Junk DNA, Rana, and Cardinale

@dsterncardinale interviews Fuz from RTB in Junk DNA. Seems like this might turn out to be a productive conversation.


For what it’s worth, I thought this was really fun and very productive. But I’m biased.


Just for purposes of discussion: productive in what way?

One thing that people like Dr. Rama need to be pushed on - many (most) of the functions they see in non- protein coding DNA are, by ID standards, low or zero information functions. Structural roles for (organizing, nuclear volume, etc.), microRNA targeting, binding of individual transcription factors, these and more involve short and/or minimally conserved sequences. This flies in the face of the ID party line.

If ID is about information, then what we know about the functioning of noncoding DNA is not consistent with ID theory.


Hi Dan
I sent this discussion to a couple of friends and called you Dr Dave by mistake again.:slight_smile: I did send a correction.

Congratulations on this video. I think it is an example of two different scientific views finding common ground and learning from each other.

One aspect I would consider is the measurement needs to include level of transcriptional activity during embryo development.

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Along the lines of junk (in general), it bears mentioning that cells devote a significant proportion of their genomic budget to turnover and degradation. Thousands of genes encode a machinery that throws aways much (most) of what the cell makes (nucleic acids and proteins). Among other things, these surveillance systems target the products of transcription of junk DNA. Thus, if one is compelled to infer function from transcriptional activity, one implies that the function of an untoward fraction of the eukaryotic genome is to make, for want of a better term, garbage.

Chemically and thermodynamically, this all makes perfect sense. But from an ID perspective, it is ludicrous.


Productive in that we were able to drill down into the specifics of where we agree and disagree and why that’s the case for the specific places where we disagree. I feel like a lot of these discussions is talking past each other, so I always try to get everyone involved to clearly and specifically articulate what their actual argument is before getting to the “disagree on the internet” part, and I think this is a pretty successful example of that.


Hi Art
Are you referring to the ubiquitin system?

Obviously not. While some people claim that there are no stupid questions…


This is weird. In essence, what you are saying is that if one infers function from some phenomenon P giving rise to some entity E targeted by some surveillance system, then one implies that the function of a fraction of the genome is to make garbage. Would you say that for P=translation and E=polypeptides ?

Fair enough. I may actually have to look at the video. One assumes that the specific places are intractable. True?

I thought one of your analogies, which Fuz seemed to get, was really helpful.

You discussed how drafty windows and rafters will make a room cooler, and the thermostat will need to compensate. The drafty features are contributing to the temperature, but it would be a mistake to think that their purpose is to lower the temp so the thermostat compensates.

That’s a good way of explaining on difference between biochemical activity and function, as ID means it.


IF one were to infer function. The alternative is to accept that there is no function for said phenomenon. @swamidass mentioned an analogy described by @dsterncardinale:

There is no need to infer a function for the draft. It exists owing to the features of the room. Likewise, for much (most) of the DNA in the eukaryotic genome, the features noted by ENCODE and other research that are associated with so-called junk DNA are like the draft - they do not reflect any sort of function but rather the inevitabilities associated with the biochemistry that underlies much of the workings of the cell.

Generally speaking, no. But I am not sure what is meant by the question.

That, as well as RNA surveillance systems (of which there are several).

And more. Consider, for example, the fact that plants possess two novel DNA-dependent RNA polymerases (Pol IV and Pol V). These two enzymes are sources of transcripts derived from particular genomic regions. These RNAs do have function - they work to suppress transcription of these regions by RNA polymerase II. Pol IV/Pol V target repetitive DNA (transposable elements and the like), and thus reduce or eliminate transcription of repetitive DNA.

Those who think along the lines of Mattick et al. would likely view the products of Pol IV/Pol V transcription (short RNAs with no protein-coding capacity) as evidence for function of repetitive DNA itself. However, they are reflections of rather the opposite.


There are no stupid questions… but there are stupid people.

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That’s what many anti-junk proponents (like the first press releases of the ENCODE fiasco) do. The mere fact that some locus is transcribed is inferred to make it functional.

They seem to completely ignore things like transcriptional level, degree of conservation, the actual properties of the sequence being expressed(for example, such as it being mutationally degrading fragments of ancient transposons), where in the body it is expressed, that much of it is actively suppressed, and crucially to Art’s point, how quickly it is degraded again and so on.

Given that all these factors are basically ignored and the mere detection of a transcript is taken as grounds for concluding it is functional, when we then learn that much of these junk transcripts are quickly degraded again, that at face value implies it’s function is to be degraded again.
It’s a reductio ad absurdum against these types of function inferences of course: We are not supposed to conclude that it’s function is to be degraded. Given an understanding of all the relevant data, the conclusion is it is functionless junk.

It is difficult to think of how else nonfunctional DNA could behave if it is insufficient to point out that it is being transcribed at a very low level, having sequences that are not being conserved by purifying selection, that look like degrading repetitive fragments of ancient transposons, which almost never leave the nucleus and have extremely short half-lives because it’s immediately targeted for degradation. Then what the hell does it take to convince anti-junkers that most of eukaryotic genomes are junk?

Their resistance to the junk conclusion from entirely reasonable and basic inferences from biochemical and comparative genetics-data is making their function-hypothesis basically unfalsifiable.


Larry Moran is (in)famous for his blog posts on junk DNA over at Sandwalk. One of my favorites over the last year or so is this article:

The post focuses on this quote from the ENCODE paper:

As laid out in the blog post, some quick math leads to a rather problematic conclusion. If these enhancers are all truly functional, then there are an average of about 50 enhancers per gene. No one knows of a single gene in the human genome whose expression is governed by 50 enhancers, much less 50 being an average. Just from this math alone, it becomes very apparent that not all of these enhancers are functional.

Moran also posted this quote:

I think that perfectly sums up the entire debate. Chemistry is messy, and biology is even messier. It isn’t at all surprising that there is junk DNA in the human genome given the number of genes and the number of bases in the genome. We should expect non-functional DNA to be transcribed, and for random non-functional sequences to bind transcription factors. Add in the lack of sequence conservation, and the conclusion seems rather unavoidable.


That’s a point I made quite a few years ago:

Interestingly, Ann Gauger actually addressed these concepts over at ENV.

It would appear that @agauger chose “lots of junk DNA” for the human genome since only a tiny fraction of sequence in the human genome produces proteins with enzymatic function.


Another very odd definition of function, since proteins can have structural, ligand, and other roles besides enzymatic activity.


And anyway, as we discussed in this thread, enzymatic activity isn’t particularly rare anyway (contra Axe).


Assuming you’re referring to Axe’s 2004 paper…I mean my goodness, the man just butchers the basics there. He “calculates” the probability of arriving at a specific functional protein fold and extrapolates that to the likelihood of any functional fold evolving. I mean, c’mon. That’s not even trying, even by DI hack standards.