Junk DNA and evolution

I’ve been reading about junk DNA on Reasons to Believe’s website. Their claim is very similar to the claims by YECs. I think they claim that any DNA that is transcribed, is functional. That is clearly an exaggeration - because scientists don’t know what most RNAs do!

And what do they mean by “function” anyway? No one ever really defines it clearly!

Anyone want to attempt responses at the three points written by Dr. Rana?

I think you already have a handle on some of the problems with assuming whatever is transcribed is ‘functional’.

On pervasive transcription:

On ‘Junk DNA’ generally:

There is absolutely no reason to believe that only functional DNA is transcribed into RNA. There is every reason to believe that leaky RNA transcriptase activity and non-specific transcription factor binding will result in the transcription of junk DNA. The null hypothesis is that an RNA molecule has no function. In order to claim that an RNA molecule has function you need evidence that it is functional. It’s mere existence is not evidence for function.[quote=“SamuraiChamploo, post:1, topic:36081”]
And what do they mean by “function” anyway? No one ever really defines it clearly!

Depends on who you talk to. The definition used by ENCODE was “changes the biochemistry of the cell”. By that definition, the trash in your kitchen trash can has function because it changes the biochemistry of the air in your kitchen. IOW, ENCODE used a definition of function that included junk DNA. Most people define function as a stretch of DNA that has sequence specific activity which impacts the fitness of the organism. This type of function is often detected by sequence conservation, although not all functional DNA can be detected by this method.[quote=“SamuraiChamploo, post:1, topic:36081”]
Anyone want to attempt responses at the three points written by Dr. Rana?

Skimming through the article, it appears that Dr. Rana uses the same bad argument that many other ID/creationists use. They play the definition game. For example, they will point out that junk DNA is non-coding DNA. They will then find some non-coding DNA that has function, and claim that there is no junk DNA. They use the Association Fallacy:

All A’s are B
B, Therefore A.

We can find other examples of this fallacy, such as “All Chevy Malibu’s are cars. My brother bought a car, therefore it must be a Malibu.” What the ID/creationists fail to understand is that no one is saying that all non-coding DNA is junk DNA. Junk DNA is just a subset of all non-coding DNA just as Chevy Malibu’s are a subset of all cars.

They also use a generalization fallacy. If they can find a 100 base pair stretch of DNA that was once thought to be junk but is now thought to have function, they will claim that this one example means that the other 2.5 billion bases of junk DNA must also have function. That’s nonsense.

However, the most basic error the make is thinking that evolution predicts junk DNA. It doesn’t. No one is saying that evolution is true because there is junk DNA. For example, the bladderwort genome is almost entirely functional, yet no one is claiming that it falsifies evolution. Evolution allows for genomes to have a lot of junk or very little junk. The only thing that junk DNA seems to clash with is the ID/creationist claim that God made genomes with 100% functionality.

If there are specific points of the article that you have questions on fee free to ask.


I couldn’t help myself and had to respond to point #1:

“Finding #1: Junk DNA Plays a Role in Embryonic Development”

This finding falls under the heading of the Association Fallacy. Scientists are saying that junk DNA includes Alu sequences. However, no scientist is saying that all Alu sequences are junk. Therefore, finding functional Alu sequences does not disprove the conclusion that many Alu sequences are junk. The same applies to ERVs.

On top of that, finding a functional Alu element that was previously thought to be junk does not prove that all Alu elements are functional. There are tons of repeat regions related to transposons and retroviruses, so it is a bit silly to say that they are all functional because you found a handful that are functional. Here is table 11 from the human genome paper:


According to the human genome paper there are just over 1 million Alu copies in the human genome, and they make up about 10% of the total human genome. Finding 100 or so functional Alu copies that span a tiny fraction of the human genome is not evidence that all 1 million Alu copies have function.


I think there’s an even more fundamental error in the article. ERVs, Alus and duplicate genes aren’t evidence of common descent because they’re junk; they’re evidence for common descent because they’re mutations that are shared across related species. We know how they occur as mutations, we see how they are shared, and we can often even date them approximately based on their genetic divergence. Because they are complex mutations, the same mutation is unlikely to occur by chance in exactly the same location, and so there’s little noise from convergent evolution. The fact that sometimes a mutation turns out to be functionally useful is irrelevant to assessing common descent.

