Sunday, September 28, 2008

Discussing Junk DNA with an Adaptationist, Again

Nils Reinton is a molecular biologist working in the field of medical diagnostics and he has been challenging the concept of junk DNA in the comment section of a recent posting. The title of that posting, Everything Is There for a Reason?, was direct response to an earlier posting from Nils where he claimed that we shouldn't label DNA as "junk" because it's a science stopper.

During the discussion in the comment to my posting, I challenged Nils to answer a number of questions. He has responded on his blog SciPhu with Hey junk people, I accept your challenge (part I). I resonded to his answers in Discussing Junk DNA with an Adaptationist.

Now Nils has weighed in with Hey junk people, I accept your challenge (part II).
Q: Why is the Fugu genome so much smaller than that of other fish?


Q: When two similar species differ in genome size by a factor of two—probably due to an ancient polyploidization—is the majority of DNA in both species functional?

A: His argument is that since the genome size differs between species, much of it must be junk. But, you could easily use the same argument towards a function, by saying that the difference in genome size is a defining (functional) difference between species. We just do not know do we ! And, why does the difference in size not give you reason to speculate on function at least in parts of these regions ? Others have however, speculated far better than me on this topic, and a thorough introduction to such research can be found at and following this link to “The Principle of Recursive Genome Function“.
No, my argument was not that the extra DNA has to be junk just because there are two similar species that differ in the sizes of their genomes.

The question was directed at adaptationists who postulate a function for everything. I wanted to know the adaptationist explanation for those observations. What is it? Following a polyploidization is it possible that most of the DNA in the larger genome becomes non-junk right away?

Incidentally, by linking to the HoloGenomics website (junk.dna), Nils does not enhance his credibility.
Q: In the human lineage there are over one million Alu sequences. They all look like degenerate versions of 7SL RNA. Are all of these sequences functional? If so, what function could they be doing? And why do the human Alus look so different from the mouse ones?

A: I am not saying all Alu-elements are functional. On the “what is junk” scale, one extreme is that everything that hasn’t been ascribed a function is junk (Larry Moran’s position !?) and on the other end is “nothing is junk”. My position is somewhere in the middle: Some of the DNA in our genome is possibly junk. A number of individual Alu-elements will undoubtedly end up in the “junk”-category when more is known about our genome. That said, it has been shown that Alu-elements can constitute (parts of) regulatory and functional elements. It’s rather hard to tell which ones are functional by just looking at them. I therefore refuse to call them “junk” by default, - I strongly feel that the “junk”-label is a dismissal of any possible function(s) and should be used with caution if at all, - even for Alu-elements.
My position is that a huge amount of the DNA in our genomes is junk. That position is based on many different lines of evidence as well as on rational extrapolation from what we know and don't know about molecular biology and evolution.

Nobody is arguing that every single Alu element is junk. That would be stupid because we know for a fact that some of them have secondarily acquired a function. The point is whether most of this repetitive sequence can be reasonably assumed to be functional, and if so, what kind of function does the adaptationist imagine for most of these sequences?

In the absence of any reasonable functional explanation, and in the face of evidence that most Alu elements are degenerate retrotransposons, it is reasonable to adopt the working hypothesis that they are junk. That's not a science stopper. It's just common sense.
Q: Most intron sequences do not seem to have a function. Why does the size of introns in the same gene vary so much in related species and why isn’t the sequence conserved in most cases?

A: This argument is similar to the genome size argument above, and the answers for bullet 5 and 6 are equally valid here. Thus, there may be many reasons for a variation in intron size and this variation is not a very good argument to support the “junk” hypothesis. Also, the intron can contain regulatory elements and the c-gamma example above goes to show that introns can even contain functional (as in transcribed) genetic elements.
The fact that we have a few examples of functional intron sequences is no reason to assume that most of them are functional in the face of abundant evidence that they are not. That's a position that only a confirmed adaptationist would take.

This is a case where the exceptions tend to prove the rule not that the exceptions make a new rule.


  1. Although I must admit I am pretty naive on genomic evolution, I thought some of the differences between you and Nils can be reconciled. Since retrotransposons are replicators in their own right, there is a good reason that they occur throughout the genome of eukaryotes: They have been following their own agenda, not that of their host. Thus, the occurrence of intronic sequences and defunctional retrotransposons in the genome makes sense in the context of adaptive evolution, but their presence is useless to their host (except for some sequences that were co-opted).

    Did that end the argument? :-)

  2. Corneel says,

    Since retrotransposons are replicators in their own right, there is a good reason that they occur throughout the genome of eukaryotes: They have been following their own agenda, not that of their host.

    The vast majority (>90%) of all retrotransposons are pseudogenes with enough mutations to make them non-functional as retrotransposons.

    How does that fit into your compromise? How can a non-functional retrotransposon be adaptive?

  3. If I recall the argument correctly, the uncontrolled spread of jumping elements results in an intragenomic conflict with the rest of the genome. Many retrotransposons will eventually be halted by the evolution of repressors, leaving them as genetic "wreckage" scattered throughout the genome. A new adaptive mutation in a transposon can than start the process again. In such a scenario, the accumulation of junk DNA is driven by natural selection, although it is in fact deleterious to the organism.

  4. "Junk" implies zero (useful) information. Mathematically, if a simple sequence is repeated a lot, the description of the genome can be compressed, implying the amount of information is low. But "low" is not necessarily the same as "zero".

    So perhaps we need a better word than "junk", although I can't think of one off the top of my head.

  5. Why would a 'description' of a genome, mathematical or otherwise, matter insofar as it's actual "information" content?

    If I describe the Mona Lisa as just another painting - does that mean that the ML is no different from the paint by numbers my 7-year old did the other day?