Bradford first informed us that Richard Sternberg was throwing down the gauntlet to Darrel Falk's rejoinder to Meyer.
Apparently Dr. Sternberg has just begun to fight.
You may read his second and third salvos here:
And his fourth salvo:
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March 17th, 2010 at 8:30 pm
I saw this and was going to blog on it. What the posts refute is the claim that all bets on junk are mere guesses. I guess that is not so when Sternberg is able to cite specific research to support his "guess."
Comment by Bradford — March 17, 2010 @ 8:30 pm
March 17th, 2010 at 9:36 pm
This is flipping amazing
I’m going to need to read Sternberg’s argument again a couple dozen times to be sure I understand it but add this observation to the recently discovered ultra conserved non-coding DNA and it looks like we might be on the cusp of something cool.
It’s always the weird anomalies that doom the reigning paradigm.
Just ask yourself which idea best explains the data.
peace
Comment by fifth monarchy man — March 17, 2010 @ 9:36 pm
March 18th, 2010 at 12:03 am
Whatever scientist came up with the term "junk" DNA really ought to be fired. Again, this is another example of sloppy thinking and shoddy science. That the vast majority of nucleotides in a human cell do not apparently encode proteins, does not lead to the conclusion that such DNA is "junk"
Indeed, from an article last year in Science Daily
If the number of genes has ranged from 150,000 to 20,500, by definition, it means that the knowledge and understanding of the precise function of cellular DNA is fluid.
So, why would it surprise anyone that non-coding DNA –previously dismissed as "junk" — might have some important function after all?
I think Sternberg is on to something here and his work should be encouraged.
Comment by David S — March 18, 2010 @ 12:03 am
March 18th, 2010 at 1:56 am
I think it is because the theory required lots of junk (not just "attic junk", but "useless, garbage, do nothing junk") to avoid mutational failure.
Comment by Pez — March 18, 2010 @ 1:56 am
March 18th, 2010 at 9:28 am
Heh. You just fired Susumu Ohno, "one of America's greatest scientists, exerting an enormous influence on our ideas about biology and evolution."
That wasn't Ohno's argument, and he proposed non-sequence specific functions for "junk DNA." Strict adaptionists rejected the notion of "junk DNA," by the way, so the claim is not unique to ID. But any scientific explanation has to explain why an onion has more DNA than you do.
Comment by Zachriel — March 18, 2010 @ 9:28 am
March 18th, 2010 at 9:54 am
I resent being compared to a vegetable
Comment by David S — March 18, 2010 @ 9:54 am
March 18th, 2010 at 10:36 am
Zach raises an interesting point about onions. Speculation and investigations abound. This from here.
Comment by Bradford — March 18, 2010 @ 10:36 am
March 18th, 2010 at 11:03 am
Onions have layers; more layers means more DNA.
Comment by SSung — March 18, 2010 @ 11:03 am
March 18th, 2010 at 12:39 pm
Are you selling appliances or comedic routines?
Comment by Bradford — March 18, 2010 @ 12:39 pm
March 18th, 2010 at 3:20 pm
[...] Telic Thoughts is an independent blog about intelligent design. « Sternberg Continues Throwing it Down [...]
Pingback by Censorship at Biologos? - Telic Thoughts — March 18, 2010 @ 3:20 pm
March 18th, 2010 at 3:22 pm
Sternberg's fourth salvo.
Comment by Bilbo — March 18, 2010 @ 3:22 pm
March 18th, 2010 at 4:31 pm
Fourth salvo here
http://www.evolutionnews.org/2...
Comment by chunkdz — March 18, 2010 @ 4:31 pm
March 18th, 2010 at 4:52 pm
I scooped both of you, Bradford and Chunk. See what happens when you stay up late partying?
Comment by Bilbo — March 18, 2010 @ 4:52 pm
March 18th, 2010 at 5:00 pm
I was just posting the correct link. And actually I stayed up all night fidgeting with a confused DSL modem.
Sternberg makes some really fascinating observations here.
Comment by chunkdz — March 18, 2010 @ 5:00 pm
March 18th, 2010 at 5:16 pm
Oops. Thanks for the correction. I won't even ban you for it.
Comment by Bilbo — March 18, 2010 @ 5:16 pm
March 18th, 2010 at 5:23 pm
Hey all,
I would love to hear some speculation as to how the features Sternberg describes might be explained by RM/NS or drift.
For the life of me I can’t think of a way this could be accounted for absent some sort of “frontloaded” mechanism.
Perhaps it could be chalked up to some strange up till now unknown predisposition inherent to the DNA molecule itself but if that is the case it begs the question of what other hidden constraints are we missing.
If this big of a deal has slipped past us who's to say it's all not predetermined.
I just hope folks understand the strength of his argument against RM/NS and drift being the cause of these patterns.
