May 23, 2003
By Paul Nesselroade
Pseudogenes have long been considered merely defective copies of functioning genes and relics of our evolutionary past. New research on mice, however, has found evidence suggesting the pseudogene Makorin1-p1 plays a crucial regulatory role in the expression of the coding gene (Makorin1) within the cell. This finding is the latest example of research discovering sub-cellular functioning where it was not expected.
Findings like these have important implications for the authority of Darwinian evolution. A major element of the Darwinian argument springs from the belief that an intelligent designer would not create biological systems that look like what biologists see. Negative evidence for a designer, then, is seen as positive evidence for the purposeless Darwinian mechanism. For example, in “Life’s Grand Design” biologist Ken Miller (1994) states,
“The theory of intelligent design [ID] cannot explain the presence of nonfunctional pseudogenes unless it is willing to allow that the designer made serious errors, wasting millions of bases of DNA on a blueprint full of junk and scribbles. Evolution, in contrast, can easily explain them as nothing more than failed experiments in a random process of gene duplication that persist in the genome as evolutionary remnants.”
So, Miller asserts that [Darwinian] evolution, and not ID, can explain the non-functionality of pseudogenes and therefore, their presence should be viewed as positive evidence for evolution. Many other Darwinists have pointed to the non-functionality of pseudogenes in debates with creationists and IDers – even a cursory search of debate transcripts on the Internet can verify this.
Now that it has been found that at least one pseudogene plays a functional role, can pseudogene functionality be used as evidence against evolution? Evidently not if you’re committed to Darwinism. In the same journal article that uncovered the functional role of Makorin1-p1 we find the following after-the-fact explanation:
“Indeed, it [the functioning pseudogene] suggests that evolutionary forces can work in both directions. The forward direction is driven by pressures to create new genes from existing ones, an imperfect process that often generates defective copies of the original.
But these defective copies need not be evolutionary dead ends, because pressures in the reverse direction could modify them for specific tasks.” (Hirotsune, et al., 2003)
So now that Darwinists know what they have to explain, the data is accommodated with a simple statement; evolution can work both ways. Without batting an eye, evolutionary theory has been modified to fit the data. Whereas prior to this research only pseudogene non-functionality was expected by evolution, now we see that pseudogene functionality is also perfectly compatible. This is a good example of the main point in last month’s essay, “Betting on All the Horses.” The horse of pseudogene functionality has been seamlessly added to the Darwinian stable. Now, according to the new model, pseudogenes are expected to be non-functional except, well… except when they’re not!
So, with this modification we now have two discrepant predictions – either of which is ready to be invoked after the data rolls in. This is rather convenient. From here on out no pseudogene findings will lack a Darwinian explanation because both functionality and non-functionality can be squarely expected. Contrary to the anxiety experienced by legitimate racetrack gamblers, Darwinists can now sit back, relax, and calmly watch the pseudogene horse races knowing that their theory has already picked each winner.
But any reasonable observer can see that pseudogene functionality was clearly not predicted by Darwinian evolution. And yet, the ease with which an after-the-fact explanation was immediately assumed to account for the findings should give all of us reason to pause and ask if we really know as much about origins as we think we do. At what point do we stop merely accounting for findings and start expecting the theory to predict findings? After all, a theory that merely explains but never predicts risks nothing and is never really in danger. Should one of science’s most important theories only be required to meet the criteria of mythology?
Darwinists like to remind us that, “nothing in biology makes sense except in the light of evolution,” (Dobzhansky, 1973). But why is it that evolution is so often what we end up trying to make sense out of? Why is it constantly responding to observations with after-the-fact modifications? Is it really helping us move forward or is it forever just playing catch-up?
It would be one thing if these modifications moved us away from ambiguity and toward tighter predictions, but so often when evolution gets modified it moves us farther away from specific predictions and closer to ambiguity (e.g., Darwinism, it now appears, indiscriminately predicts both functional and non-functional pseudogenes).
Theories are free, of course, to predict discrepant observations. Most big theories do. But in order for these discrepant observations to be seen as supporting evidence, the theory must make specific predictions concerning EXACTLY when each type of observation will appear. If it fails to do this, the theory isn’t explaining anything and the observations are just that – mere observations.
For example, any of a myriad of human relations theories can construct an after-the-fact explanation as to why one marriage fell apart and another stayed together. A good human relations theory, however, will tell us ahead of time exactly when to expect a marriage to fall apart and exactly when to expect it to endure. Can, in the words of Daniel Dennett (1995), the “single best idea anyone has ever had” tell us up front when we can expect to find functional pseudogenes and when we can expect not to?
A clairvoyant isn’t expected to pick heads on every coin toss. She is free to predict either outcome. But, she can’t pick them both at the same time and still be considered a psychic. If she does, her after-the-fact explanations become useless and her customers would be wise to look elsewhere for advice.
Dr. Nesselroade is Associate Professor of Psychology at Asbury College in Kentucky. Readers are welcome to respond to this column at the ARN Discussion Forum.
Copyright 2003 Paul Nesselroade. All rights reserved. International
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File Date: 05.23.03