But what you really ought to do is read about transposons, which are super cool; and once you see how transposons work, I think you’ll see why we don’t have to imagine that they all have advantageous functions for us, any more than we imagine that the cold or flu viruses are advantageous to us. For the most part we have them because we can’t get rid of them; they’re ‘alive’ for themselves, not for us.

If they are functional, and not junk, then don’t you need more numbers to justify why you lumped in the entire amount of transposable elements as junk, say, numbers to suggest which fraction of transposable elements have not been co-opted for evolutionary fitness and which have? The OP says “Indeed, we are now finding many interesting examples of transposon-derived stuff being co-opted for organismal function (but these are the exception, not the rule).” The last clause makes a definitive statement (upper bound on prevalence), while the opening clause suggests the number is increasing: is there data to suggest an upper bound? Are you saying “these are currently the exception, not the rule, and it’s my belief this won’t change”?

The OP says “The ‘junk DNA’ question is about how much DNA has essentially no direct impact on the organism’s phenotype – roughly, what DNA could I remove (if I had the technology) and still get the same organism.” That, too, is imprecise: is a human with HER2 mutation the same phenotype as one without? If you removed introns completely, would RNA splicing work? What if it worked only half the time, is that a different phenotype? What if the intron required a certain minimum number of base pairs for splicing to work, which part of the intron is functional and which is not, and could the standard measures of selective pressure identify function? If you removed everything in a 5′ UTR except the exact regulatory sequence, would that work, or is the “regulatory sequence” a sequence-specific part plus a non-sequence-specific spacing to allow a 3D molecule to bind a certain sequence and still have room to accomodate the rest of its structure? Which is functional, and can you measure the selective pressure for that? Is it about REMOVING that DNA, or is it in practice about which stretches of DNA repress point mutations, and thus are non-redundant and sequence-specific?

Wandering further off, if you eliminated the introns and the spliceosome, such that the same transcript got generated, is that the same phenotype and organism? Or have you created a new, intron-and-spliceosome-free organism? If that organism proved horribly more susceptible to attack/disabling by transposable elements, such that it died out, would that constitute proof that those parts of DNA were not junk but selectively functional? What if it didn’t die out, but became obviously different? If there were multiple splicings, and in your non-splicing organism you duplicated each as a separate gene, does that extra DNA constitute proof that the non-splicing organism doesn’t need those additional base pairs (it’s a bunch of extra DNA in virtually identical organisms)?

You wrote “I agree, and I think that’s part of the slipperiness of the term ‘function’, and why the term ‘junk’ is only a colloquialism. The junk on my desk is junk, but if you suddenly removed it, my coffee cup would fall over and spill into my laptop; the junk has become part of the system.” Wait…are you saying that spacer DNA has a secondary function, but not a selective one? Or are you acknowledging it can have a selective function, but would still consider it “junk”? If the spacer DNA has a selective function–let’s say complete removal of the spacer ultimately results in death of the fetus–is that identifiable and measurable right now? How is it classified according to the numbers you’ve given? It might even have a transposable element in the middle.

D. Allan Drummond writes, “A better definition is ‘a change whose fitness effect is detectable by natural selection’. Set aside for the moment our inability to measure fitness effects; this is true, unfortunate, and irrelevant to the question of whether the definition is correct.” This is on a post which is essentially ranting about ENCODE’s numbers for functioning DNA, so if you concede you can’t actually measure your correctly defined “functional” entities, why are you quibbling about somebody else’s numbers? If your hugely conservative estimator function for your “correct definition” is known to underpredict, and they’ve chosen an optimistic “incorrect definition” that acts as a liberal estimator for your definition, why are you quibbling? They can point out DNA which your estimator wrongly excludes, and you can point out DNA their definition wrongly includes.

nr comments about how little information it would take to encode spacing rather than sequence. If I understand his point, the density of information encoded by a base pair isn’t relevant when deciding whether it is under selective pressure or not. True, in information-theoretic terms it is wasteful to use say 100 base pairs to convey a binary message “yes, transcribe this DNA” or “no, do not transcribe”. But it isn’t _coding_ for a spacer, it _is_ the spacer. It acts in sort of an epistatic way.