In the case of the ultraconserved noncoding DNA the argument was that surely there was some unknown function that was being selected for thus conserving the sequence but in this case the sequence is not conserved at all yet the pattern is.
Like I said it's flipping amazing
To top it off I'm floored that the Scientific community knew about this for decades and this is the first I’m hearing about it.
peace
Comment by fifth monarchy man — March 18, 2010 @ 5:23 pm
March 18th, 2010 at 5:50 pm
Hi FMM,
Frankly, I have no idea if Sternberg is on to something or not. But it is at least intriguing.
Comment by Bilbo — March 18, 2010 @ 5:50 pm
March 18th, 2010 at 5:54 pm
Obviously they have some important, undetermined function.
Of course that would support Meyer's assertion from Signature.
Comment by chunkdz — March 18, 2010 @ 5:54 pm
March 18th, 2010 at 6:24 pm
hey chunkdz,
Are you suggesting function for the pattern itself but not for the sequence or are you saying a separate unknown sequence is responsible for the preservation of the pattern?
I think we can agree that this feature is there for a reason but what I don't understand is how it can be selectable given the current paradigm.
Regulatory switches in noncoding DNA are preserved because they have inportant effects on the coding stuff. Are we to surmise that the pattern here has some vital role to play yet apparently this function is not important at all in animals with less DNA.
just trying to understand
peace
Comment by fifth monarchy man — March 18, 2010 @ 6:24 pm
March 18th, 2010 at 7:15 pm
I haven't got a clue. But I can imagine a test similar to a knockout test where instead of removing segments we simply re-order them, or try a different pattern. Wonder if it's been done yet or if nobody ever thought to try it before since these were thought to be junk.
You and me both, man. I've been fascinated by this stuff ever since I found out that I was highly advanced nanotechnology.
Comment by chunkdz — March 18, 2010 @ 7:15 pm
March 18th, 2010 at 7:47 pm
Most SINEs are sequence repetitions. Co-localization of SINEs could be due to hotspots or biased deletions. Simplistic notions of random mutation doesn't give a very accurate picture of genome evolution where "local genomic context strongly shapes local genomic features and rates of evolution."
Comment by Zachriel — March 18, 2010 @ 7:47 pm
March 18th, 2010 at 8:28 pm
What would cause a spot to be hot or a deletion to be biased so as to preserve a pattern while ignoring a the sequence involved?
“hot spot” and “biased deletion” are not explanations but simply descriptions of the phenomena at issue.
Feel free to provide a more nuanced notion of random mutation that would create a identical pattern in genomes separated by millions of years while not caring about the actual sequences involved.
"local context" is not an explanation either. What sort of "local context" would account for what is reported?
I’m not trying to start a argument and I have zero interest in parsing terms with you Zach.
Just hoping for a possible explanation that's all
peace
Comment by fifth monarchy man — March 18, 2010 @ 8:28 pm
March 18th, 2010 at 9:42 pm
More particularly, the distribution is the phenomena, hotspots and biased deletion are posited processes.
It's important to understand that the genome itself has a geography. Some areas of the genome are rich in genes and GC bases, while other areas are poor in genes but rich in AT bases. This basic geography is inherited from the common ancestor and it influences events that occur after divergence, including the behavior of interspersed repeated sequences.
LINEs tend to reside in AT-rich regions of the genome, while SINEs accumulate in GC gene-rich regions. There is no consensus yet, but a number of testable mechanisms for the distribution of SINEs have been proposed, including biased insertion, increased recombination in gene-rich regions, recombinogenic properties in clusters of SINEs, ectopic exchange in AT-regions areas, and negative selection for new SINEs.
Comment by Zachriel — March 18, 2010 @ 9:42 pm
March 18th, 2010 at 10:22 pm
So how would the basic geography produce this effect? and if it can produce this effect with out RM/NS are there any limits to it's power.
Lets see
Why would a insertion be biased to produce this effect?
Why would increased recombination that produced this effect be selected ?
Why would recombinogenic properties that produced this effect be selected ?
Why would an ectopic exchange that produced this effect be selected?
Why would negative selection for new SINEs produce this effect?
These are not explanations they are are only mechanisms I can think of all kinds of ways this effect might be produced if I wanted to make it happen.
I just don’t know why RM/NS (nuanced or not) would favor it.
Is that all you got?
I guess a possible explanation is too hard for Zach to give and life is too short for me to keep banging my head against this particular wall.
Anyone else want to give it a try.
I just want to understand
peace
Comment by fifth monarchy man — March 18, 2010 @ 10:22 pm
March 18th, 2010 at 10:47 pm
I'll just wait to see what Sternberg proposes.