One of the nice things about duplicated genes, by the way, is that some of them are not merely duplicated DNA: they’re actually produced from mRNA that’s been processed (introns removed, poly-A tail added) and then copied back into DNA before being incorporated into the genome. The new gene bears the tell-tale marks of duplication, which is an odd state of affairs if you think an all-powerful designer put it there apart from natural processes – why not just create a new gene out of whole cloth?

Final note: the possibility that sequence bulk has a selective advantage – that the total amount of DNA matters, regardless of the sequence – is not a new one, nor is it relevant to the question of junk DNA. Junk DNA is defined as DNA whose sequence composition has no effect on the organism; by that definition, DNA that is useful only because it bulks up the nucleus can easily be junk. The hypothesis has been around since at least the early 70s, and evidence has been advanced for it on more than one occasion.

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I thought about discussing that as well. All too often I have come across creationists who think that evolutionists are citing ERVs as evidence because they are junk. Little do they know that ERVs would be smoking gun evidence for common ancestry even if every single one of them was functional. The divergence of the 5’ and 3’ LTR of an individual ERV is also a compelling piece of evidence.[quote=“glipsnort, post:5, topic:36081”]
Junk DNA is defined as DNA whose sequence composition has no effect on the organism; by that definition, DNA that is useful only because it bulks up the nucleus can easily be junk.

To use an analogy, bulk DNA is as functional as the trash in a landfill.

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I agree with the responses of the others, but to see the absurdity of the article, we only have to go through the title to see a blatant straw man fallacy:

“Three (More) Reasons Why Junk DNA Is No Longer Evidence for Evolution”

If all evolution was Darwinian, there should be no junk DNA–in reality junk DNA is evidence supporting non-Darwinian evolution (neutral or drift).

Of course, admitting the very existence of non-Darwinian evolution throws a wrench into their polemics about “Darwinists.” How can a scientist be an evil “Darwinist” if she studies non-Darwinian evolutionary mechanisms?

It’s a bit like arguing against the existence of gravity by pointing to non-Newtonian gravitational effects, like the precession in Mercury’s orbit.

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Hi T -

Not being a professional biologist, I have no idea what an LTR is. Would you be so kind as to elaborate? Thanks and have a great weekend!

Chris Falter

I love talking about this subject, so I would be happy to.

The first part is understanding what 5’ and 3’ are. These refer to the carbons in the sugar molecule that makes up the backbone of a DNA molecule.

This is what gives “direction” to the molecule. The proteins that copy DNA start at the 5’ side of the molecule and move towards the 3’ side.

LTR stands for long terminal repeats. These are like the bookends of the retroviral genomes. They are regions with repeating letters of DNA that cause RNA transcriptases to bind to the string of DNA and produce RNA from the viral genes. You have often heard that retroviruses “take over the cells machinery and force it to make many copies of new viruses”. Well, the LTRs are what does that.


As you can see, there is an LTR on the 5’ side of the DNA and one on the 3’ side. That is what they are called the 5’ and 3’ LTRs. The interesting part of this whole story is that before integration of the retroviral genome into the host genome the viral proteins use one LTR to create the other LTR. Therefore, at the time of insertion into the host genome the LTRs have identical sequence.

Why is this important? Since they are identical at the time of insertion we know that any differences between the LTRs of a single ERV are due to the accumulation of mutations since the time of insertion. This allows us to use LTR divergence as a genetic marker for tracing evolution. The longer an ERV has been in the host genome the more differences we should see between the LTRs. Therefore, one can predict that an ERV insertion shared by all primates should have more more divergence between the 5’ and 3’ LTRs than an ERV shared by just chimps and humans, and that is exactly what we see.

If you are interested in reading the technical peer review paper on the subject, it can be found here:

“Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A). Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication.”


It’s worth noting that there’s plenty of junk translation too, in the sense that RNAs and proteins whose absence is lethal are expressed long (weeks in mice, months in humans) before the time at which one can detect any phenotype in a null mutant.

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