Ancient signalling machinery
by Krauze
Chordates may have started with this little eel-like critter, known as Pikaia, but today spans a diverse range of animals, such as mammals, birds, and fish. In a surprising discovery, a group of researchers have found that some of the signalling machinery used by chordates dates far further back.
Chordates use a signal molecule called retinoic acid (RA) to construct their bodies during development. Since RA seemed to be restricted to chordates, it was assumed to have arisen relatively recently, in conjunction with the origin of chordates. In an article published in the scientific journal Evolution & Development, a group of researchers have discovered pieces of the "RA genetic machinery" in a sea-urchin, pushing its origin back in evolutionary time. When more species have their genomes sequenced, the machinery may in fact turn out to be even older. As the authors note, it is possible that the parts of the RA machinery had a different function in its early ancestor, handling another signal molecule than retinoic acid.
This illustrates an important point about front-loading. A designer wanting to front-load the evolution of life need not have inserted useless genes for eyes and hearts in a unicellular organism, where mutations would erase them in a few million years. Instead, the designer could have designed genes that could be adapted to multiple functions, so that a gene could serve one function in a unicellular organism and another in a multicellular organism. Flexibility - not micro-managing - is the key.
Cañestro C., et al., "Is retinoic acid genetic machinery a chordate innovation?", Evolution & Development 8(5):394-406 (2006)
doi:10.1111/j.1525-142X.2006.00113.x
November 5th, 2006 at 10:40 pm
Have RAs or related molecules been discovered in unicellular organisms?
Comment by Bilbo — November 5, 2006 @ 10:40 pm
November 6th, 2006 at 12:55 am
Krauze, is your view that there was a single front-loading event, that the first organism was created front-loaded to become all that we know about life, or do you see this only as one front-loading view?
Comment by bFast — November 6, 2006 @ 12:55 am
November 6th, 2006 at 9:23 am
Bilbo and bFast,
"Have RAs or related molecules been discovered in unicellular organisms?"
No, the researchers only surveyed the genomes of multicellular organisms.
bFast, I'm not quite sure what it is you're asking about, so you'll have to excuse me if I don't get it right.
I favor a single front-loading event, but I'm open to the possibility that bacteria and eukaryotes were deposited at two different events.
Front-loading, as originally conceived by Mike Gene, doesn't claim that the designer had "all that we know about life" in mind. I've written more about this here.
Comment by Krauze — November 6, 2006 @ 9:23 am
November 6th, 2006 at 11:39 am
It seems to me that a designer is not necessary in this case. If at one point in evolution a toolbox evolved from which a plethora of other functions can be constructed (the LEGO building block concept), it would be indistinguishable from your 'front-loading with designer' hypothesis.
Comment by AdR — November 6, 2006 @ 11:39 am
November 6th, 2006 at 1:43 pm
Hi AdR,
My thoughts about front-loading don't hinge on it being "necessary". After all, if front-loading is indistinguishable from the atelological approach, that means that the atelological approach is also indistinguishable from front-loading. It also means that all of those claims about front-loading being impossible are without basis in fact.
Now, it might be possible that future research will allow us to tweeze these two perspectives apart. But until that happen, I see no reason to give up on what looks like an interesting hypothesis.
Comment by Krauze — November 6, 2006 @ 1:43 pm
November 6th, 2006 at 1:47 pm
Thanks Krauze, you fully answered my question. I also agree that nature looks to me like a true experiment, where the experimenter did not micromanage the end result. That's the only explanation I can find for why the cambrian explosion produced dozens of phila, but only a few survived.
It seems like life is a machine that is tuned to benefit optimally from whatever the environment throws at it. However, I still wonder if there hasn't been some tweaking along the way. I consider a recent report about the HAR1F gene that is all but identical between birds and chimps, but has taken on a number of mutations in man. If the HAR1F gene is all but identical in birds and chimps it must be extremely resistant to random mutation. As the mutatons that did happen seem to be key to that which makes us human, one would think that the only mechanism available to obtain such mutations is, well intention.