Comment by Bilbo — March 18, 2010 @ 10:47 pm
March 18th, 2010 at 11:15 pm
A couple of things, one of which I have mentioned before. First, just because DNA is being transcribed doesn't mean the transcripts are functional. Secondly, genomic areas with extensive repeats are highly variable, subject to inserts and deletions of blocks of repeats due to slipped-strand mispairing. These highly repetitive areas, by their physical structure, can become recombinational hot spots, increasing the probability of unequal crossing over, which can result in insertions and deletions and gene duplications. All of this activity can bring transcription initiation sequences (like promoters) near different mishmashes of nonsense sequences, resulting in transcription, but for non-functional transcripts. The activity can also bring new combinations of sequences under transcription that now have the ability to affect expression of genes elsewhere, i.e., that now have a function. This latter possibility, that of new function coming about by reshuffling of sequences via purely stochastic forces, cannot be considered as evidentiary support for front-loading. Intelligent Design advocates, therefore, will need to carefully sift through these and rule out what I have described above before claiming genomic evidence of design.
Comment by KC — March 18, 2010 @ 11:15 pm
March 19th, 2010 at 6:25 am
Hey KC
Yet for some reason in this case they have produced a nearly identical pattern, strange huh
So you agree with Sternberg against Falk that these areas have function?
This is strange given the fact that other organisms get along just fine with out them and apparently two organisms arrived at nearly the exact same structure independently?
So much for evolutionary picture of a blind watchmaker that cobles together broken parts that just barely get the job done.
How improbable does the pattern have to be before we can make that claim?
Keep in mind for now I'm only saying these areas are not junk and I’m flabbergasted at their appearance and am looking for an explanation.
If you add this finding to the ultraconserved unexpressed sequences it makes you wonder what is going on does it not?
peace
Comment by fifth monarchy man — March 19, 2010 @ 6:25 am
March 19th, 2010 at 8:09 am
Just because there is sorting doesn't mean it was sorted by an agent. Natural forces sort things all the time. If we have two similar geologies, it is no surprise that water flows and fills the same basins.
Sternberg's argument is that there is a pattern that emerges independently in separate lineages. But this is incorrect. The pattern is already there, inherited from the common ancestor. That means his argument is unfounded.
Despite the analogy, a genome is not a computer, but chemistry. It does matter about ATGC. Some of your questions were answered by KC. Others can be found if you do a bit of research.
Comment by Zachriel — March 19, 2010 @ 8:09 am
March 19th, 2010 at 8:41 am
Wrong.
Comment by MikeGene — March 19, 2010 @ 8:41 am
March 19th, 2010 at 8:49 am
Zachriel wrote:
If the pattern was inherited from the unknown common ancestor of mouse and rat, then what sequences occupied the SINE positions, within the pattern, in that unknown ancestor? The SINE elements in mouse and rat are not homologous.
You're inferring common ancestry in the face of a clear signal of non-homology.
But let's suppose common ancestry is the case. What mechanism would remove SINE elements from their positions in lineages stemming from the unknown common ancestor — that is, those elements were originally homologous (this is entailed by your assumption of common ancestry) — while simultaneously substituting unrelated SINEs in two independent lineages?
Comment by Paul Nelson — March 19, 2010 @ 8:49 am
March 19th, 2010 at 9:10 am
The genome is already sorted by AT-rich and gene GC-rich areas. This creates a landscape upon which other features interact.
http://telicthoughts.com/stern...
Comment by Zachriel — March 19, 2010 @ 9:10 am
March 19th, 2010 at 9:17 am
Hi Mike,
Does the front-loading hypothesis predict this to occur, say as a kind of "unfolding"?
Comment by KC — March 19, 2010 @ 9:17 am
March 19th, 2010 at 9:18 am
To Zachriel:
What genetic mechanism (a) deletes or removes originally homologous SINEs in two diverging lineages, while simultaneously (b) substituting unrelated SINEs in the same positions, in those lineages?
Is the mechanism one of these?
Please specify. "Creates a landscape upon which other features interact" is a nice-sounding metaphor.
Comment by Paul Nelson — March 19, 2010 @ 9:18 am
March 19th, 2010 at 9:34 am
Hi fmm,
Intriguing, yes.
Is Falk actually saying all non-coding DNA is non-functional? We know that is false, and have known it for some time.
Functions, even new ones, don't necessarily have to have positive adaptive value.
Personally, I think we have to know a lot more about how genomic architecture comes about before we can really say. Work by Michael Lynch makes the intriguing suggestion that much of it may be due to non-adaptive processes like genetic drift. I suggest his fascinating book The Origins of Genome Architecture. The patterns these kinds of forces may have on the distribution of things like SINEs have not yet been fully determined, as far as I know.
Some of the areas are proving to have function, and in some wonderfully unexpected ways.
I wonder about it a lot.
Comment by KC — March 19, 2010 @ 9:34 am
March 19th, 2010 at 9:36 am
It's largely irrelevant to Sternberg's argument that there is a pattern that emerges independently in separate lineages. The pattern is already there, inherited from the common ancestor. There is no consensus on the mechanism that sorts SINEs.
