (mostly defective). The presence of the these insertions show us that cells don't discriminate between intron sequences that make up 25% of the genome and the remaining 65% that's mostly junk. They are all targets for inserting small genes and transposons. No surprises here.

Finally, on the last page of Chapter 4, Wells devotes two paragraphs to a genuine scientific argument. The idea is that long introns might be necessary to delay transcription. This idea has been around for a long time. It was originally proposed over 25 years ago as an explanation for the long introns found in Drosophila HOX genes, especially Ubx.

If a gene has several long introns it can stretch out over 100 kb (100,000 bp). The typical RNA polymerase II elongation complex transcribes at a rate of 50 bp per second so it will take more than 30 minutes to transcribe these long genes. The idea is that the presence of long introns delays appearance of the regulatory proteins during development. This seems unlikely because there are many other, more efficient, ways of regulating gene expression. As a matter of fact, the argument can be easily turned upside down.

Genes that need to be transcribed quickly have very short introns or none at all. The heat shock inducible genes, for example, don't even have introns. These genes need to be expressed rapidly when a cell encounters stressful conditions. Their non-inducible homologues all have respectable introns so it looks like there has been selection for losing introns in these genes.

Similarly, there are often testes specific genes than lack introns. The supposition is that these variant family members have lost introns so they can be quickly transcribed during spermatogenesis. The globin genes have relatively small introns and they are also expressed at a high rate in erythroblasts.

Genes that are infrequently transcribed tend to accumulate large introns. This includes most developmentally regulated transcription factors that only need to produce a small number of proteins at a specific time in the life of the organism. These observations are consistent with the idea that excess junk in intron sequences is removed when necessary. It's actually evidence that those sequences are junk.

So far we covered the evidence of probable function in Chapter 3 and seen that Wells does not critically examine the data on pervasive transcription but simply assumes it is correct. He then makes the unsubstantiated claim that evidence of transcription is evidence of function. He's wrong about the claim that most of our genome is transcirbed and he's wrong to assume that all transcripts are functional. Nothing in that chapter supported his claim that junk DNA is a myth.

In this chapter we see the first evidence for specific functions of noncoding DNA. The presence of regulatory sequences in introns has been well known for decades and it has no impact on the estimates of junk DNA. The idea that big introns might be adaptive regardless of sequence is possible but not reasonable. In fact, the evidence suggests strongly that big introns full of junk DNA can be detrimental in some cases. Nothing in Chapter 4 provides convincing evidence that junk DNA is a myth.

What about pseudogenes? Are they a myth? That's covered in Chapter 5.

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A note about references
The IDiots are promoting this book by bragging about multiple references that challenge the concept of junk DNA [Jonathan Wells offers over 600 references to recent peer-reviewed literature]. Chapters 1 and 2 were introductions to the problem. They had a total of 51 references. Chapter 3 had 62 references but, as we have seen, they don't add up to a convincing case. There were plenty of references that should have been included if a scientific case was going to be made. Chapter 4 has 63 references but only three of them address a substantive argument against junk DNA in introns. All three make the same point; namely that long introns delay transcription.

That's a total of 176 references so far with nothing much to show for them. There are 432 references in the rest of the book. There are 26 references to known IDiots including 8 references to the work of Jonathan Wells.

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Junk & Jonathan: Part 6—Chapter 3

This is part 6 of my review of The Myth of Junk DNA. For a list of other postings on this topic see the link to Genomes & Junk DNA in the "theme box" below or in the sidebar under "Themes."

We learn in Chapter 9 that Wells has two categories of evidence against junk DNA. The first covers evidence that sequences probably have a function and the second covers specific known examples of functional sequences. In the first category there are two lines of evidence: transcription and conservation. Both of them are covered in Chapter 3 making this one of the most important chapters in the book. The remaining category of specific examples is described in Chapters 4-7.

The title of Chapter 3 is Most DNA Is Transcribed into RNA. As you might have anticipated, the focus of Wells' discussion is the ENCODE pilot project that detected abundant transcription in the 1% of the genome that they analyzed (ENCODE Project Consortium, 2007). Their results suggest that most of the genome is transcribed. Other studies support this idea and show that transcripts often overlap and many of them come from the opposite strand in a gene giving rise to antisense RNAs.

The original Nature paper says,

... our studies provide convincing evidence that the genome is pervasively transcribed, such that the majority of its bases can be found in primary transcripts, including non-protein-coding transcripts, and those that extensively overlap one another.

The authors of these studies firmly believe that evidence of transcription is evidence of function. This has even led some of them to propose a new definition of a gene [see What is a gene, post-ENCODE?]. There's no doubt that many molecular biologists take this data to mean that most of our genome has a function and that's the same point that Wells makes in his book. It's evidence against junk DNA.

