Over at BioLogos, Dennis Venema provides the conventional view of transposons through a non-teleological prism. Like many others, he thinks of transposons as parasites:
They are the perfect parasites: using their host to provide resources so they can replicate themselves, and with a “lifestyle” so simple that replication is essentially its only feature.
Despite their parasitic nature, sometimes the host species can exploit transposons as a source of genetic novelty.
Yet it is not really accurate to describe transposons as parasites.
A few people have notified me to let me know that front-loading is being discussed on UD by someone with the moniker ‘genomicus.’ In one place, genomicus states that cytosine deamination is a prediction of front-loading. Someone else with the moniker “eigenstate” disagrees and writes:
The fail point here in this item is “so why would a front-loader choose cytosine as a base in DNA?”. It’s not sufficient to offer us *a* reason why you think cytosine would be chosen (and this is particularly devastating if you are offering this putative prediction in the context of an “intelligent design” explanation, an explanation with an unknown, inscrutable, mysterious designer). The choice must follow NECESSARILY from the hypothesis.
You are quite conspicuously working backwards from your conclusion. Coming up with a plausible choice — and given an unspecified, unknown, potentially omniscient and omnipotent designer, ALL choices are plausible — does not ground a prediction. First you lay out the hypothesis, the proposed mechanism, and then you deduce from that NECESSARY implications that proceed from that. If you can affirm what is entailed from your model, you got something! Sometimes those predictions are trivial or banal, and so don’t carry much weight. Other times they just don’t distinguish the hypothesis from other, competing hypotheses. But in this case, if you COULD establish that such a choice was ENTAILED from your proposed model, that would be quite substantial, indeed, I think.
I would not agree with genomicus that front-loading predicts the cytosine deamination story. That whole story is more subtle and complex than that. Let me explain.
Over at Jerry Coyne’s blog, biologist Greg Mayer wrote:
One of the most important lessons of comparative anatomy is that evolution usually proceeds by the modification of pre-existing structures (or, stated more precisely, the modification of the pre-existing developmental programs that produce those structures). Certain changes are easier to evolve because the developmental system can be modified to produce them—evolution follows the developmental path of least resistance. In terms of the skeleton of vertebrates, this means that most evolutionary changes are reduction, fusion, loss, lengthening, shortening, thickening, and narrowing of bones. Evolution uses what’s already there, and rarely do wholly new structures arise. (from “Tinkering with elephants’ feet”)
All of this is true, yet we can proceed beyond this conventional thinking and ask a couple of questions:
WHY does evolution follow the developmental path of least resistance?
WHAT are the implications of evolution following the developmental path of least resistance?
Philosopher Michael Ruse objects to a recent comment from Pope Benedict:
“If man were merely a random product of evolution in some place on the margins of the universe, then his life would make no sense or might even be a chance of nature. But no, reason is there at the beginning: creative, divine reason.”
According to Ruse, this view is a no-no because it contradicts science. To show this, he, well, quotes from Stephen Jay Gould:
“Since dinosaurs were not moving toward markedly larger brains, and since such a prospect may lie outside the capabilities of reptilian design, we must assume that consciousness would not have evolved on our planet if a cosmic catastrophe had not claimed the dinosaurs as victims. In an entirely literal sense, we owe our existence, as large and reasoning mammals, to our lucky stars.”
Well, that just settles it once and for all. He then adds:
Gould was not saying that human evolution was uncaused or random in that sense. But he was saying that there is no design. Human evolution had no more forethought than, say, the pattern that a pile of sand makes when emptied from a bucket.
Yeah, I understand the argument and position, but where are the actual data that show “there is no design” and there was no, NO, NO foresight involved in human evolution?
Posted in design
Here are six points that lay at the foundation of my approach. All six points are quite reasonable. In fact, I would maintain that not only are they all reasonable, but they are also more reasonable than the position that would deny them:
Posted in design
Over in the comments section at BioLogos, Bilbo summarizes my position:
He begins with the hypothesis that the first cells were designed to make evolving (by neo-Darwinian processes) in a certain direction more likely.
And someone then asks: What does he think happened before life was cellular, then?
Given the paucity of solid information, I’m not quite sure what to think. However, there are really only two options: the planet was seeded with life or the planet spawned life. Both explanations are supported by circumstantial evidence.