Comment by Zachriel — March 19, 2010 @ 9:36 am
March 19th, 2010 at 9:56 am
Zachriel wrote:
Point to Sternberg.
In order for the pattern to exist in an unknown common ancestor, some SINE elements must occupy the relevant positions in that ancestor. However, those positions are occupied in the mouse and rat by non-homologous SINEs.
This means that, without a genetic mechanism to sort SINEs in two diverging lineages — "no consensus" means we don't know the mechanism, sorry — there are no grounds, other than bald assertion, for saying that the pattern was inherited from a common ancestor.
"Largely irrelevant" is flat-out false, Zachriel.
Comment by Paul Nelson — March 19, 2010 @ 9:56 am
March 19th, 2010 at 9:58 am
We may have:
1. extreme similarity not due to selection
2. possible function that is mostly invisible to selection (recall if something is strongly redundant, it is not mostly visible to selection)
It would suggest seleciton had little to do with the patterns and functionality. Oddly the ability to change these areas show that neutralism is a bad explanation as well. It is possible for something to be functional without being very selectable. See: Airplane Magnetos Contingency Designs and Reasons ID will Prevail
This is deeply suggestive of design. Some areas are a testable hypothesis, and I alluded to this in various posts related to genetic entropy. If anyone remembers, I said something to the effect, "test the areas of supposed deep conservation"
See:
comment #152: Stephen Meyer's Book Ranked #1
I suggested we first looke at SNP between mice and humans, but Sternberg might have and equally better idea: mice and rats.
KC, if I recall, you had a specialty with order rodentia?
Sal
One need no such mechanism if life came from an act of recent special creation. Such problems are more reasons, on scientific grounds alone to doubt the geological record. Even if the world is Billions of years old, the geological record, as interpreted by Darwinists, could be totally out to lunch.
Comment by Salvador T. Cordova — March 19, 2010 @ 9:58 am
March 19th, 2010 at 10:31 am
Common Descent is already determined from a great deal of independent evidence. Are you disputing Common Descent? If so, you can't just look at one piece of evidence in isolation, but have to consider the body of supporting evidence.
Sternberg is only considering new SINE insertion events.
Mouse-specific and rat-specific refers to events that occurred after divergence. Sternberg is claiming the pattern only occurred after divergence, and this represents a problem for evolutionary theory. But the topology predates the posited divergence, completely consistent with evolutionary theory. This is directly contrary to his argument. There are a number of plausible mechanisms to sort new SINEs, but that's irrelevant to the point.
Puddle Logic.
Comment by Zachriel — March 19, 2010 @ 10:31 am
March 19th, 2010 at 10:41 am
Assuming you are speaking in general terms,
Retrotransposons replicate themselves in the genome, often many many times. There's still a lot unknown about how this interacts with other processes or its effect on hereditary variation.
Not necessarily the case. Duplication can increase the amount of activity.
Comment by Zachriel — March 19, 2010 @ 10:41 am
March 19th, 2010 at 11:17 am
Hi KC,
Huh? You don't know? You made the truth claim about the hypothesis. You asserted, as matter of fact, that "new function coming about by reshuffling of sequences via purely stochastic forces, cannot be considered as evidentiary support for front-loading."
Yet it turns out you don't even understand what front-loading is. Thank you for showing your cards.
Comment by MikeGene — March 19, 2010 @ 11:17 am
March 19th, 2010 at 11:31 am
Zachriel wrote:
What topology? Take away the SINEs, and the pattern disappears. To observe any topology (i.e., pattern) at all, inferred to be present in the unknown common ancestor, one needs SINE elements to give the particular or distinctive distribution along the chromosome. The only way the pattern can predate the divergence is if SINEs are present, at just the right positions, in the common ancestor.
But the SINEs in rat and mouse topologies are non-homologous.
Thus, if their chromosomal SINE distributions share common ancestry, one needs a mechanism to remove the ancestral SINES from the original topology, and to swap in new elements, in two diverging lineages.
No such mechanism is known. Point to Sternberg.
I'm curious, Zachriel: how would you reproduce this distribution in the unknown common ancestor of mouse and rat, without SINE elements?
Comment by Paul Nelson — March 19, 2010 @ 11:31 am
March 19th, 2010 at 11:39 am
Hi Mike,
Well, if I'm misrepresening front-loading, then I apologize for being ignorant. Would it it be asking too much to answer my question then?
Comment by KC — March 19, 2010 @ 11:39 am
March 19th, 2010 at 12:25 pm
SINEs represent about 7% of the rodent genomes studied, with less than 2% being lineage specific. Take away the lineage specific SINEs and the pattern remains.
http://www.zachriel.com/images...
A+T content of the rat, and density in the rat genome of LINEs and SINEs that originated since the last common ancestor of human, mouse and rat. Pink boxes highlight regions of the chromosome in which substitution rates, A+T content and LINE density are correlated. Blue boxes highlight regions in which SINE density is high but LINE density is low.
