Mutation Protocols: Cut-And-Paste DNA with Built-In Tuning Knobs
| September 15, 2012 | Posted by johnnyb under Intelligent Design |
We have been discussing lately the idea that mutations, rather than being haphazard, may actually be directed by cellular machinery. In a recent volume of the Annals of the New York Academy of Sciences, several scientists presented evidence in favor of this view. One of these scientists has a paper on what he calls “mutation protocols” – that is, repeated patterns of mutations whose behavior is not only physical, but also logical. In other words, the pattern that the mutation follows is consistent with the overall architecture of the organism. You might call these design-consistent mutations.
In any case, David King gives us examples of two mutation protocols – cut-and-paste functional segments, and tuning knobs.
Tuning knobs are generally implemented in the cell through short sequences of repetitive DNA (called SSRs) — one of the types of DNA previously thought to be junk. The idea was, if it is the same, short DNA sequence over and over again, how can it be useful? If mutations are likely to increase or decrease copy number, aren’t the copies just the result of random copying errors? But it turns out that these short sequences are actually usable *because* they mutate by adding/removing copies, and because of their special placement. These sequences act as “tuning knobs” for the genome. Adding copies is like turning a volume knob one way, and removing copies is like turning it the other. You can also tell that these are specially placed, because if a mutation creates an SSR where there wasn’t one to begin with, this often leads to diseases and even cancer.
So, by having certain sequences signal to the genome “hey I’m a tuning knob”, the mutation system can easily and fairly safely adjust organismal parameters across generations.
The second mutation protocol discussed by King is the copy-and-paste protocol implemented by Transposable elements. These were previously considered “genomic parasites”, but have recently been shown to play a role in providing robust variation in organisms. In other words, transposons can import necessary functions into new sites.
But, what’s even more amazing, is that the functions that the transposons import may themselves have tuning knobs! So, not only is it importing function, it is importing a function with control knobs!
The author also makes an interesting observation – mutations have historically (and in fact still are) described in textbooks to be copying errors, while sexual recombination – which is in fact a mutation – has not been considered in the category of “mutation” because the organism expends considerable energy to accomplish it, and it is so useful for the longevity of the organism. In other words, it wasn’t considered an “error” since it seems to be a part of the design. Likewise, we are finding more and more mutations to actually be part of the design rather than being “errors”.
Of course, this is why I proposed a second-level classification of mutations. A while ago, I proposed separating mutations out into design-consistent and design-inconsistent mutations, and described how one might be able to classify these empirically. I still think this is a useful road to follow.
3 Responses to Mutation Protocols: Cut-And-Paste DNA with Built-In Tuning Knobs
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johnnyb, this may be of interest:
i.e. now this may be a bit simplistic for what you are trying to accomplish, but if dedicated, and sophisticated, molecular mechanisms are specifically changing portions of DNA, and diligently correcting ‘truly random chemical fluctuations and replication errors’ to DNA, as Shapiro has noted, then why in the world do Darwinists presuppose that ANY of these directed changes to DNA, that are mediated by these sophisticated molecular mechanisms, are random in the first place? It simply makes no sense for them to mandate that they are ‘random’ changes! In fact, as Koonin recently noted here, finding direct evidence for mediated changes to the genome, by epigentic mechanisms, are in direct violation of the Central Dogma of the modern synthesis of neo-Darwinism:
johnnyb, since you have been specifically studying the different types of mutations for a while, I was wondering if you knew how the following mutation rate of 60, which brought the mutation rate down from 100-300 per generation, was specifically derived? i.e. Exactly what type of mutations are they counting and how did they classify them so as to arrive at their ’60′ number.
Supplemental notes:
on repetitive DNA:
recent note on sexual recombination
As to fixing ‘random’ mutations once they have arisen, well that is another story altogether
I usually enjoy your posts. But I am particularly uncomfortable with the “factual” tone of your post. This paper argues in favor of a hypothesis (i.e., We shouldn’t automatically regard all mutations as haphazard accidents; evolution ought to be able to shape mutational
mechanisms, such as “tuning knobs” based on SSRs, which could plausibly facilitate evolvability). But your post appears to treat
the “tuning knob” hypothesis as established fact.
I am also especially uneasy with certain of your phrases: “because of their special placement” and “these are specially placed”. Although in certain places a newly-arising (and expanding) SSR can certainly cause disease (there are good examples in the literature), the word “often” surely exaggerates the probability of this eventuality. I doubt whether the placement of SSRs is really “special” — I suspect that that there are so many “safe” places for SSRs in the genome that the location of any particular SSR might not be at all special. (It’s just that SSRs in maladaptive locations should be quickly eliminated by selection.) I also suspect that only a fraction (of hundreds of thousands) of SSRs in a genome have a current function; many are probably indeed “junk”.
Starbuck -
Those are all excellent points, and you are certainly right on the current state of knowledge. I think that my assertions will be shown to be correct in the long run, but you are correct that as of current knowledge, there isn’t yet a plurality of known function of SSRs. I probably should have been more tentative in my statements, but my excitement sometimes gets the better of me.
However, the deeper question is which is the best and most effective way to generalize in biology? I would argue that the far more effective mode of generalization is that if you find something where form and function are intertwined, that recurs often, and where we have several known instances of function, that the leap to view this as a general functional pattern is well-justified. I don’t know of a good justification to think that this is not a generalized pattern – the simple fact that we haven’t yet elucidated one yet is simply a Darwin-of-the-gaps reasoning. However, there might be other, better reasons that I am missing.
Similarly, we don’t know what every gene in every organism does, but I think that we are well-justified in assuming, at least as a default assumption, that they do perform some function, because they match a pattern which is regular within biology and which intertwines form and function.