Posted in design
Biologists find themselves in the uncomfortable position of studying something that is difficult to define. Traditionally, they define life by listing several features characteristic to life, including metabolism, growth and development, responsiveness, and reproduction. Because of its central importance in evolution, many emphasize reproduction. Yet Daniel Koshland tells this story:
What is the definition of life? I remember a conference of the scientific elite that sought to answer that question. Is an enzyme alive? Is a virus alive? Is a cell alive? After many hours of launching promising balloons that defined life in a sentence, followed by equally conclusive punctures of these balloons, a solution seemed at hand: “The ability to reproduce–that is the essential characteristic of life,” said one statesman of science. Everyone nodded in agreement that the essential of a life was the ability to reproduce, until one small voice was heard. “Then one rabbit is dead. Two rabbits–a male and female–are alive but either one alone is dead.” At that point, we all became convinced that although everyone knows what life is there is no simple definition of life. 
Koshland himself defines life by citing seven features that are both universal and essential to life: “P(rogram), I(mprovisation), C(ompartmentalization), E(nergy), R(egeneration), A(daptability), S(eclusion), PICERAS, for short–are the fundamental principles on which a living system is based.”  That life resists attempts to define it in an efficient and simplistic manner may speak to manner in which reductionism fails to account for it.
In 2001, Bernard Korzeniewski used a cybernetic approach to come up with a definition of life that turns out to be quite helpful when thinking of evolution as a process that was designed.
Let me add one more comment concerning Avise’s PNAS paper. In the last entry, I focused on his argument that introns counts as evidence against intelligent design. We saw the whole argument fails if we envision design working through evolution. But I want to you to notice something else. In the paragraph preceding the discussion of introns, Avise wrote:
Approximately 1% of all known genes in the human genome encode molecular products that our cells employ to build spliceosomes and conduct splicing operations on premRNA. All this rigmarole has some advantages (e.g., opportunities for alternative splicing during ontogeny and exon shuffling during evolution, both of which can generate functional protein diversity), but such benefits do not come without major fitness costs.
Note that Avise describes alternative splicing as something that confers “some advantage.” Some advantage. As if alternative splicing is just a minor factor in evolution.
Now let’s contrast this to the abstract from a paper by Stephanie Boue, Ivica Letunic, and Peer Bork (Alternative splicing and evolution. BioEssays 2003 25:1031–1034):
Alternative splicing is a critical post-transcriptional event leading to an increase in the transcriptome diversity. Recent bioinformatics studies revealed a high frequency of alternative splicing. Although the extent of AS conservation among mammals is still being discussed, it has been argued that major forms of alternatively spliced transcripts are much better conserved than minor forms.(1) It suggests that alternative splicing plays a major role in genome evolution allowing new exons to evolve with less constraint.
“A major role in genome evolution” sounds a tad more than “some advantage “ to me. In fact, consider the conclusion of Boue et al.:
So what is the consequence of Avise’s false dichotomy? The bulk of his paper is a detailed exploration of the “outlandish features of the human genome that defy notions of ID by a caring cognitive agent.” While this is an argument that works against design that is coupled to special creation, it fails against design that is coupled to evolution. To see this, let’s pick one of the outlandish features that Avise explores – introns. I chose this example simply because I have already written about it.
Avise’s core argument is as follows:
There are good reasons to think that cells might be better off without introns, in an ideal world.
Let me now add to this argument with the following point:
There are good reasons to think that evolution might be worse off without introns.
In other words, if introns are an “outlandish features of the human genome,” we might also point out that without this outlandish feature, there is no evidence to think that evolution would have cobbled together a human, or human-like, genome.
Recall that I have used the teleological perspective of front-loading to propose a testable hypothesis about introns – they have facilitated the emergence of metazoan-type complexity – that is supported by evidence (here, here, here, and here) and has been successfully defended. (If you have not read these essays, then what follows below will not make much sense to you).
If the design objective is to nudge the emergence of metazoan-type complexity, and not to ensure that cells would be “better off,” then we can see that Avise’s core argument has collapsed.
Nevertheless, let’s have a look at Avise’s reasons.
In the last entry, we saw that biologist John Avise argues that traits which are gratuitously complicated, function poorly, and debilitate their bearers, all count as evidence against design. And as I noted, I agree with this assessment. In fact, Avise is unknowingly participating in one facet of the Design Matrix – the criterion of rationality. What’s missing from his argument are two things: 1) Assign a numerical score to better nail down and communicate this judgment of irrational design and 2) An acknowledgement that a fair-minded and open-ended analysis would have to include the willingness to score things in the other direction, such that traits which are not gratuitously complicated, function exceedingly well, and do not debilitate their bearers, count as evidence for design. To argue otherwise would be to engage in apologetics.
But there is a more fundamental problem with Avise’s argument.