Comment by bFast — November 6, 2006 @ 1:47 pm
November 6th, 2006 at 2:07 pm
bfast,
Yes. How many times have you heard the phrase "evolution is a tinkerer", or "evolution offered a creative solution". Of course, evolution doesn't tinker, nor was it completely front-loaded into one or two ancient events.
Comment by chunkdz — November 6, 2006 @ 2:07 pm
November 6th, 2006 at 8:59 pm
Hmmm…there may be a problem here for front-loading. If we can't find RAs or related molecules (that they could have evolved from) in unicellular organisms, then it would seem to point to at least a second design event, wouldn't it?
Comment by Bilbo — November 6, 2006 @ 8:59 pm
November 6th, 2006 at 9:44 pm
Hi Bilbo,
It's not an issue of researchers not being able to find them, but of them simply not having looked for them there.
That being said, I'm not staking any claim that RA definitely is an example of front-loading. The current find certainly increases the likelihood of that being the case, but even if RA was found a unicellular organism, that wouldn't be enough to conclude that it had been put there with chordates in mind. To make that jump, you need a theoretical framework that isn't in place yet. Hopefully, I'll be able to write a "Design Matrix" of my own some day, rectifying this.
The point of a post like this is simply to point at interesting leads for front-loading, as well as to use some real-life examples to illustrate the logic behind the conjecture (in this case, that a designer doesn't have to stuff useless genes into a defenseless microbe).
Comment by Krauze — November 6, 2006 @ 9:44 pm
November 7th, 2006 at 12:46 am
Why? At least two other explanations are fully consistent with standard evolutionary theory: (1) relaxation of selective constraint in the lineage leading to humans (i.e. the function previously performed by this gene is no longer required in humans), or (2) positive selection for new functions in the lineage leading to humans. Given the rate of change in this gene the researchers favour explanation (2) for HAR1F, but (1) is still a live possibility.
Note that "the mutatons that did happen seem to be key to that which makes us human" is pure speculation that has been lapped up by the mainstream media. All we know is that this region of the genome shows accelerated sequence changes in the human lineage; we don't know what functional effects these changes had, and we certainly don't know that these changes were critical to any of the evolutionary changes that make humans unique.
Comment by Mesk — November 7, 2006 @ 12:46 am
November 7th, 2006 at 2:08 am
Mesk, at 2 mutations in 600 million years, the HAR1F is clearly very resistant to genetic drift. To be this resistant one would expect that there are very active constraints, and probably multiple constraints. In light of this, I would expect that your position 2, "positive selection for new functions", would also require position 1, "relaxation of selective constraints". If this is correct, then position 1 must be the case, even if position 2 is also. If there are multiple constraints, then position 1 becomes all the more unlikely.
The article that I obtained my information from does state that the function of the HAR1F is not clearly established. However, there seems to be good reason to suspect that it is involved in the development of the remarkable human cerebral cortex.
Nothing may have been established in fact, but this certainly looks to me very suspiciously like an area where the great genetic engineer did a bit of engineering.
Comment by bFast — November 7, 2006 @ 2:08 am
November 7th, 2006 at 2:59 pm
Mesk,
Your 2 positions become even more tenuous as one considers that HAR1F is a non-coding RNA that is likely a regulator for a cascade of enourmously complex developmental systems. Stability for such a highly regulatory gene is paramount, as evidenced by it's conservation. It also appears to have a structure that is completely novel among non-coding RNA's, meaning that a radical change occured - apparently without destroying the entire neurodevelopmental system. So far, nothing about HAR1F says gradualism. Everything about HAR1F so far says "tinkering with thought to the consequences".
Comment by chunkdz — November 7, 2006 @ 2:59 pm
November 7th, 2006 at 6:10 pm
The cavalry has come, the reinforcements are here! Thanks Chunkdz.