Comment by Zachriel — March 19, 2010 @ 12:25 pm
March 19th, 2010 at 12:42 pm
Actually, since you made the bold claim, I'd actually be interested in what you think the front-loading hypothesis is, given that you like to argue against it.
What is front-loading?
Comment by chunkdz — March 19, 2010 @ 12:42 pm
March 19th, 2010 at 1:41 pm
Chunk,
As I understand the Mike Gene flavor of front-loading (which I wasn't specifically addressing in my original comment), front loading suggests that life on earth was seeded with organisms which were designed in such a way as to take advantage of evolutionary processes to accomplish the original design goal. It is not, as other FL flavors suggest, an idea that those organisms had all of the essential genes packed in the genome, ready to be turned on. But it does suggest, as I said, an unfolding of the design over time. However, if we look at the processes I was talking about, i.e., new functions arising from stochastic shuffling and fortuitous joining of non-coding DNA with initiator sequences littered throught the genome, I don't see how their existence in any way is evidentiary support for front loading. They may be consistent with the hypothesis, but I would think, in order to be considered evidentiary support for it they would have to have something by which to distinguish them from the non-front-loading hypotheses, preferably as part of specific predictions.
Comment by KC — March 19, 2010 @ 1:41 pm
March 19th, 2010 at 2:19 pm
KC, front loading relies upon "new function coming about by reshuffling of sequences via purely stochastic forces".
Evidentiary support means consistency with the hypothesis. A successful front-loading program is expected to be highly adaptable.
Comment by chunkdz — March 19, 2010 @ 2:19 pm
March 19th, 2010 at 2:22 pm
Any function? If so, how can one claim that supports design?
Comment by KC — March 19, 2010 @ 2:22 pm
March 19th, 2010 at 2:56 pm
A function that displays foresight, rationality, analogy, or discontinuity would lean toward what we expect from design.
Comment by chunkdz — March 19, 2010 @ 2:56 pm
March 19th, 2010 at 3:55 pm
Zach
The problem with this argument is it proves too much.
If an intricate spot for this pattern to rest in was present in the LCA waiting to find expression then anything is possible.
Maybe the architecture for multicellulaity was present in the LCA just waiting for the proper sequences to fall in to it like a peg to a hole.
There is no need for NS in this scheme even noncoding DNA will do.
Maybe there was a spot just waiting for the gene that codes for language or consciousness or altruism.
Maybe the sequences that lead us to believe there was a LCA in the first place
Peace
Comment by fifth monarchy man — March 19, 2010 @ 3:55 pm
March 19th, 2010 at 4:04 pm
would oncogenes be a good example of front loading and design?
Or perhaps the cytochrome P450 isozymes which on occasion produce reactove (and toxic) metabolites, eg., CYP450-4E and the metabolism of acetaminophen resulting in liver damage/failure?
Comment by Acipenser — March 19, 2010 @ 4:04 pm
March 19th, 2010 at 4:07 pm
Hi chunk,
Hypothetical situation:
In a butterfly, a non-coding sequence is brought adjacent to an initiation sequence by a deletion caused by unequal crossing over. The result is a microRNA transcript which interferes in the expression of a specific gene, resulting in a minor change in wing shape. In lowland meadows, the change is adaptively neutral. However, in fields at slightly higher altitudes, this wing shape stabilizes flight better during wind gusts, providing a reproductive advantage when trying to escape from predators.
How does this new function fit (or not fit) with the criteria you gave above? I'm not trying to pose some trick question here, just trying to get an idea for what you mean by your stated criteria.
Comment by KC — March 19, 2010 @ 4:07 pm
March 19th, 2010 at 4:13 pm
deleted —-duplicate post.
Comment by Acipenser — March 19, 2010 @ 4:13 pm
March 19th, 2010 at 4:34 pm
Mike Gene:
KC:
I too am a little puzzled. Perhaps Mr Gene could refer us to the current consensus definition of front-loading. There often is much discussion of the inadequacies of some aspect of evolutionary theory but less about the adequacies of competing theories.
Comment by zykander — March 19, 2010 @ 4:34 pm
March 19th, 2010 at 5:03 pm
Some might.
Take Myc, for instance. Since it is thought to have been crucial for the development of metazoa, it seems to have the hallmarks of foresight.
I score it a +2 on the design matrix.
Sorry, don't know much about this.
Comment by chunkdz — March 19, 2010 @ 5:03 pm
March 19th, 2010 at 5:17 pm
Minor phenotype modifications are perfectly within the purported abilities of a blind, stupid tinkerer.
However, the choice of proteins as the original building material to allow such adaptive facility – that certainly seems like an extremely fortuitous choice for a blind, stupid tinkerer to make.
And for a blind, stupid tinkerer to choose a globally optimal code right from the get go, well that was extremely lucky as well, no?