What are these transcripts doing? Wells devotes a section to "Specific Functions of Non-Protein-Coding RNAs." These RNAs may be news to most readers but they are well known to biochemists and molecular biologists. This is not the place to describe all the known functional non-coding RNAs but keep in mind that there are three main categories: ribosomal RNA (rRNA), transfer RNA (tRNA), and a heterogeneous category called small RNAs. There are dozens of different kinds of small RNAs including unique ones such as the 7SL RNA of signal recognition factor, the P1 RNA of RNAse P and the guide RNA in telomerase. Other categories include the spliceosome RNAs, snoRNAs, piRNAs, siRNAs, and miRNAs. These RNAs have been studied for decades. It's important to note that the confirmed examples are transcribed from genes that make up less than 1% of the genome.

One interesting category is called "long noncoding RNAs" or lncRNAs. As the name implies, these RNAs are longer that the typical small RNAs. Their functions, if any, are largely unknown although a few have been characterized. If we add up all the genes for these RNAs and assume they are functional it will account for about 0.1% of the genome so this isn't an important category in the discussion about junk DNA.

Theme

Genomes
& Junk DNASo, we're left with a puzzle. If more than 90% of the genome is transcribed but we only know about a small number of functional RNAs then what about the rest?

Opponents of junk DNA—both creationists and scientists—would have you believe that there's a lot we don't know about genomes and RNA. They believe that we will eventually find functions for all this RNA and prove that the DNA that produces them isn't junk. This is a genuine scientific controversy. What do their scientific opponents (I am one) say about the ENCODE result?

Criticisms of the ENCODE analysis take two forms ...

• The data is wrong and only a small fraction of the genome is transcribed
• The data is mostly correct but the transcription is spurious and accidental. Most of the products are junk RNA.

Criticisms of the Data

Several papers have appeared that call into question the techniques used by the ENCODE consortium. They claim that many of the identified transcribed regions are artifacts. This is especially true of the repetitive regions of the genome that make up more than half of the total content. If any one of these regions is transcribed then the transcript will likely hybridize to the remaining repeats giving a false impression of the amount of DNA that is actually transcribed.

Of course, Wells doesn't mention any of these criticisms in Chapter 3. In fact, he implies that every published paper is completely accurate in spite of the fact that most of them have never been replicated and many have been challenged by subsequent work. The readers of The Myth of Junk DNA will assume, intentionally or otherwise, that if a paper appears in the scientific literature it must be true.

But criticism of the ENCODE results are so widespread that they can't be ignored so Wells is forced to deal with them in Chapter 8. (Why not in Chapter 3 when they are first mentioned?) In particular, Wells has to address the van Bakel et al. (2010) paper from Tim Hughes' lab here in Toronto. This paper was widely discussed when it came out last year [see: Junk RNA or Imaginary RNA?]. We'll deal with it when I cover Chapter 9 but, suffice to say, Wells dismisses the criticism.

Criticisms of the Interpretation

The other form of criticism focuses on the interpretation of the data rather than its accuracy. Most of us who teach transcription take pains to point out to our students that RNA polymerase binds non-specifically to DNA and that much of this binding will result in spurious transcription at a very low frequency. This is exactly what we expect from a knowledge of transcription initiation [How RNA Polymerase Binds to DNA]. The ENCODE data shows that most of the genome is "transcribed" at a frequency of once every few generations (or days) and this is exactly what we expect from spurious transcription. The RNAs are non-functional accidents due to the sloppiness of the process [Useful RNAs?].

Wells doesn't mention any of this. I don't know if that's because he's ignorant of the basic biochemistry and hasn't read the papers or whether he is deliberately trying to mislead his readers. It's probably a bit of both.

It's not as if this is some secret known only to the experts. The possibility of spurious transcription has come up frequently in the scientific literature in the past few years. For example, Guttmann et al. (2009) write,

Genomic projects over the past decade have used shotgun sequencing and microarray hybridization to obtain evidence for many thousands of additional non-coding transcripts in mammals. Although the number of transcripts has grown, so too have the doubts as to whether most are biologically functional. The main concern was raised by the observation that most of the intergenic transcripts show little to no evolutionary conservation. Strictly speaking, the absence of evolutionary conservation cannot prove the absence of function. But the remarkably low rate of conservation seen in the current catalogues of large non-coding transcripts (less than 5% of cases) is unprecedented and would require that each mammalian clade evolves its own distinct repertoire of non-coding transcripts. Instead, the data suggest that the current catalogues may consist largely of transcriptional noise, with a minority of bona fide functional lincRNAs hidden amid this background.

This paper is in the Wells reference list so we know that he has read it.

