15 May 2011

Alu need to know about parasitic DNA: telling the whole story about Alu elements and "design"

So, Alu elements are mobile DNA modules that can exert diverse influences on genomes and the organisms harboring them. They can affect genome function in constructive ways, by altering gene expression or supporting chromosome structure. And they can be damaging, even deadly. There are more than a million of them in the human genome, and we don't know what each one does. But, as I explained in the first post in this series, we do know that they can play both helpful and harmful roles, in the same way that other kinds of parasites can be good, bad, or indifferent.

Alu elements and other genome-wide repeats are a big problem for intelligent design (ID) theorists of some stripes. Any ID proponent who claims that genomes are carefully-designed, well-optimized systems must deal with the reality of the enormous numbers of mobile elements in (for example) the human genome. Now, I can think of various ways such an ID theorist might discuss Alu elements. She could propose that all of their characteristics (including their mobility) are part of their design, such that they can bring new design features quickly into being; she could propose that their mobility is a "bug" rather than a "feature," and perhaps speculate on how things went wrong; she could postulate that the damage caused by their expression and their mobility is being misattributed to the genome when it is instead caused by some other external process. (Or she could say, "We're still working on that one.")

Well, sadly, there's one other option for an ID apologist. She could tell only part of the story, claiming that Alu elements are one of God's gifts to humankind, while omitting the most important facts about them.

Consider what we know about Alu elements. Here is a list of what we might call their "positive" attributes:
  • They can participate in the control of gene expression.
  • They can participate in structural functions in the genome.
  • They can be converted into functional genes.
That list should not be ignored or underestimated. Alu elements, like other genome-wide repeats, can be put to use by the genome.

And here is a list of what we might call their "negative" attributes:
  • They can cause harmful mutations by hopping into the middle of essential genes.
  • They can destabilize the genome by facilitating damaging large-scale physical interactions.
  • They can generate toxic RNA molecules that must be controlled by other cellular systems.
And so, while we continue to learn more about these fascinating genomic components, we must keep both of those lists in mind. Recent reviews by experts on the topic have strongly emphasized that balance.

Troublingly, one ID advocate at Reasons To Believe (RTB) has chosen a different approach. Dr. Patricia Fanning is a "visiting scholar" at RTB, and she recently completed a six-part series on Alu elements at RTB's blog. Her articles are clear summaries of the first bullet list. She describes recent work on Alu elements and their structure, and her overviews of their effects on gene expression are very nicely written. I don't much care for her claim that non-function is a key assertion of evolution biologists with respect to genome-wide repeats (that's just not true), but we've been over that before, and I think that her mistake there is an easy one to make. What I find so discouraging and disappointing is her complete omission of the best-known facts about Alu elements.

First, she omits the entire second bullet list. She makes no mention at all of the documented cases of genetic illness caused by Alu-mediated mutation. She makes no mention at all of the well-known phenomenon of damaging recombination caused by genome-wide repeats. And although the macular degeneration article was published in Nature on 17 March, two weeks before she began her series, she makes no mention of this important and influential new finding.

But much worse, she wrote six blog posts, including one that emphasizes the structural components in each Alu element, without mentioning the one thing that is best understood about Alu elements: the fact that they are mobile. It is a systematic omission that makes the entire series profoundly misleading. Once that central fact about Alu elements is re-introduced, many of Dr. Fanning's claims about their form and function and placement are seen to be well-explained by common ancestry and purifying selection.

It would be like advertising "dwelling for sale: one room, windows, air conditioning, heat, furnishings," omitting key facts that would be readily apparent upon seeing the advertised "dwelling." That's how serious I consider Dr. Fanning's omission to be.

Dr. Fanning may be right that Alu elements were designed by God and situated in the human genome according to design or a plan. Her enthusiasm for design-based explanation of genomic structure is legitimate, and I don't wish to criticize her or RTB for expressing that preference. But I am troubled by the choice to tell an incomplete, inaccurate, and misleading story about Alu elements. In my opinion, RTB should consider an addendum to the series, noting that Alu elements are mobile and that their activity is known to be damaging as well as beneficial. This would not require abandoning the pro-design position, and it would be a welcome step toward a more responsible and credible RTB.

Comments are most welcome.

2 comments:

Berend de Boer said...

 RTB is an old earth "creationist" society, so mobile elements probably don't fit in well with the story. On the other hand, they have millions of years of death before Adam and Eve, so why ignore harmful stuff?

I assume young earth creationists are a bit more enthusiastic with the mobile element as they need to generate quite a few species since the Ark...

Preston G. said...

One might guess that they are ignoring the fact that Alus are mobile because it creates a big problem for their denial of common descent. There are millions of instances of the same transposable element (Alus or others) inserted at the same site in different primate species. Without common descent, you have to have millions of identical transposition events in parallel in multiple primate species, and there is no evidence that Alus (or any of the other transposable elements in primates) have that kind of target specificity. Or, against all the evidence, you could argue that Alus and other elements are not really transposable. Is that where RTB is going? Who knows. Either way they have a big problem.