Comment by chunkdz — March 19, 2010 @ 5:17 pm
March 19th, 2010 at 5:50 pm
Hi Chunk,
So acquisition of functionality for non-coding DNA of this nature is not considered evidentiary support for front-loading because it can be accomplished via blind, stochastic forces. Interesting. That was my original point.
Comment by KC — March 19, 2010 @ 5:50 pm
March 19th, 2010 at 6:13 pm
given that oncogenes/proto oncogenes are found at every step involved in all aspects of cell divison, growth, signal transduction, ect which ones should we consider front loaded and which ones not so much?
For example p53 is perhaps the most commonly found mutation in cancers and p53 controls the cell cycle during division. Is the gene that encodes this protein considered as being front loaded given its importance in control of cell division?
Is cancer the hallmark of foresight?
There are a host of metabolic enzymes (gene products) that produce reactive and/or genotoxic metabolites. One is the example I gave above and another would be the metabolism of benzo(a)pyrene. Do you think the formation of metabolic end products (toxic or not) are representative of front loading?
Comment by Acipenser — March 19, 2010 @ 6:13 pm
March 19th, 2010 at 6:29 pm
No your point was a negative one – namely "This latter possibility, that of new function coming about by reshuffling of sequences via purely stochastic forces, cannot be considered as evidentiary support for front-loading." [emph. mine]
What if the mechanisms for reshuffling were designed to harness the power of the blind stupid tinkerer?
Comment by chunkdz — March 19, 2010 @ 6:29 pm
March 19th, 2010 at 6:40 pm
Would the Philadelphia chromosome be an example of this front loading functionality?
Comment by Acipenser — March 19, 2010 @ 6:40 pm
March 19th, 2010 at 6:52 pm
Again, the criteria are foresight, rationality, analogy, and discontinuity.
Personally, I find an oncogene that facilitates multicellularity would have been a rational foresight for a designer who was hoping to create metazoa.
I assume this is just your snarky version of a "no true designer" argument?
I assume this is also part of your "no true designer" fallacy?
Comment by chunkdz — March 19, 2010 @ 6:52 pm
March 19th, 2010 at 6:58 pm
Space Shuttles explode. I suppose they weren't designed then.
Comment by chunkdz — March 19, 2010 @ 6:58 pm
March 19th, 2010 at 7:04 pm
nope, no snarkyness at all but they are very real examples (and extremely common at that) that I think someone should be able to address with the front loading hypothesis/theory.
pretty much all oncogenes promote multicellularity and the problem with that is the "loss of control" over cell division. Basically what you appear to be saying is that cancer is a sign of a designer.
Proto oncogene, on the other hand, protein products also result in multcellularity/differentiation but are not characterised by a 'loss of control' of the process. However, these proto oncogenes are easily transformed into oncogenes with simple point mutations (as well as other mutations/translocations/transductions) and if these most important genes are not representative of front loading which ones are representative of front loading?
Comment by Acipenser — March 19, 2010 @ 7:04 pm
March 19th, 2010 at 7:08 pm
The Philadelphia chromosome is a result of translocation of portions of two genes…the process that you argue is representative of front loading. So given your remark (snarky or not) I suppose then that cancer is a characteristic of a designer or, alternately, that the front loading concept has some serious issues it needs to address with better answers than the space shuttle explodes and since it is designed then the Philadelphis chromosome is also designed. Seems like a very poor analogy that you are makng but whatever floats your boat.
Comment by Acipenser — March 19, 2010 @ 7:08 pm
March 19th, 2010 at 7:34 pm
No, I said foresight, rationality, analogy, and discontinuity were hallmarks of design.
The problem with harnessing a blind stupid tinkerer to do your work for you is that he is, well, blind and stupid. Left to his own devices and given dirt to play with he will pretty much just swirl dirt around the sandbox. But if you give the blind stupid tinkerer some advanced tools to play with, he can turn those tools into beautiful and extravagantly complex conscious lifeforms.
And yes, they will all die someday at the blind stupid tinkerers hand.
Comment by chunkdz — March 19, 2010 @ 7:34 pm
March 19th, 2010 at 7:44 pm
No. Foresight, rationality, analogy, and discontinuity are characteristics of design.
Point mutations are the tinkerings of blind stupid tinkerers.
Comment by chunkdz — March 19, 2010 @ 7:44 pm
March 19th, 2010 at 7:50 pm
Hi chunk,
You gave the criteria for determining whether or not functionality could be considered evidentiary support for design, then ruled out my example (and other functionality arising purely stochastic forces), saying they were well within the realm of the "blind stupid tinkerer". Now you're saying they COULD be considered evidentiary support if we NOW accept the premise that the designer set up the blind stupid tinkerer in the first place!
Is there a good reason to think that? If not, I smell the signs of ad hocery !