What these authors are saying is that the data is consistent with spurious transcription (noise). Part of the evidence is the lack of any sequence conservation among the transcripts. It's as though they were mostly derived from junk DNA.

Sequence Conservation

Recall that the purpose of Chapter 3 is to show that junk DNA is probably functional. The first part of the chapter reportedly shows that most of our genome is transcribed. The second part addresses sequence conservation.

Here's what Wells says about sequence conservation.

Widespread transcription of non-protein-coding DNA suggests that the RNAs produced from such DNA might serve biological functions. Ironically, the suggestion that much non-protein-coding DNA might be functional also comes from evolutionary theory. If two lineages diverge from a common ancestor that possesses regions of non-protein-coding DNA, and these regions are really nonfunctional, then they will accumulate random mutations that are not weeded out by natural selection. Many generations later, the sequences of the corresponding non-protein-coding regions in the two descendant lineages will probably be very different. [Due to fixation by random genetic drift—LAM] On the other hand, if the original non-protein-coding DNA was functional, then natural selection will tend to weed out mutations affecting that function. Many generations later, the sequences of the corresponding non-protein-coding regions in the two descendant lineages will still be similar. (In evolutionary terminology, the sequences will be "conserved.") Turning the logic around, Darwinian theory implies that if evolutionarily divergent organisms share similar non-protein-coding DNA sequences, those sequences are probably functional.

Wells then references a few papers that have detected such conserved sequences, including the Guttmann et al. (2009) paper mentioned above. They found "over a thousand highly conserved large non-coding RNAs in mammals." Indeed they did, and this is strong evidence of function.¹ Every biochemist and molecular biologist will agree. One thousand lncRNAs represent 0.08% of the genome. The sum total of all other conserved sequences is also less than 1%. Wells forgets to mention this in his book. He also forgets to mention the other point that Guttman et al. make; namely, that the lack of sequence conservation suggests that the vast majority of transcripts are non-functional. (Oops!)

There's irony here. We know that the sequences of junk DNA are not conserved and this is taken as evidence (not conclusive) that the DNA is non-functional. The genetic load argument makes the same point. We know that the vast majority of spurious RNA transcripts are also not conserved from species to species and this strongly suggests that those RNAs are not functional. Wells ignores this point entirely—it never comes up anywhere in his book. On the other hand, when a small percentage of DNA (and transcripts) are conserved, this gets prominent mention.

Wells doesn't believe in common ancestry so he doesn't believe that sequences are "conserved." (Presumably they reflect common design or something like that.) Nevertheless, when an evolutionary argument of conservation suits his purpose he's happy to invoke it, while, at the same time, ignoring the far more important argument about lack of conservation of the vast majority of spurious transcripts. Isn't that strange behavior?

The bottom line hear is that Jonathan Wells is correct to point to the ENCODE data as a problem for junk DNA proponents. This is part of the ongoing scientific controversy over the amount of junk in our genome. Where I fault Wells is his failure to explain to his readers that this is disputed data and interpretation. There's no slam-dunk case for function here. In fact, the tide seems to turning more and more against the original interpretation of the data. Most knowledgeable biochemists and molecular biologists do not believe that >90% of our genome is transcribed to produce functional RNAs.

UPDATE: How much of the genome do we expect to be transcribed on a regular basis? Protein-encoding genes account for about 30% of the genome, including introns (mostly junk). They will be transcribed. Other genes produce functional RNAs and together they cover about 3% of the genome. Thus, we expect that roughly a third of the genome will be transcribed at some time during development. We also expect that a lot more of the genome will be transcribed on rare occasions just because of spurious (accidental) transcription initiation. This doesn't count. Some pseudogenes, defective transposons, and endogenous retroviruses have retained the ability to be transcribed on a regular basis. This may account for another 1-2% of the genome. They produce junk RNA.

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1. Conservation is not proof of function. In an effort to test this hypothesis Nöbrega et al. (2004) deleted two large regions of the mouse genome containing large numbers of sequences corresponding to conserved non-coding RNAs. They found that the mice with the deleted regions showed no phenotypic effects indicating that the DNA was junk. Jonathan Wells forgot to mention this experiment in his book.

Guttman, M. et al. (2009) Chromatin signature reveals over a thousand highly conserved non-coding RNAs in mammals. Nature 458:223-227. [NIH Public Access]

Nörega, M.A., Zhu, Y., Plajzer-Frick, I., Afzal, V. and Rubin, E.M. (2004) Megabase deletions of gene deserts result in viable mice. Nature 431:988-993. [Nature]

The ENCODE Project Consortium (2007) Nature 447:799-816. [PDF]

A Poll: How Much of the Human Genome Is Junk?

It's time for another poll. Please answer the question in the sidebar.

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