Comment by bFast — November 7, 2006 @ 6:10 pm
November 7th, 2006 at 6:27 pm
Krauze:
But from the article, all that we know is that RAs have been found in chordates and in sea urchins — both multicellular organisms. It hasn't been demonstrated that RAs or their precursors existed in unicellular organisms. Until then, I don't see how this supports front-loading.
Comment by Bilbo — November 7, 2006 @ 6:27 pm
November 8th, 2006 at 7:04 pm
Chunkdz:
Certainly "tinkering with thought to the consequences" is synonymous with ID. The question then, what further evidence could be gathered from researching HAR1F which would support the premise that the uniqueness of the human HAR1F is the product of "tinkering with thought to the consequences" Certainly experiments could be run demonstrating that the HAR1F is "a regulator for a cascade of enourmously complex developmental systems", and that "Stability for such a highly regulatory gene is paramount".
This one gene may provide a complete and strong positive case for ID.
Comment by bFast — November 8, 2006 @ 7:04 pm
November 8th, 2006 at 8:10 pm
bFast,
Thank you for alerting me to HAR1F. I'm surprised no one at TT has addressed it yet, although there is still much to be learned about it. Check out this figure from the Nature article. It offers a visual indication of just how radically different human HAR1F is.
Comment by chunkdz — November 8, 2006 @ 8:10 pm
November 9th, 2006 at 12:55 am
Chunkdz, thanks for the link.
I am not a biologist, but I am finding something here that doesn't seem mutatable to me. This seems to be irreduceably complext on the individual mutation level.
Tell me if my biology is just not rich enough, but it seems to me that we have a number of substitutions which must occur in matched sets to maintain reasonable folding. My guess, considering how conserved this dear thing is, is that if this gene doesn't fold right, the animal will be painfully dysfunctional at best, therefore these matched pairs of mutations must have occurred simultaneously. Would that not be outside of reasonably possible within the framework of NDE?
Am I correct when I say that the folding is calculated using the EvoFold program? Could one not produce every possible single mutation in an attempt to get from the chimp to human and see if there is any pattern that maintains a reasonable fold by single mutation events? If it could be demonstrated that multiple mutation pairs were required to get from chimp to man, how big of a challenge would this be to the status quo?
Comment by bFast — November 9, 2006 @ 12:55 am
November 9th, 2006 at 3:02 am
bFast,
I was thinking the exact same thing. One should be able to calculate the probability of randomly evolving the human version by determining which mutations are deleterious, and determining a reasonable mutation rate. Seems a fertile patch of ground for an ID research program.
Comment by chunkdz — November 9, 2006 @ 3:02 am
November 10th, 2006 at 6:42 pm
I don't mean to distract the disputants discussions (both informative and even more entertaining) about books hardly anyone reads (but a few Cretinists and Evilutionists), theocratic conspiracies (that fail every election cycle), and gratuitous cartoon homoeroticism, but I found this very interesting paper about "front-loading" in PLoS today:
Mayo AE, Setty Y, Shavit S, Zaslaver A, Alon U (2006) Plasticity of the cis-Regulatory Input Function of a Gene. PLoS Biol 4(4): e45
http://biology.plosjournals.or...
I'm putting this here Krauze because one of the things I've questioned is that the "front-loading" concept has always seemed to focus more on isolated exemplars apparently drawn at random (Like the paper you cited?) rather than what I would expect from a front-loading strategy, and that is to load the potential for innovations and adaptations"¦ up front!
Front-loading would therefore, or so it seems to me, be better served by exploring for those examples (of potentiality, creativity, adaptability, evolvability) that are universal.
Comment by Rock — November 10, 2006 @ 6:42 pm
November 10th, 2006 at 7:07 pm
Hi Rock,
You write:
The examples that Krauze (and I) often provide are part teaser and part potentially significant data point. But your point is on target. That's why this will be a very helpful guide to those interested in front-loading (although its not all about front-loading).
Comment by MikeGene — November 10, 2006 @ 7:07 pm