Lastly, in a more philosophic vein, I think the whole wasted time around “junk DNA” springs from using inappropriate terminology. When you use words in a substantially different manner than society at large, it should come as no surprise there will be much confusion and you will have to explain your precise meaning over and over. And you really don’t have much of a leg to stand on if some of your colleagues decide to use the word in a manner more closely fitting general useage.

In particular, Brenning (and Ohno too?) differentiate between junk you keep, and garbage you throw away. Here are relevant meanings from a dictionary description:

Junk
n.
1. Discarded material, such as glass, rags, paper, or metal, some of which may be reused in some form.
2. Informal
a. Articles that are worn-out or fit to be discarded: broken furniture and other junk in the attic.
b. Cheap or shoddy material.
c. Something meaningless, fatuous, or unbelievable: nothing but junk in the annual report.
tr.v. junked, junk·ing, junks
To discard as useless or sell to be reused as parts; scrap.
adj.
1. Cheap, shoddy, or worthless: junk jewelry.

In particular, I would highlight the repeated theme that junk should be thrown out, has been thrown out, or is being thrown out. And yet, “junk DNA” is widely acknowledged to have all sorts of benefits and uses, it just is not currently under selective pressure, and is presumed to be separate from “garbage DNA” which more closely corresponds to the given definition for junk.
It’s no wonder there’s confusion and scorn when conveyed to the general English-speaking public, and as with the musician Prince/artist-formerly-known-as, explaining the special meaning for the characters doesn’t completely fix things.

Please be aware that my criticism originates in a genuine desire to understand the genome- that is my life’s work. I believe that we have a long way to go to understand the genome, and the technology we have today to interrogate the genome is far from capable to explain some of the “apparently” paradoxical genome size question.

Your preprint’s primary use is in clearly stating the assumptions and reasoning you made. And that’s what’s important here: being explicit about the assumptions and reasoning you made makes it a lot easier to argue about the underlying facts. For example you make the assumption “Selfish DNA
elements function for themselves, rather than having an adaptive function for their host.” (although you allude to a far more subtle interplay between organismal transposition and its abuse by self-replicating entities).

The problem is that all you or ENCODE is doing when debating the 80% figure is arguing about definitions, which isn’t particularly interesting. What would be more interesting is to look at the ENCODE data in detail, and understand the WHY of what they observe. If we can explain it with null hypotheses, rather than overreaching conclusions, that’s a good thing. If instead the new data helps us understand something vexing, that’s a *great* thing.

Ultimately, i think we can resolve the entire debate by having ENCODE:
1) admit that their function definition is very loose
2) admit some of their claims are overreaching
3) spend a lot more time coming up with significantly more sensitive and accurate methods to determine actual “functionalism” in genomic DNA.

and having ENCODE’s detractors:
1) spend a lot more time looking at the ENCODE data
2) trying to disprove some of their own beliefs and assumptions. I have a hunch that ENCODE’s data is telling us something,

Since then, I posted in Science five mini-essays outlining some of the key tenets associated with this model, which might solve the C-value and jDNA enigmas ( http://comments.sciencemag.org/content/10.1126/science.337.6099.1159).

As discussed in the original paper (1) and these mini-essays, the so called jDNA serves as a defense mechanism against insertional mutagenesis, which in humans and many other multicellular species can lead to cancer.

Expectedly, as an adaptive defense mechanism, the amount of protective DNA varies from one species to another based on the insertional mutagenesis activity and the evolutionary constrains on genome size.

1. Bandea CI. A protective function for noncoding, or secondary DNA. Med. Hypoth., 31:33-4. 1990.