Comment by KC — March 19, 2010 @ 7:50 pm
March 19th, 2010 at 7:56 pm
OK, if point mutations are the tinkerings of blind stupid tinkerers then should we consider all the other mechanisms that are known to mutate a proto oncogene into a oncogene as also being the work of a blind stupid tinkerer?
If your answer is yes, then that really leaves nothing for the front loading theory to work with given the number and variety of mechanisms that are known to mutate proto oncogenes.
Where do oncogenes/proto oncogenes fit into the front loading scenario?
Given that >1% of human genes are proto oncogenes should we toss them out of consideration of the front loading theory? Especially, since foresight should have made someone/something/some designer realize that a single screw up in those genes promotes cancer development. By analogy killing the product of design via design flaw represents poor design….kinda like a Ford pinto.
Then maybe we can get back to metabolism and its foibles.
Comment by Acipenser — March 19, 2010 @ 7:56 pm
March 19th, 2010 at 8:35 pm
We know deletion events occur and that they can enhance or alter function.
Maybe. Maybe not. If a designer wanted to seed a planet to produce conscious metazoa, he would likely have incorporated the toolkit for metazoan life in the pre-multicellular stage. There is evidence to suggest this is the case, and this bears the hallmarks of design.
Might be wrong, but I find it intriguing.
Comment by chunkdz — March 19, 2010 @ 8:35 pm
March 19th, 2010 at 8:49 pm
Yes, the blind stupid tinkerer has many, many ways of tinkering with things. Sometimes they get better, sometimes they don't. He sure is stupid! Makes you wonder how people ever got the crazy idea that he made life from dirt!
Not every Pinto exploded. Not every metazoan gets cancer.
Yet both bear the hallmarks of design.
Comment by chunkdz — March 19, 2010 @ 8:49 pm
March 19th, 2010 at 9:11 pm
The pinto was removed from production in recognition of the design flaw.
In any case it seems to me that if we assign all the mechanisms that can mutate a proto oncogene to the stupid blind tinkerer there are no tools remaining in the front loaders toolbox.
I think you answered your own question.
Comment by Acipenser — March 19, 2010 @ 9:11 pm
March 19th, 2010 at 9:21 pm
Yet it was designed.
And we will all likely be removed from production someday. Flaws and all.
The stupid blind tinkerer IS a tool. The design occurred long ago.
Do you believe the blind stupid tinkerer made dirt come alive?
Comment by chunkdz — March 19, 2010 @ 9:21 pm
March 19th, 2010 at 9:26 pm
KC,
How about the fact that we have indisputable knowledge of multiple designers who are capable of setting up "blind stupid tinkerers" with intention and foresight, and have demonstrably done so. Meanwhile, not only do we have no such knowledge of blind stupid tinkerers brutely existing or "just popping into existence uncaused", etc, but such knowledge – even if it were true – will in principle forever elude us by its nature.
Of course, I'd also throw in that any blind stupid tinkerer who was set up and is working as intended can hardly be called blind or stupid in any relevant or meaningful sense. Hell, there's problems with "tinkerer", but that's less of an issue.
Comment by nullasalus — March 19, 2010 @ 9:26 pm
March 19th, 2010 at 9:49 pm
Was the 'tool' designed as well? I would also assume (perhaps incorrectly) that you would think that the foresight of the 'tool's' actions would/is incorporated into the design.
If yes, then we are back to cancer(s) of all manner are front loaded into the organism by design. You seemed to argue against this earlier but now seem to have come full circle.
Comment by Acipenser — March 19, 2010 @ 9:49 pm
March 19th, 2010 at 10:51 pm
Frontloading is a hypothesis about life's origin only.
Yes, I'd presume that the designer was aware of the capabilities of the stupid blind tinkerer, since this is an integral part of evolution.
Not just cancer, but death of all sorts. We all die at the hands of the blind stupid tinkerer. (Turns out he's pretty stupid and he doesn't care.)
But we also evolve. Not just endless forms most beautiful, but conscious and aware that we are created. Intelligent. Creative. A successful project.
We can then conclude one of two things based upon our working assumption. Either the designer (1) failed at his goal of creating creatures that would never suffer and never die, or…
(2)…the designer was wildly successful at the goal of turning dirt into conscious life, and the goal was apparently NOT to create living creatures that never suffered and never died.
Whichever one it was, the hallmarks of design are present.
Comment by chunkdz — March 19, 2010 @ 10:51 pm
March 19th, 2010 at 11:14 pm
chunkdz, if the mechanisms of evolution are the mechanisms of the stupid blind tinkerer then we need to consider option three and that is:
3) The stupid blind tinkerer has done a wonderful job at evolving endless forms of life and since the stupid blind tinkerer was not designed there is no need for a designer to explain anything.
What would unconcious life look, or act, like?
And logically cancer is a hallmark of design.
Comment by Acipenser — March 19, 2010 @ 11:14 pm
March 20th, 2010 at 7:29 am
Acipencer,
I have no problem attributing things like cancer to the designer. My theology demands as much.
I am the LORD, and there is no other, besides me there is no God; I equip you, though you do not know me, that people may know, from the rising of the sun and from the west, that there is none besides me; I am the LORD, and there is no other. I form light and create darkness, I make well-being and create calamity, I am the LORD, who does all these things.
(Isaiah 45:5-7)
If you have a hang up with accepting that such things could be the result of design I would suggest that there are other venues to get that fixed. It is probably not helpful to let it influence your evaluation of the evidence.
The fact that you don't like the implications is no excuse to deny the obvious.
peace
Comment by fifth monarchy man — March 20, 2010 @ 7:29 am
March 20th, 2010 at 11:17 am
Puddle logic. The intricacy of the landscape is irrelevant. Sternberg's argument depends on the pattern not being there in the common ancestor.
Comment by Zachriel — March 20, 2010 @ 11:17 am
March 20th, 2010 at 6:50 pm
It might be irrelevant as to whether this particular DNA is junk but it is very relevant to the TOE in general.
If you are willing to concede that something this intricate can be preserved with out reference at all to actual selection then nothing in the genome can be attributed to NS selection. Perhaps it all is just due geography.
You have just given away the entire Darwinist farm.
I'm really not concerned with Sternberg's argument one way or the other right now. The exact amount of junk DNA is just a side issue IMHO.
What does interest me greatly is that you are conceding that there is a built in ability to conserve such a large and intricate pattern in the genome for millions of years with no regard to what it’s actual genetic content does.
We have just found the mother of all frontloading mechanisms and Zach is the one arguing for it.
Like I said Flipping amazing
peace
peace
Comment by fifth monarchy man — March 20, 2010 @ 6:50 pm
March 21st, 2010 at 10:55 pm
Imagine you want to hire a stupid blind tinkerer to make conscious metazoans. Wouldn't you give him the best tools available to maximize his chances of success? Wouldn't you give him seeds with a metazoan toolkit in place? Or would you give him a handful of dirt and wait patiently as he moves his hands back and forth through the sandbox?
Makes much more sense the first way, no?
Viruses?
Proto-oncogenes probably are. And cancer cells bear all the hallmarks of normal cells as far as mature design goes.
I've answered many of your questions, acipenser, but you haven't answered mine.
Do you believe that the blind stupid tinkerer made dirt become alive?
Comment by chunkdz — March 21, 2010 @ 10:55 pm
March 22nd, 2010 at 8:19 am
We were addressing just the one particular of Sternberg's argument, that the similar pattern of SINEs across the genomes in mice and rates postdates the divergence.
The topology predates the posited divergence, consistent with evolutionary theory.
Huh? Some of the topology consists of genes and regulatory regions under selection. Other sections are drifting, but the rate of genomic change is small compared to the short time scales involved, about 22 million years. Furthermore, there are many changes to the genomes not encompassed in such a comparison. For instance, the rat genome is estimated to be about 2.75 GB, while the mouse genome is estimated to be about 2.6 GB.
You can't understand evolution by only looking at AT-GC enrichments across the genome.
It was the thread topic, after all.
Of course it's conserved. Rates of evolution tend to be small compared to the timescales involved; except in cases of strong selection, then the changes tend to be very localized.
Comment by Zachriel — March 22, 2010 @ 8:19 am
March 23rd, 2010 at 4:06 pm
As examples of what random effects can do to a good design.
ID does not say that random effects do not occur or that they do not have any affect.
Comment by ID guy — March 23, 2010 @ 4:06 pm
March 23rd, 2010 at 4:08 pm
So you say but when push comes to shove it never pans out.
Heck you once thought- and probably still do- that Common Descent expects a nested hierarchy.
IOW you aren't in any position to talk about evidence.
Comment by ID guy — March 23, 2010 @ 4:08 pm
March 23rd, 2010 at 7:26 pm
Amen to that!
http://www.topical-bible-studi...
I find the suggestion that God would never create death to be silly at best, ignorant at worst.
Comment by chunkdz — March 23, 2010 @ 7:26 pm
March 25th, 2010 at 3:54 pm
Zachiel
Those of your critics who are interested in that topology may have a look into Farwick et al. (2006) Automated Scanning for Phlegmatically Informative Transposed Elements in Rodents Syst Biol 55: 936-948
That new SINES are inserted in orthologous loci may be caused by the insertion mechanism that uses parts of the LINE machinery. As Yang and co-workers stated:
( Yang S (2004) Patterns of Insertions and Their Covariation With Substitutions in the Rat, Mouse, and Human Genomes. Genome Res 14:517-527
Comment by sparc — March 25, 2010 @ 3:54 pm
March 26th, 2010 at 1:17 am
Unfortunately, I didn't notice that my spell checker changed "phylogentically" to "phlegmatically". Sorry for that. The link still works though.
Comment by sparc — March 26, 2010 @ 1:17 am